Ribonucleic acid-based therapy for aging-associated diseases and Lifespan extension: LncRNA CCAT1  inhibits the interaction of DBC1 with PARP1, increases the PARP1 activity, promotes DNA repair, augments tolerance against radiation, cancer, and aging, via down-regulation of its target gene, 3/March/2019, 8.50 am

Combinatorial therapy for attenuating prostate cancer bone metastasis: A pharmaceutical mixture encompassing  Simvastatin and Navitoclax (SAN) inhibits the expression of Monoamine oxidase A (MAOA), inhibits Shh-IL6-RANKL signaling network, suppresses tumor-stromal interactions, reduces prostate cancer metastasis and prolongs survival via upregulation of its target gene, 3/March/2019, 8.33 am
March 3, 2019
Ribonucleic acid-based therapy for inflammation and arthritis:  LncRNA ZFAS1 (zinc finger antisense (ZFAS)1 increases IL-9 levels, augments proliferation of ILC2s (type 2 innate lymphoid cells) and regulatory T (Treg) cells, promotes resolution of inflammation, attenuates cartilage destruction, decreases bone loss, and inhibits pathological features associated with arthritis via up-regulation of its target genes, 3/March/2018, 9.13 am
March 3, 2019
Show all

Introduction: What they say

A study from Department of Genetics, Paul F. Glenn Center for the Biology of Aging, Harvard Medical School, Boston, MA, USA; and Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, New South Wales 2052, Australia shows that “A conserved NAD+ binding pocket that regulates protein-protein interactions during aging.” This research paper was published, in the 24 March 2017 issue of the journal “Science [One of the best research journals in Science with an I.F of 34+], by Prof. David A. Sinclair, Jun Li, and others.


What we say:

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that:   Ribonucleic acid-based therapy for aging-associated diseases and Lifespan extension: LncRNA CCAT1  inhibits the interaction of DBC1 with PARP1, increases the PARP1 activity, promotes DNA repair, augments tolerance against radiation, cancer, and aging, via down-regulation of its target gene


What is known?

Prof. David A. Sinclair’s research team has recently shown that: (a) increased levels of NAD+ (found in non-aged tissues) inhibits the interaction the between DBC1 (deleted in breast cancer 1) and PARP1 [poly(adenosine diphosphate–ribose) polymerase]; and promotes DNA repair; (b) decreased levels of NAD+ (found in aged tissues) promotes the interaction between DBC1 and PARP1 and inhibits DNA repair; (c) aged cells/tissues that are low in NAD+ are radiation-sensitive, cancer-prone and prone to accelerated ageing; and (d) ageing-associated diseases can be reversed by increasing the concentration of NAD+ in ageing tissues, suggesting that ageing-associated diseases, in part, can be reversed by NAD+ supplementation in older animals.


From research findings to therapeutic opportunity:

This study suggests an RNA-based therapy for both ageing-associated diseases and life-span extension. LncRNA CCAT1, by decreasing the expression of its target gene, it may increase the levels of NAMPT and NMN/NAD+. Thereby, it may: (1) increase plasma NMN levels and tissue NAD+ availability; (2) inhibit the interaction between DBC1 and PARP1; (3) augment PARP1’s DNA repair activity; (4) protect against radiation; (5) protect against cancer; and (6) prevent age-associated gene expression pattern and accelerated ageing. Thus, pharmacological formulations encompassing “lncRNA CCAT1 or its activators, either alone or in combination with other compounds,” may be used to suppress age-associated overall physiological decline and improve health/lifespan.[easy_payment currency=”USD”]

Figure1. LncRNA CCAT1 may act as an anti-aging and a longevity-promoting agent. LncRNA CCAT1,  by increasing NAD+ levels, may suppress ageing-associated overall physiological decline, ageing-associated diseases

Figure 2. LncRNA CCAT1 promotes health/lifespan by increasing the levels of NAD+


Details of the research findings: 

Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.

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

Undisclosed mechanistic information: How does LncRNA CCAT1  increase the levels of NMN/NAD?

Amount: $300#

* Research cooperation

For purchase and payment details, you may reach us at info@genomediscovery.org


References:

Citation: Boominathan, L., Ribonucleic acid-based therapy for aging-associated diseases and Lifespan extension: LncRNA CCAT1  inhibits the interaction of DBC1 with PARP1, increases the PARP1 activity, promotes DNA repair, augments tolerance against radiation, cancer, and aging, via down-regulation of its target gene, 3/March/2019, 8.50 am, Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org

Web: http://genomediscovery.org or http://newbioideas.com

Courtesy: When you cite us, kindly drop us a line

Comments are closed.