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.NoIdeas based on Nobel Laureate’s work is posted by GBMD’s Director-cum-Chief ScientistDr L Boominathan PhD
1Celastrol, an antioxidant and  anti-inflammatory drug, suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target geneThe 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 Discoverycenter (GBMD), http://genomediscovery.org
2Treating human cancer with  Thunder of God vine: Celastrol, an antioxidant & anti-inflammatory drug from herb Thunder of God vine, increases the expression of tumorsuppressor p16(Ink4a) via down regulation of its target geneNoble 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 oxidesynthase) 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 oftumor 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
3Treating cancer with longevity promoting  drugs: Resveratrol, a longevity promoting  small molecule, suppresses the expression of NOS2 via up regulation of its target geneNoble 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 howResveratrol inhibits the expression of NOS-2To cite: Boominathan, 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 Discoverycenter (GBMD), http://genomediscovery.org– See more at: http://genomediscovery.org/research/news
4Treating 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/
5Mechanistic insights into Cancer therapy: NOS-2 increases the levels of cell cycle protein Cyclin D1 via up regulation of its target geneNoble 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 oxidesynthase) may have a therapeutic value in a number of cancers. In connection with this finding,                    Dr LBoominathan, Director-cum-chief scientist of GBMD, reports that: Mechanistic insights into Cancer therapy: NOS-2 increases the levels of cell cycle proteinCyclin 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
6Molecular insights into Cancer therapy: NOS-2 suppresses the expression of  tumor suppressor TNFAIP8L2  via up regulation of its target geneNoble 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 oxidesynthase) 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 Discoverycenter (GBMD), http://genomediscovery.org – See more at: http://genomediscovery.org/research/news
7Molecular insights into Cancer therapy: NOS-2 suppresses the expression of  tumor suppressor RECK via up regulation of its target geneNational 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 servedbasis.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 tumorsuppressor 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 Discoverycenter (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 geneNoble 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 tumorsuppressor 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 Discoverycenter (GBMD), http://genomediscovery.org – See more at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf
9Molecular 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 Discoverycenter (GBMD), http://genomediscovery.org – See more at: http://genomediscovery.org/research/news/#sthash.iwFq4ewT.dpuf
10Molecular insights into Cancer therapy: NOS-2 suppresses the expression of pro-apoptotic protein BTG2  via up regulation of its target geneNoble 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 improvecaner 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
11Molecular 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 tumorsuppressor 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
12Molecular insights into Cancer therapy: NOS-2 suppresses the expression of DNA repair protein hMSH2 via up regulation of its target geneNoble 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
13Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor GRHL3  via up regulation of its target geneNoble 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 improvecaner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression oftumor 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
14Molecular insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor PDCD4 via up regulation of its target geneNoble 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 improvecaner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression oftumor 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 geneNoble 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 improvecaner therapy. To cite: Boominathan, Insights into Molecular cancer therapy: NOS-2 suppresses the expression oftumor 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
16Insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor KRIT1/CCM1 via up regulation of its target geneNoble 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:Breaking News
17Insights into Cancer therapy: NOS-2 suppresses the expression of tumor suppressor TPM1 via up regulation of its target geneNoble 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:Breaking News
18Dismantling stem cell network: Tumor suppressor p53 inhibits the embryonic stem cell transcriptional network through induction of its target gene peptidylargininedeiminase-4Prof. 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
19Celastrol, an antioxidant and  anti-inflammatory drug, suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target geneThe 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:Breaking News
20BRMS1 (Breast cancer metastasis suppressor 1) suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target geneThe 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:Breaking News
21NFKB suppresses the expression of epigenetic integrator UHRF1 via up regulation of its target geneThe 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
22Insights into the regulation of a mid-gestation developmental program: Metformin decreases Nr6a1 and embryonic gene expression programs in adult cellsNoble 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
23Insights into the regulation of a mid-gestation developmental program: Estrogens (E2) decrease Nr6a1 and embryonic gene expression programs in adult cellsNoble 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:Breaking News
24Insights 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:Breaking News
25Insights into the regulation of a mid-gestation developmental program: 1,25-Dihydroxyvitamin D3 suppresses Nr6a1 and  embryonic gene expression programs in adult cellsNoble 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:Breaking News
26Let-7 miRNA increases the expression of tumor suppressor p53 homologue p73 via down regulation of its target geneNoble 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
27LIN-41/TRIM71 suppresses the expression of p53 homologue p73 via down regulation of its target geneThe 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:Breaking News
28ATRA (Vitamin A) decreases IFN regulatory factor 4 (IRF4) expression via up regulation of its target geneNoble 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 Mф/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  Mф/Immune cell activation. Together, this study suggests that Vitamin-A can be used to augment immune cell activation. To cite: Boominathan, L, Vitamin-mediated Mф/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:Breaking News
29The Follow-up of Nobel laureates’s (Sudhof C Thomas) favoritework: Drosha inhibits the induction of functional neurons from human IPSCs and ESCs, 24/October/2013, 6.33 amAmount – $ 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 neuronsIdea 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
30Connecting with Nobel’s [Sudhof C Thomas] findings: Size doesn’t matter- action matters: p53/p63/p73-dependentmicroRNAs regulate the induction of functional neurons from human IPSCs and ESCs, 23/October/2013, 13.42Amount – $ 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 overexpressionrapidly 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/
31Connecting 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 amAmount – $ 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 miRNAsThis finding provides mechanistic insight into the pathology of autism and other cognitive diseasesIdea 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/
32Connecting 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, 22.28Amount – $ 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 numbersIdea 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/
33Connecting 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 amAmount – $ 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 SynaptotagminsIdea 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 thecomplexins/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
34The Follow-up of Nobel laureates’s (Sudhof C Thomas) favoritework: miR-135 inhibits the expression of CPLX1, an essential activator of calcium-induced exocytosis, 12/October/2013, 6.11 amAmount – $ 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
35The Follow-up of Nobel laureates’s (Sudhof C Thomas) favoritework: p53/p63/p73 regulates the expression of synaptotagmin III through its target miRNAs, 10/October/2013, 5.07 amAmount – $ 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/
36The Follow-up of Nobel laureates’s (Sudhof C Thomas) favoritework: p73 regulates the expression of calcium sensor proteins that play a central role in insulin release, 10/October/2013, 4.36 amAmount – $ 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 traffickingIn 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/
37The 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 amAmount – $ 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, DrBoominathan 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/
38The Follow-up of Nobel laureates’s(Sudhof) favorite work: p63/p73 regulates compensatory synaptic vesicle endocytosisthrough its target gene, 9/October/2013, 9.13 amAmount – $ 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/
39p73 connects with Nobel Laureate’s(Sudhof) finding: The tumorsuppressor p73 functions as a calcium sensor for spontaneous Neurotransmitter release via Synaptoagmin-1, 9/October/2013, 5.37 amAmount – $ 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/
40The Follow-up of Nobel’s(Schekman Randy) favorite work: Thetumor suppressor p63/p73/p53 regulates Sec23 expression through its target gene, 8/October/2013, 7.40 amAmount – $ 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/
41The tumor suppressor gene p53/p63/p73 regulates the expression of Wave1 through its target genes, 24/September/2013, 20.42Amount – $ 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 inoocytes 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 utilityIdea Proposed byDr L Boominathan Ph.D.Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditionsTo 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/
42p53/p63/p73 regulates reversion of reprogramming via induction of its target gene, 5/September/2013, 6.44 amAmount – 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 specialWe 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/
43Regulating lymphoid development: p53/p63/p73 controls the expression of ZBTB1 through its target miRNAs, 4.35 amAmount – $ 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 cite: Boominathan, 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/
44The 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 amAmount – $ 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 cite: Boominathan, 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/
45N(obel)FKB’s companion: miR-146 regulates the expression of p53/p63/p73, 14/July/2013, 19.14Amount – $ 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 by: Dr L Boominathan Ph.D.Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/To cite: Boominathan, 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/
46Nobel 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 ofembroyonic 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/
47Interrupting the mid-gestation developmental program: p53/p63/p73 promotes continual suppression of embroyonicgene 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 cite: Boominathan, 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.orgNobel 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/
48The tumor suppressor p53 controls telomere elongation by suppressing CDK1 expression through its target miRNA, 17/August/2013, 17.04Amount – $ 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-dependentphosphorylation 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 cite: Boominathan, 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/
49INK4a regulates telomere elongation by suppressing CDK1 through its target miRNA, 9/August/2013, 7.33 amAmount – $ 500/-Noble Laureate Prof. Elizabeth H. Blackburn has reported in Cell that  Cdk1-dependent phosphorylation of Cdc13 coordinates telomere elongation during cell-cycleустановка 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 cite: Boominathan, 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/
50The tumor suppressor p53-miR-145 pathway suppresses the expression of Glis1-Noble laureate S. Yamanaka’s pro-reprogramming factor that facilitates clinical applications ofiPSC technology 13/October/2012Amount – $ 500/-Idea Proposed by: Dr L Boominathan Ph.D.Terms & Conditions applyhttp://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/