Noble Laureate’s work tracked by GBMD

 

We have followed the research work published by Nobel laureates Profs. Schekman Randy, Sudhof C Thomas, Shinya Yamanaka, Gurdon JB, Phil Sharp, David Baltimore, Elizabeth H. Blackburn, Carol W Greider, Beutler A Bruce, Ferid M and Ignarro LJ  and published a number of ideas related to their research work:

S.No

Ideas based on Nobel Laureate’s work is posted by GBMD’s
Director-cum-Chief Scientist

Dr L Boominathan PhD

1

 

1

Celastrol, an antioxidant and  anti-inflammatory drug, suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target gene

The Nobel Prize Winner in Physiology/Medicine (1975) Prof. David Baltimore from California Institute of Technology (Caltec), California, USA, has
reported in a number of prestigious journals that
NFKB regulates the expression of a number of miRNAs. In connection with Nobel Laureate Baltimore’s findings,                                 Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports that  Celastrol, an antioxidant and  anti-inflammatory drug, suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target gene. To cite: Boominathan, Molecular cancer therapy: Celastrol, an antioxidant and anti-inflammatory drug, suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target gene,  7/February/2014, 22.13, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more at:

http://genomediscovery.org/research/news

2

Treating human cancer with  Thunder of God vine: Celastrol, an antioxidant & anti-inflammatory drug from herb Thunder of God vine, increases the expression of tumor suppressor p16(Ink4a) via down regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Ferid M (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers. In connection with this
finding,                
Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Treating human cancer with  Thunder of God vine: Celastrol, an antioxidant & anti-inflammatory drug from herb Thunder of God vine, increases the expression of tumor suppressor p16(Ink4a) via down regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may aid cancer therapy. To cite: Boominathan, Treating human cancer with Thunder of God vine: Celastrol, an antioxidant & anti-inflammatory drug from herb Thunder of God vine, increases the expression of tumor suppressor p16(Ink4a) via down regulation of its target gene, 14/March/2014, 23.42, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org.

– See more at: http://genomediscovery.org/research/news

3

Treating cancer with longevity promoting  drugs: Resveratrol, a longevity promoting  small molecule, suppresses the expression of NOS2 via up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Ferid M (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers. In connection with this finding, Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Treating cancer with longevity promoting  drugs: Resveratrol, a longevity promoting  small molecule, suppresses the expression of NOS2 via up regulation of its target gene. This study provides mechanistic insights into how Resveratrol inhibits the expression of NOS-2To citeBoominathan, Treating cancer with longevity promoting  drugs: Resveratrol, a longevity promoting  small molecule, suppresses the expression of NOS2 via up regulation of its target gene, 13/March/2014, 11.55, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

– See more at: http://genomediscovery.org/research/news

4

Treating cancer with  Thunder of God vine: Celastrol, an
antioxidant & anti-inflammatory drug from herb Thunder of God vine, suppresses the expression of NOS2 via up regulation of its target gene 

Noble Laureate in Medicine (1998) Prof. Dr Ferid M (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition
of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers. In connection with this finding, 
Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Treating cancer with Thunder of God vine: Celastrol, an antioxidant & anti-inflammatory drug from herb Thunder of God vine, suppresses the expression of NOS2 via up regulation of its target gene. This study provides mechanistic insights into
how Celastrol inhibits the expression of  NOS-2. To cite: Boominathan, Treating cancer with  Thunder of God vine: Celastrol, an antioxidant & anti-inflammatory drug from herb Thunder of God vine, suppresses the expression of NOS2 via up regulation of its target gene, 13/March/2014,
11.45, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

– See more at: http://genomediscovery.org/research/news/

 

5

Mechanistic insights into Cancer therapy: NOS-2 increases the levels of cell cycle protein Cyclin D1 via up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Ferid M (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers. In connection with this finding,                    Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Mechanistic insights into Cancer therapy: NOS-2 increases the levels of cell cycle protein Cyclin D1 via up regulation of its target gene. This study provides mechanistic insights into
why increased expression of NOS-2 promotes tumorigenesis, while inhibition of its expression  improves
caner therapy. To cite: Boominathan, Mechanistic insights into Cancer therapy: NOS-2 increases the levels of cell cycle protein Cyclin D1  via up regulation of its target gene, 11/March/2014, 13.47, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See
more at: http://genomediscovery.org/research/news

6

Molecular insights into Cancer therapy: NOS-2 suppresses the expression of  tumor suppressor TNFAIP8L2  via
up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Ferid M (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers. In connection with this finding,                          

Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of
tumor 
suppressor TNFAIP8L2  via up regulation of its target gene
. This study provides mechanistic insights into how inhibition of NOS-2 may improve caner therapy.To cite: Boominathan, Insights
into Molecular cancer therapy: NOS-2 suppresses the expression of tumor suppressor TNFAIP8L2 via up regulation of its target gene, 3/March/2014, 8.50 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more at: http://genomediscovery.org/research/news

7

Molecular insights into Cancer therapy: NOS-2 suppresses the expression of  tumor suppressor RECK via
up regulation of its target gene

National Science day special: We wish everyone a very happy National Science day. On this special occasion, we are happy to announce that ideas posted today (28/February/2014) will be available to the use of Scientists/Professors/Physicians/Researchers for free. So, there will be no terms and conditions for the ideas posted today (28/February/2014). Each idea posted will be served first come, first served basis.Write to info@genomediscovery.org for more details about the ideas posted.-Dr L Boominathan PhD, Director, GBMD.

Noble Laureate in Medicine (1998) Prof. Dr Ferid M (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers. In connection with this finding,  Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor RECK via up regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may improve caner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of  RECK tumor suppressor via up regulation of its target gene, 28/February/2014, 9.05 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

8

 Molecular insights into Cancer therapy: NOS-2 suppresses
the expression of  tumor suppressor lncRNA GAS5 via up regulation of its
target gene

Noble Laureate in Medicine (1998) Prof. Dr Ferid M  (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers. In connection with this finding, Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor lncRNA GAS5 via up regulation of its target gene. This study provides mechanistic insights into
how inhibition of NOS-2 may improve caner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of  tumor suppressor lncRNA GAS5  via up regulation of its
target gene, 27/February/2014, 8.56 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

9

Molecular insights into Cancer therapy: NOS-2 suppresses the expression of pro-apoptotic protein Fas Ligand
(FasL)  via up regulation of its target gene 

Noble Laureate in Medicine (1998) Prof. Dr Ferid M  (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have
a therapeutic value in a number of cancers. In connection with this finding,                                                 Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights
into Cancer therapy: NOS-2 suppresses the expression of pro-apoptotic protein Fas Ligand (FasL)  via
up regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may improve caner therapy To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of  pro-apoptotic protein Fas Ligand (FasL) via up regulation of its target gene, 24/February/2014, 10.00 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
– See more at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

10

Molecular insights into Cancer therapy: NOS-2 suppresses the expression of pro-apoptotic protein BTG2  via up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Ferid M  (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers.   In connection with this finding, Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of pro-apoptotic protein BTG2  via
up regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may improve caner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of  pro-apoptotic protein BTG2 via up regulation of its target gene, 22/February/2014, 22.13, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
– See more at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

11

Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor p53 homologue TAp63  via up regulation of its target gene 

Noble Laureate in Medicine (1998) Prof. Dr Ferid M  (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have
a therapeutic value in a number of cancers.  In connection with this finding, Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor p53 homologue TAp63  via up regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may improve cancer therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of tumor suppressor p53 homologue TAp63 via up regulation of its target gene, 20/February/2014, 7.43 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
– See more at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

12

Molecular insights into Cancer therapy: NOS-2 suppresses the
expression of DNA repair protein hMSH2 via up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Ferid  M (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have
a therapeutic value in a number of cancers.   In connection with this finding,                                                Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of DNA repair protein hMSH2 via up regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may improve caner
therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of DNA repair protein hMSH2 via up regulation of its target gene, 19/February/2014, 10.13 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more
at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

13

Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor GRHL3  via up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Feirid  (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers.   In connection with this finding, Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor GRHL3  via up regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may improve caner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of tumor suppressor GRHL3 via up regulation of its target gene, 18/February/2014, 10.49 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

14

Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor PDCD4 via up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Feirid  (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers.   In connection with this finding, Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor PDCD4 via up regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may improve caner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of tumor suppressor PDCD4 via up regulation of its target gene, 17/February/2014, 8.54 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more
at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

15

 Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor TIMP3 via up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Feirid  (The University of Texas, Houston, Texas, USA) has suggested in a number of papers that inhibition of NOS2 (Nitric oxide synthase) may have a therapeutic value in a number of cancers.  In connection with this finding, Dr L Boominathan, Director-cum-chief scientist of GBMD, reports that: Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor TIMP3 via up regulation of its target gene. This study provides mechanistic insights into how inhibition of NOS-2 may improve caner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression of tumor suppressor TIMP3 via up regulation of its target gene, 16/February/2014, 7.18 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more
at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

16

Insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor KRIT1/CCM1 via up regulation of its target gene

Noble Laureate in Medicine (1998) Prof. Dr Feirid  (The University of Texas, Houston,
Texas, USA) has suggested in a number of papers that inhibition
of NOS2 (Nitric oxide synthase) may have
a therapeutic value in a number of cancers.  In connection with this
finding, Dr L Boominathan, Director-cum-chief
scientist of GBMD, reports that: Insights into Cancer therapy: NOS-2
suppresses the expression of tumor
suppressor KRIT1/CCM1 via up regulation of its target
gene. This study provides mechanistic insights into how inhibition of
NOS-2 may improve caner therapy. To
cite: Boominathan, Insights into Cancer
therapy: NOS-2 suppresses the expression of tumor
suppressor KRIT1/CCM1 via up regulation of its target gene,
15/February/2014, 14.40, Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

17

Insights into Cancer therapy: NOS-2 suppresses the expression
of tumor suppressor TPM1 via up regulation of its
target gene

Noble Laureate in Medicine (1998) Prof. Dr Feirid  (The University of Texas, Houston,
Texas, USA) has suggested in a number of papers that inhibition
of NOS2 (Nitric oxide synthase) may have
a therapeutic value in a number of cancers.  In connection with this
finding, Dr L Boominathan, Director-cum-chief
scientist of GBMD, reports that: Insights into Cancer therapy: NOS-2
suppresses the expression of tumor suppressor TPM1
via up regulation of its target gene. This study provides mechanistic
insights into how inhibition of NOS-2 may improve caner
therapy. To cite: Boominathan, Insights
into Cancer therapy: NOS-2 suppresses the expression of tumor
suppressor TPM1 via up regulation of its target gene, 15/February/2014,
14.35, Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

18

Dismantling stem cell network: Tumor suppressor p53
inhibits the embryonic stem cell transcriptional network through induction of its target gene peptidylarginine deiminase-4

Prof. Dr Kouzarides and
the Nobel Prize Winner in
Physiology/Medicine (2012)  Prof Dr Gurdon
JB  from  Cancer Research Gurdon Institute, Cambridge,
UK reports in the prestigious journal Nature
(2014) that “Citrullination regulates pluripotency….”  On the foundation of this
interesting finding, Dr L Boominathan PhD,
Director-cum-chief Scientist of GBMD, reports that: Dismantling stem
cell network: Tumor suppressor p53 inhibits
the embryonic stem cell transcriptional network through induction of its
target gene peptidylarginine
deiminase-4. Furthermore, Dr Boominathan
identifies the mechanism by which p53 and its homologues p63 and p73 regulate citrullination of arginine residues
in proteins. This exciting finding explains how stress induced p53 and
its homologues TA-p63 and TA-p73  inhibit
the pluripotency transcriptional network in normal
cells and in cancer cells.  To cite: Boominathan,
Dismantling stem cell network: Tumor
suppressor p53 inhibits the embryonic stem cell transcriptional network
through induction of its target gene peptidylarginine
deiminase-4, 10/February/2014, 8.34 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more
at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

19

Celastrol, an antioxidant and  anti-inflammatory drug, suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target gene

The Nobel Prize Winner in Physiology/Medicine
(1975), Prof.
David Baltimore from California Institute of
Technology (Caltec), California, USA, has
reported in a number of prestigious journals that NFKB regulates
the expression of a number of miRNAs. In connection
with Nobel Laureate Baltimore’s findings, Dr Boominathan,
Founder Director-cum-chief scientist of GBMD, reports that  Celastrol, an
antioxidant and  anti-inflammatory drug, suppresses the expression
of epigenetic integrator UHRF1 via up regulation of its
target gene. To cite: Boominathan, Molecular
cancer therapy: Celastrol, an antioxidant
and  anti-inflammatory drug, suppresses the expression
of epigenetic integrator UHRF1 via up regulation of its
target gene,  7/February/2014, 22.13, Genome-2-Bio-Medicine
Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

20

BRMS1 (Breast cancer metastasis suppressor 1) suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target gene

The Nobel Prize Winner in Physiology/Medicine
(1975), Prof. David Baltimore from California Institute of
Technology (Caltec), California, USA, has
reported in a number of prestigious journals that NFKB regulates the
expression of miR-146. In connection with Nobel Laureate Baltimore’s
findings, Dr Boominathan, Founder
Director-cum-chief scientist of GBMD, reports
that  BRMS1 (Breast cancer metastasis suppressor
1) suppresses the expression of epigenetic integrator UHRF1 via up regulation
of its target gene. To cite: Boominathan, BRMS1 (Breast
cancer metastasis suppressor 1) suppresses the expression of epigenetic
integrator UHRF1 via up regulation of its target gene, 6/February/2014,
12.39 pm, Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

21

NFKB suppresses the expression of epigenetic integrator UHRF1
via up regulation of its target gene

The Nobel Prize Winner in Physiology/Medicine
(1975), Prof. David Baltimore from California Institute of
Technology (Caltec), California, USA, has reported
in a number of prestigious journals that NFKB regulates the expression
of a number of miRNAs. In connection with Nobel
Laureate Baltimore’s findings, Dr Boominathan,
Founder Director-cum-chief scientist of GBMD, reports that  NFKB suppresses the expression of epigenetic
integrator UHRF1 via up regulation of its target gene. To cite: Boominathan, NFKB suppresses the expression of
epigenetic integrator UHRF1 via up regulation of its target
gene, 6/February/2014, 12.29 pm, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more
at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

22

Insights into the regulation of a mid-gestation developmental program: Metformin decreases Nr6a1 and embryonic gene expression programs in adult cells

 

Noble Laureate Prof. Phil Sharp (from MIT,
Cambridge, USA) has published a paper in the Journal Genes &
Development stating that Let-7 represses Nr6a1 and a mid-gestation
developmental program in adult cells.  This study suggests that
“let-7 is required for the continual suppression of embryonic gene expression
in adult cells.“   In connection with this
finding, Dr L Boominathan, Director-cum-chief
scientist of GBMD, reports that:  Insights into the regulation of a
mid-gestation developmental program: Metformin decreases
Nr6a1 and embryonic gene expression programs in adult cells. This study
may through light into the tumor suppressive action
of  Metformin. To
cite: Boominathan, Insights into the
regulation of a mid-gestation developmental program: Metformin decreases
Nr6a1 and embryonic gene expression programs in adult
cells,  29/December/2013, 7.33 am, Genome-2-Bio-Medicine Discovery
center (GBMD), http://genomediscovery.org –
See more at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

23

Insights into the regulation of a mid-gestation developmental program: Estrogens (E2) decrease Nr6a1 and embryonic gene expression programs in adult cells

Noble Laureate Prof. Phil Sharp (from MIT,
Cambridge, USA) has published a paper in the Journal Genes &
Development stating that Let-7 represses Nr6a1 and a mid-gestation
developmental program in adult cells.  This study suggests that
“let-7 is required for the continual suppression of embryonic gene expression
in adult cells.“   In connection with this
finding, Dr L Boominathan, Director-cum-chief
scientist of GBMD, reports that:  Insights into the regulation of a
mid-gestation developmental program: Estrogens (E2) decrease Nr6a1
and embryonic gene expression programs in adult cells. This study may
through light into the tumor suppressive action of
Estrogens. To cite: Boominathan, Insights
into the regulation of a mid-gestation developmental
program: Estrogens decrease Nr6a1 and embryonic gene
expression programs in adult cells, 24/December/2013, 8/56
am,Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

24

Insights into the regulation of a mid-gestation developmental program: Androgens decrease Nr6a1 and embryonic gene expression programs in adult cells 

 

Noble Laureate Prof. Phil Sharp (from MIT,
Cambridge, USA) has published a paper in the Journal Genes &
Development stating that Let-7 represses Nr6a1 and a mid-gestation
developmental program in adult cells.  This study suggests that
“let-7 is required for the continual suppression of embryonic gene expression
in adult cells.“   In connection with this
finding, Dr L Boominathan, Director-cum-chief
scientist of GBMD, reports that:  Insights into the regulation of a
mid-gestation developmental program: Androgens decrease Nr6a1 and
embryonic gene expression programs in adult cells. This study may
through light into the tumor suppressive action of  androgens. To cite: Boominathan, Insights
into the regulation of a mid-gestation developmental program: Androgens
decrease Nr6a1 and embryonic gene expression programs in adult cells, 24/December/2013,
7.35 am,Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

25

Insights into the regulation of a mid-gestation developmental program: 1,25-Dihydroxyvitamin D3 suppresses Nr6a1 and  embryonic gene expression programs in adult cells

Noble Laureate Prof. Phil Sharp (from MIT,
Cambridge, USA) has published a paper in the Journal Genes &
Development stating that Let-7 represses Nr6a1 and a mid-gestation
developmental program in adult cells.  This study suggests that
“let-7 is required for the continual suppression of embryonic gene expression
in adult cells.“   In connection with this
finding, Dr L Boominathan, Director-cum-chief
scientist of GBMD, reports that:  Insights into the regulation of a
mid-gestation developmental program: 1,25-Dihydroxyvitamin
D3 suppresses Nr6a1 and  embryonic gene expression programs in adult
cells. This study may through light into the tumor
suppressive action of  1,25-Dihydroxyvitamin
D3. To cite: Boominathan, Insights into
the regulation of a mid-gestation developmental program:
1,25-Dihydroxyvitamin D3 suppresses Nr6a1 and embryonic gene
expression programs in adult cells, 24/December/2013, 7.24
am,Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

26

Let-7 miRNA increases the expression of tumor suppressor p53 homologue p73 via down
regulation of its target gene

 

Noble Laureate Prof. Shinya Yamanaka (from San
Francisco, USA) has reported in the journal Cell Stem Cell that
“The let-7/LIN-41 Pathway Regulates Reprogramming to Human Induced Pluripotent Stem Cells by Controlling Expression of Prodifferentiation Genes.“ As a follow-up of this
study, here, Dr Boominathan,
Chief-Scientist-cum-Director of GBMD, reports that Let-7 miRNA increases the expression of tumor
suppressor p53 homologue p73 via down regulation of its target gene,
14/December/2013, 8.44 am. To cite: Boominathan, The
Follow-up of Noble laureates’s (Shinya Yamanaka) favorite work: Let-7 miRNA
increases the expression of tumor
suppressor p53 homologue p73 via down regulation of its target
gene, 14/December/2013, 8.44 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org – See more
at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

27

LIN-41/TRIM71 suppresses the expression of p53 homologue p73 via down regulation of its target gene

 

The Follow-up of Noble laureates’s
(Shinya Yamanaka) favorite work: LIN-41/TRIM71
suppresses the expression of p53 homologue p73 via down regulation of its
target gene, 14/December/2013, 8.31 am. Noble Laureate Prof. Shinya
Yamanaka (from San Francisco, USA; Japan) has reported in the journal
Cell Stem Cell that “The let-7/LIN-41 Pathway Regulates
Reprogramming to Human Induced Pluripotent Stem
Cells by Controlling Expression of Prodifferentiation
Genes.“ As a follow-up of this study, here, Dr Boominathan,
Chief-Scientist-cum-Director of GBMD, reports that LIN-41/TRIM71
suppresses the expression of p53 homologue p73 via down regulation of
its target gene, 14/December/2013, 8.31 am. To cite: Boominathan, The Follow-up of Noble laureates’s (Shinya Yamanaka) favorite
work: LIN-41/TRIM71 suppresses the expression of p53 homologue p73 via
down regulation of its target gene, 14/December/2013, 8.31 am,
Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

28

ATRA (Vitamin A) decreases IFN regulatory factor 4 (IRF4) expression via up regulation of its target gene

 

Noble Laureate Prof. David Baltimore (USA) has
reported in the Journal Immunology ( J Immunol. 2011 Nov 15;187(10):5062-8) that
miRNAs play a significant role in stimulating
/Immune cell
activation.  In connection with this study, here, Dr L Boominathan, Director-cum-chief Scientist of GBMD,
reports that ATRA (Vitamin A) decreases IFN regulatory factor 4 (IRF4) expression via up regulation of its target gene.
Thereby, ATRA (Vitamin A) augments  /Immune cell activation. Together, this
study suggests that Vitamin-A can be used to augment immune cell
activation. To cite: Boominathan, L,
Vitamin-mediated /Immune cell activation:
ATRA (Vitamin A) decreases IFN regulatory factor 4 (IRF4) expression via up
regulation of its target gene, 7/December/2013, 5.49
am,  Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org – See more at:
http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf

29

The Follow-up of Nobel laureates’s (Sudhof C Thomas) favorite work: Drosha inhibits the induction of functional neurons from human IPSCs and ESCs, 24/October/2013, 6.33 am

Amount – $ 500*/-

This year’s Nobel prize winner for Physiology
or Medicine 
Prof. Sudhof
C Thomas
 (from Stanford University,
California, USA) has published a paper in the Journal Neuron stating
that ”
Rapid single-step induction of
Functional neurons from Human pluripotent stem
cells
.”  This study suggests that
“Neurogenin-2 overexpression rapidly transforms
ESCs and iPSCs into neurons.”

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports thatDrosha inhibits the induction of functional neurons from human IPS cells This finding suggests that targeting the expression of nuclear miRNA-processing
enzyme, Drosha, in iPScs
and ESCs may aid the generation of functional neurons

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, The Follow-up of Nobel laureates’s (Sudhof C Thomas) favorite work:
Drosha inhibits  the induction of
functional neurons from human IPSCs and ESCs, 24/October/2013, 6.33
am, Genome-2-Bio-Medicine Discovery center
(GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at: http://genomediscovery.org/drosha-inhibits-the-induction-of-functional-neurons-from-human-ipscs-and-escs-via-down-regulation-of-its-target-gene-24october2013-6-33-am/#sthash.KPLvtJ97.dpuf

30

Connecting with Nobel’s [Sudhof C Thomas] findings: Size doesn’t matter- action matters: p53/p63/p73-dependent microRNAs regulate the induction of functional neurons from human IPSCs and ESCs, 23/October/2013, 13.42

Amount – $ 500*/-

This year’s Nobel prize winner for Physiology or
Medicine Prof. 
Sudhof C Thomas (from Stanford University, California, USA) has published a
paper in the Journal Neuron stating that ”
Rapid single-step induction of Functional neurons from Human pluripotent stem cells.”  This study suggests that “Neurogenin-2 overexpression rapidly
transforms ESCs and iPSCs into neurons.”

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports thatSize doesn’t matter- action matters:
p53/p63/p73-dependent microRNAs regulate the
induction of functional neurons from human IPS cells
 This finding suggests that targeting the expression of p53/p63/p73-dependent microRNAs in iPScs and
ESCs may aid the generation of functional neurons. 

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, Connecting with Nobel’s[Sudhof C
Thomas] findings: Size doesn’t matter- action
matters: p53/p63/p73-dependent microRNAs
regulate the induction of functional neurons from human IPSCs and ESCs,
23/October/2013, 13.49, Genome-2-Bio-Medicine Discovery center (GBMD), 
http://genomediscovery.org

– See more at:
http://genomediscovery.org/connecting-with-nobels-sudhof-c-thomas-findings-size-doesnt-matter-action-matters-micrornas-inhibit-induction-of-functional-neurons-from-human-ips-cells-23october2013-13-42/

31

Connecting with Nobel’s (Sudhof C Thomas) Cognitive work: p53/p63/p73 regulates Neuroligin and Neurexin expression via up regulation of its target miRNAs, 14/October/2013, 8.01 am

Amount – $ 300/-

This year’s Nobel prize winner for Physiology or
Medicine 
Prof. Sudhof
C Thomas
 (from Stanford University,
California, USA) has published an article in the Journal Nature (2008)
stating that ” 
Neuroligins and Neurexins link synaptic function to cognitive disease.” In this study, the author explains  how:  (1) “Neurexins and neuroligins– synaptic cell-adhesion
molecules–connect presynaptic and postsynaptic
neurons at synapses, mediate signalling across the synapse, and shape the
properties of neural networks by specifying synaptic functions
“; and (2) synaptic cell
adhesion is linked to cognition and its disorders
 (Sudhof, 2008, Nature).

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports
that 
p53/p63/p73 regulates Neuroligins and Neurexins expression
via up regulation of its target miRNAs
This finding provides mechanistic insight into the pathology of autism and other cognitive diseases

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, Connecting with Nobel’s (Sudhof C
Thomas) Cognitive work: p53/p63/p73 regulates  Neuroligins
and Neurexins expression via up
regulation of its target miRNAs, 14/October/2013,
8.01 am, Genome-2-Bio-Medicine Discovery center
(GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/connecting-with-nobels-sudhof-c-thomas-cognitive-work-p53p63p73-inhibits-neurexin-expression-via-up-regulation-of-its-target-mirnas-14october2013-8-01-am/

32

Connecting with Nobel’s (Sudhof C Thomas) favorite work:
p53/p63/p73 inhibits IGF-1 exocytosis via up regulation of its target miRNAs, 13/October/2013,
22.28

Amount – $ 500*/-

This year’s Nobel prize winner for
Physiology or Medicine 
Prof. Sudhof C Thomas (from
Stanford University, California, USA) has published a paper in the
Journal Cell (2011) stating that ” 
Activity-dependent IGF-1 exocytosis is
controlled by the Calcium-sensor synaptotoagmin-10
.” This study suggests that deletion of synaptotoagmin-10 results
in (i) impaired secretion of IGF-1; (ii)  smaller neurons; and (iii) an overall decrease in
synapse numbers.

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports that p53/p63/p73 inhibits IGF-1 exocytosis via up regulation of its target miRNAsThis finding
suggests that 
p63/p73/p53 may (i)
inhibit IGF-1 secretion through its target miRNAs;
and (ii)  decrease synapse numbers

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, Connecting with Nobel’s (Sudhof C
Thomas) favorite work: p53/p63/p73 inhibits
IGF-1 exocytosis via up regulation of its target miRNAs, 13/October/2013,
22.28, Genome-2-Bio-Medicine Discovery center
(GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at: http://genomediscovery.org/connecting-with-nobels-sudhof-c-thomas-favorite-work-p53p63p73-inhibits-igf-1-exocytosis-via-up-regulation-of-its-target-mirnas-13october2013-22-28/

33

Connecting with Nobel’s (Sudhof C Thomas) favorite
work: p53/p63/p73 regulates the CPLXs/synaptotagmins
switch via its target genes, 12/October/2013, 8.28 am

Amount – $ 500*/-

This year’s Nobel prize winner for
Physiology or Medicine 
Prof. Sudhof C Thomas (from
Stanford University, California, USA) has published a paper in the
Journal Cell (2006) stating that 
“A complexin/synaptotagmin 1
switch controls fast synaptic vesicle exocytosis.”
  Subsequently, he  has published an article in Journal of
Neuroscience (2013) stating that 
Complexin
activates exocytosis of distinct secretory vesicles controlled by different synaptotagmins

In connection with these findings, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports
that 
p53/p63/p73 regulates the complexins/synaptotagmins
switch via its target genes
. This finding
suggests that 
p63/p73/p53 may
regulate Calcium-triggered exocytosis by
controlling the expression of Complexins (CPLXs)
and Synaptotagmins

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan,Connecting with Nobel’s (Sudhof C Thomas) favorite work: p53/p63/p73 regulates the complexins/synaptotagmins
switch via its target genes, 12/October/2013, 8.34
am, Genome-2-Bio-Medicine Discovery center
(GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/connecting-with-nobels-sudhof-c-thomas-favorite-work-p53p63p73-regulates-the-cplxssynaptotagmins-switch-via-its-target-genes-12october2013-8-28-am

34

The Follow-up of Nobel laureates’s (Sudhof C Thomas) favorite work: miR-135 inhibits the expression of CPLX1, an essential activator of calcium-induced exocytosis, 12/October/2013, 6.11 am

Amount – $ 300*/-

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan,The Follow-up of Nobel laureates’s (Sudhof C Thomas) favorite work:
miR-135 inhibits the expression of CPLX1, an essential activator of
calcium-induced exocytosis, 12/October/2013, 6.11
am, Genome-2-Bio-Medicine Discovery center
(GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/the-follow-up-of-nobel-laureatess-sudhof-c-thomas-favorite-work-mir-135-inhibits-the-expression-of-cplx1-an-essential-activator-of-calcium-induced-exocytosis-12october2013-6-11-am

35

The Follow-up of Nobel laureates’s (Sudhof C Thomas) favorite work: p53/p63/p73 regulates the expression of synaptotagmin III through its target miRNAs, 10/October/2013, 5.07 am

Amount – $ 500*/-

This year’s Nobel prize winner for
Physiology or Medicine 
Prof. Sudhof C Thomas (from
Stanford University, California, USA) in his research has elucidated the role
of  synaptotagmins in
calcium sensing, secretory protein release, and
vesicular traficking

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports that  p53/p63/p73 regulates the expression of  synaptotagmin
III through its target miRNAs
.  Earlier research has shown that synaptotagmin
III plays a critical role in insulin exocytosis.
Considered together, Dr Boominathan
believes that 
p73/p63/p53 may play a central role in
insulin exocytosis
.

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, The Follow-up of Nobel laureates’s (Sudhof C Thomas) favorite work:
p53/p63/p73 regulates the expression of  synaptotagmin
III through its target miRNAs, 10/October/2013,
5.07 am, Genome-2-Bio-Medicine Discovery center
(GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/the-follow-up-of-nobel-laureatesssudhof-c-thomas-favorite-work-p53p63p73-regulates-the-expression-of-synaptotagmin-iii-through-its-target-mirnas-10october2013-5-07-am/

36

The Follow-up of Nobel laureates’s (Sudhof C Thomas) favorite work: p73 regulates the expression of calcium sensor proteins that play a central role in insulin release,
10/October/2013, 4.36 am

Amount – $ 500*/-

This year’s Nobel prize winner for
Physiology or Medicine 
Prof. Sudhof C Thomas (from
Stanford University, California, USA) in his research has elucidated the role
of  synaptotagmins
in calcium sensing, secretory protein
release, and vesicular trafficking

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports that  p73 regulates  the expression of  calcium sensor
proteins that play a central role in insulin release
.  Based on this result, Dr Boominathan
believes that p73 may play a central role in the disease pathogenic
mechanisms of 
diabetes.

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, The Follow-up of Nobel laureates’s (Sudhof C Thomas) favorite
work: p73 regulates  the expression of calcium sensor
proteins that play a central role in insulin release, 10/October/2013, 4.36
am, 10/October/2013, 4,36 am Genome-2-Bio-Medicine Discovery center (GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at: http://genomediscovery.org/the-follow-up-of-nobel-laureatesssudhof-c-thomas-favorite-work-p73-regulates-calcium-sensors-that-play-a-central-role-in-insulin-release-10october2013-4-36-am/

37

The Follow-up of Nobel laureates’s(Sudhoffavorite work: p53/p73/p63 suppresses synaptotagmin-2 transcription in cortical neurons through its target genes, 9/October/2013,
9.22 am

Amount – $ 500*/-

This year’s Nobel prize winner for
Physiology or Medicine 
Prof. Sudhof (Stanford
University, California, USA) has published a paper namely ”
Calmodulin suppresses synaptotagmin-2 transcription in cortical neurons.” (J Biol Chem. 2010
Oct 29;285(44):33930-9)

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports that  p53/p73/p63 suppresses synaptotagmin-2 transcription in cortical
neurons through its target genes
. This finding
may explain how 
p53/p63/p73 regulates exocytosis via synaptotagmin-2. Based on this result, Dr Boominathan
believes that p53/p63/p73 may play a critical role in the disease pathogenic
mechanisms of 
asthma.

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, The Follow-up of Nobel laureates’s(Sudhof) favorite
work: p53/p73/p63 suppresses synaptotagmin-2 transcription in
cortical neurons through its target genes, 9/October/2013, 9.22
am Genome-2-Bio-Medicine Discovery center
(GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at: http://genomediscovery.org/the-follow-up-of-nobel-laureatesssudhof-favorite-work-p53p73p63-suppresses-synaptotagmin-2-transcription-in-cortical-neurons-through-its-target-genes-9october2013-9-22-am/

38

The Follow-up of Nobel laureates’s(Sudhoffavorite work: p63/p73 regulates compensatory synaptic vesicle endocytosis through its target gene, 9/October/2013, 9.13 am

Amount – $ 500*/-

This year’s Nobel prize winner for
Physiology or Medicine 
Prof. Sudhof (from Stanford
University, California, USA) has published numerous articles in journals
relating to 
Synaptotagmins and their role in calcium sensing, membrane/vesicular
trafficking, release of neurotransmitters
 etc. In connection with these findings, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports
that 
the tumor
suppressor p53 homolog, p63/p73 regulates compensatory synaptic
vesicle endocytosis through its target gene.  

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, The Follow-up of Nobel laureates’s(Sudhof) favorite work: p63/p73
regulates compensatory synaptic vesicle endocytosis
through its target gene, 9/October/2013, 8.54 am,  Genome-2-Bio-Medicine
Discovery center (GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/the-follow-up-of-nobel-laureatesssudhof-favorite-work-p63p73-regulates-compensatory-synaptic-vesicle-endocytosis-through-its-target-gene-9october2013-9-13-am/

39

p73 connects with Nobel Laureate’s(Sudhof) finding: The tumor suppressor p73 functions as a calcium sensor for spontaneous Neurotransmitter release via Synaptoagmin-1, 9/October/2013, 5.37
am

Amount – $ 500*/-

This year’s Nobel prize winner for
Physiology or Medicine 
Prof. Sudhof (Stanford
University, California, USA) has published a paper in Nature
Neuroscience (2009) stating that “
Synaptotagmin-1
functions as a calcium sensor for spontaneous release
.” 

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports
that 
The tumor
suppressor p73 functions as a calcium sensor for spontaneous release via
Synaptoagmin-1
. This finding suggests that the
expression of p63/p73/p53 may regulate 
spontaneous Neurotransmitter release via Synaptoagmin-1.  Based on
this result Dr Boominathan believes that
p53/p63/p73 may play a critical role in the disease pathogenic mechanisms
of 
diabetics.

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, p73 connects with Nobel Laureate’s(Sudhof)
finding: The tumor suppressor p73 functions as a
calcium sensor for spontaneous Neurotransmitter release via Synaptoagmin-1,
9/October/2013, 5.37 am,  Genome-2-Bio-Medicine Discovery center (GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at: http://genomediscovery.org/p73-connects-with-nobel-laureatessudhof-finding-the-tumor-suppressor-p73-functions-as-a-calcium-sensor-for-spontaneous-neurotransmitter-release-via-synaptoagmin-1-9october2013-5-07-am/

40

The Follow-up of Nobel’s(Schekman Randy) favorite work: The tumor suppressor p63/p73/p53 regulates Sec23 expression through its target gene, 8/October/2013, 7.40 am

Amount – $ 500*/-

This year’s Nobel prize winner for Physiology or Medicine Prof. Schekman Randy (from Univ of California, Berkeley, USA) has highlighted
the importance of the 
COPII
component Sec23 in vessicle traficking and normal craniofacial development
.  

In connection with this finding, Dr Boominathan, Founder Director-cum-chief scientist of GBMD, reports that the tumor
suppressor p53/p63/p73 regulates Sec23 expression through its target gene
. This finding suggests that the expression of p63/p73/p53 may regulate vessicle traficking and normal craniofacial development through Sec23.  Furthermore, p53/p63/p73-regulated Sec23a may
control the secretion of metastasis-suppressive proteins. 

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, The Follow-up of  Nobel’s(Schekman
Randy) favorite work: The tumor
suppressor p63/p73/p53 regulates Sec23 expression through its target gene,
8/October/2013, 7.40 am,  Genome-2-Bio-Medicine Discovery center (GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/the-follow-up-of-nobelsschekman-randy-favorite-the-tumor-suppressor-p63p73p53-regulates-sec23-expression-through-its-target-gene-8october2013-7-40-am/

41

The tumor suppressor gene p53/p63/p73 regulates the expression of Wave1 through its target genes, 24/September/2013, 20.42

Amount – $ 500*/-

The Nobel Prize Winner in
Physiology or Medicine (2012),
 Gurdon JB  from Wellcome Trust/Cancer Research Gurdon Institute, Cambridge, UK reports in
the prestigious journal
 Science that Nuclear Wave1 is required for reprogramming transcription in oocytes and for normal development.  Based on this remarkable finding,
Dr
L Boominathan PhD, Director-cum-chief
Scientist of GBMD
, reports
that 
the tumor
suppressor gene p53/p63/p73 regulates the expression of Wave1 through its
target genes.
 Furthermore, Dr Boominathan identifies the mechanism through which p53
and its homologues p63 and p73 regulate the maternal reprogramming factor
Wave1. This exciting finding explains how stress induced p53 may cause
abnormal development. Therefore, Dr Boominathan
believes that this finding has great 
clinical utility

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions

To citeBoominathan, The tumor suppressor gene p53/p63/p73
regulates the expression of Wave1 through its target genes,
24/September/2013, 20.42, Genome-2-Bio-Medicine Discovery center (GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/the-tumor-suppressor-gene-p53p63p73-regulates-the-expression-of-wave1-through-its-target-genes-24september2013-20-42/

42

p53/p63/p73 regulates reversion of reprogramming via induction of its target gene, 5/September/2013, 6.44 am

Amount – Free/-

Nobel Laureate Prof. Shinya Yamanaka has
reported in the journal PNAS that “
Maturation, not
initiation, is the major roadblock during reprogramming toward pluripotency
…”,  Proc Natl
Acad Sci U S A.
 2013
Jul 23;110(30):12172-9. 
As a follow-up of
this study, here, 
Dr Boominathan, Chief-Scientist-cum-Director of GBMD, reports that p53/p63/p73
regulates reversion of reprogramming via induction of its target gene,
5/September/2013, 6.45 am.

Teacher’s day special

We are happy to announce that ideas posted today (5/September/2013)
will be available to the use of
 Scientists/Professors/Teachers for free. So, there are no terms and conditions will apply. Each idea
posted will be served first come, first served basis to three to five
research teams.Write to 
Drboomi@genomediscovery.org for more
details.

– See more at: http://genomediscovery.org/p53p63p73-regulates-reversion-of-reprogramming-via-induction-of-its-target-gene-5september2013-6-44-am/

43

Regulating lymphoid development: p53/p63/p73 controls the expression of ZBTB1 through
its target miRNAs, 4.35 am

Amount – $ 300*/-

Nobel laureate Beutler B has reported in JEM that
ZBTB1 plays an essential role in lymphoid development 
(Sigg,.. Beutler B

, JEM, 2012). Here, Dr Boominthan, Director-cum-chief scientist of GBMD, reports
that
 p53/p63/p73
controls the expression of ZBTB1 through its target miRNAs.

Idea Proposed
by
Dr L Boominathan Ph.D.

Terms &
Conditions
 apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, Regulating
lymphoid development: p53/p63/p73 controls the expression of ZBTB1 through
its target miRNAs, 4.35 am,
Genome-2-Bio-Medicine Discovery center
(GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/regulating-lymphoid-development-p53p63p73-controls-the-expression-of-zbtb1-through-its-target-mirnas-4-35-am/

44

The Follow-up of Nob(Beutler)el’s screen: p53 regulates B-1 B/T-cell development, germinal center formation, and memory B-cell responses via its target miRNA, 14/August/2013,
4.10 am

Amount – $ 300*/-

Nobel laureate Beutler B has
conducted a genetic screen to identify a role for 
Nfkbid, Zeb1, and Ruvbl2 in humoral
immunity 
(Arnold CN,.. Beutler B, PNAS, 2012). In relation to this finding, Dr Boominathan, Director-cum-chief scientist of GBMD,
reports that
 p53 regulates B-1 B/T-cell development, germinal center formation, and memory B-cell responses via its
target miRNA.

Idea Proposed
by
Dr L Boominathan Ph.D.

Terms &
Conditions
 apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, The
Follow-up of Nob(Beutler)el’s
screen: p53 regulates B-1 B/T-cell development, germinal center
formation, and memory B-cell responses via its target miRNA,
14/August/2013, 4.10 am,  Genome-2-Bio-Medicine Discovery center (GBMD), 
http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/following-nobbeutlerels-screen-p53-regulates-b-1-bt-cell-development-germinal-center-formation-and-memory-b-cell-responses-via-its-target-mirna-14august2013-4-10-am/

45

N(obel)FKB’s companion: miR-146 regulates the expression of p53/p63/p73, 14/July/2013, 19.14

Amount – $ 300*/-

Nobel laureate Baltimore D has reported that miR-146 is a transcriptional
target of NFKB. Here, Dr L Boomianthan PhD,
Chief-Scientist-cum-Director of GBMD, reports that NFKB-induced miR-146 may
regulate the expression of 
p53/p63/p73. 

Idea Proposed byDr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, N(obel)FKB’s companion:miR-146 regulates the expression of
p53/p63/p73, 14/July/2013, 19.14  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

* Research cooperation

– See more at:
http://genomediscovery.org/nfkbs-companion-mir-146-regulates-the-expression-of-p53p63p73-14july2013-19-14/

46

Nobel laureate Sharp PA has reported that “Let-7 represses Nr6a1 and a mid-gestation developmental program in adult cells”

Dr L Boomianthan
PhD, Chief-Scientist-cum-Director of GBMD, reports that 
p53/p63/p73 promotes continual suppression of embroyonic gene expression in adult cells by regulating
the Let-7-Nr6a1 pathway through its target genes. 

http://genomediscovery.org/interrupting-the-mid-gestation-developmental-program-p53p63p73-promotes-continual-suppression-of-embroyonic-gene-expression-in-adult-cells-by-regulating-the-let-7-nr6a1-pathway/

– See more at:
http://genomediscovery.org/nobel-laureate-sharp-pa-has-reported-that-let-7-represses-nr6a1-and-a-mid-gestation-developmental-program-in-adult-cells/

47

Interrupting the mid-gestation developmental program: p53/p63/p73 promotes continual suppression of embroyonic gene expression in adult cells by regulating the Let-7-Nr6a1 pathway,

Amount – $
500*/-

Idea Proposed
by
Dr L Boominathan Ph.D.

Terms &
Conditions
 apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan,
Interrupting the mid-gestation developmental program: p53/p63/p73
promotes continual suppression of embroyonic gene
expression in adult cells by regulating the Let-7-Nr6a1 pathway, 10/July/2013,
8.44 am , Genome-2-Bio-Medicine Discovery center
(GBMD), http://genomediscovery.org

Nobel laureate Sharp PA has
reported recently that “Let-7 represses Nr6a1 and a mid-gestation developmental program in
adult” cells

* Research cooperation

– See more at:
http://genomediscovery.org/interrupting-the-mid-gestation-developmental-program-p53p63p73-promotes-continual-suppression-of-embroyonic-gene-expression-in-adult-cells-by-regulating-the-let-7-nr6a1-pathway/

48

The tumor suppressor p53 controls telomere elongation by suppressing CDK1 expression through its
target miRNA, 17/August/2013, 17.04

Amount – $ 500*/-

Noble Laureate Carol W Greider  had reported in
the journal 
Molecular Cell  (2006 Nov
3;24(3):423-32) that the cyclin-dependent
kinase CDK1 regulates teomere
elongation. Subsequently, Noble Laureate Prof. 
Elizabeth
H. Blackburn
 had reported in the journal Cell (2009 Jan 9;136(1):50-61) that  Cdk1-dependent phosphorylation of Cdc13 coordinates telomere elongation
during cell-cycle progression
Based
on these observations, here,
 Dr L Boominathan,
Director-cum-chief Scientist of GBMD, reports that 
the tumor suppressor p53 controls telomere elongation by
suppressing CDK1 expression through its target miRNA
.

Idea Proposed
by
Dr L Boominathan Ph.D.

Terms &
Conditions
 apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, The tumor suppressor p53 controls telomere elongation by
suppressing CDK1 expession through its target miRNA, 17/August/2013, 17.04, 
http://genomediscovery.org

* Research
cooperation

– See more at:
http://genomediscovery.org/the-tumor-suppressor-p53-controls-telomere-elongation-by-suppressing-cdk1-through-its-target-mirna-17august2013-17-04/

49

INK4a regulates telomere elongation by suppressing CDK1 through its target miRNA, 9/August/2013, 7.33 am

Amount – $
500/-

Noble Laureate Prof.
Elizabeth H. Blackburn 
has reported in Cell that  Cdk1-dependent phosphorylation
of Cdc13 coordinates telomere elongation during cell-cycle
установка кондиционеров недорого в витебской области progression
Here, 
Dr L
Boominathan
, Director-cum-chief Scientist of
GBMD, reports that
 INK4a regulates telomere elongation by suppressing
CDK1 through its target miRNA.

Idea Proposed
by
Dr L Boominathan Ph.D.

Terms &
Conditions
 apply http://genomediscovery.org/registration/terms-and-conditions/

To citeBoominathan, INK4a
regulates telomere elongation by suppressing CDK1 through its target miRNA, 9/August/2013, 7.33 am, 
http://genomediscovery.org

* Research
cooperation

– See more at:
http://genomediscovery.org/ink4a-regulates-telomere-elongation-by-suppressing-cdk1-through-its-target-mirna-9august2013-7-33-am/

50

The tumor suppressor p53-miR-145 pathway suppresses the
expression of Glis1-Noble laureate S. Yamanaka’s pro-reprogramming factor that facilitates clinical applications of iPSC technology 13/October/2012

Amount – $
500/-

Idea Proposed
by
Dr L Boominathan
Ph.D.

Terms &
Conditions apply

http://genomediscovery.org/registration/terms-and-conditions/

– See more at:
http://genomediscovery.org/the-tumor-suppressor-p53-mir-145-pathway-suppresses-the-expression-of-glis-1-the-noble-laureate-s-yamanakas-pro-reprogramming-factor-that-facilitates-clinical-applications-of-ipsc-technology-13se/