Ribonucleic acid-based therapy for aging-associated diseases and Lifespan extension: LncRNA PCAT5  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, 2/July/2019, 11.58 pm

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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 PCAT5  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 PCAT5, 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  PCAT5  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.

 

Figure1. LncRNA PCAT5 may act as an anti-aging and a longevity-promoting agent. LncRNA PCAT5 , by increasing NAD+ levels, may suppress ageing-associated overall physiological decline, ageing-associated diseases and improve health/lifespan

Figure 2. LncRNA PCAT5 promotes health/lifespan by increasing the levels of NAD

Figure 3. While restoring NAD+ levels attenuate ageing features and promote DNA repair activity,, LncRNA PCAT5 may promote 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 PCAT5 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 PCAT5  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, 2/July/2019, 11.58 pm, Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org

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

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