Ribonucleic acid-based Lifespan extension therapy: A therapeutic mix encompassing lncRNA-TUG1 and/or Ursolic acid, Maresin, DIM, Ursolic acid  Lutein, Maresin, Cholecalciferol, Catalpol, Isoliquiritigenin (UMDULMCCI)  activates autophagy, promotes leanness, increases insulin sensitivity, improves motor function, alleviates ageing feature and extends lifespan via upregulation of its target gene ATG5 (Autophagy-related 5), 14/March/2018, 11.01 pm

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Introduction: What they say

A study from the Global Research Laboratory, Seoul National University, Korea shows that Overexpression of Atg5 in mice activates autophagy and extends lifespan.” This study was published, in the online journal “Nature Communications”,  by Prof. Jung YK, Pyo Jo, and others.

Earlier, Prof. Yoshinori Ohsumi, from Institute of Innovative Research, Tokyo Institute of Technology, who won the Nobel prize in Physiology or Medicine, in 2016, discovered the mechanisms of Autophagy, including the role of ATG5 in the regulation of autophagy.


What we say: 

On the foundation of these interesting findings, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that:   Ribonucleic acid-based Lifespan extension therapy: A therapeutic mix encompassing lncRNA-TUG1 and/or Ursolic acid, Maresin, DIM, Ursolic acid  Lutein, Maresin, Cholecalciferol, Catalpol, Isoliquiritigenin (UMDULMCCI activates autophagy, promotes leanness, increases insulin sensitivity, improves motor function, alleviates ageing feature and extends lifespan via upregulation of its target gene ATG5 (Autophagy-related 5)


From research findings to therapeutic opportunity: 

This study suggests, for the first time, that a therapeutic mix encompassing  LncRNA TUG1 and/or Ursolic acid, Maresin, DIM, Ursolic acid  Lutein, Maresin, Cholecalciferol, Catalpol, Isoliquiritigenin (UMDULMCCI), by regulating the expression of its target genes, it may increase the expression of ATG5 (Autophagy-related 5). Thereby, it may: (1) enhance autophagy, (2) promote leanness; (3) increase insulin sensitivity; (4) improve motor function; and (5) alleviate aging features (Fig.1).

Figure1. A therapeutic mix encompassing Ursolic acid, Maresin, DIM, Ursolic acid  Lutein, Maresin, Cholecalciferol, Catalpol, Isoliquiritigenin (UMDULMCCI) and/or LncRNA TUG1 functions as a longevity promoting agent. The UMDULMCCI and/or LncRNA TUG1 increases ATG5 expression and promotes leanness, insulin sensitivity, motor function and longevity.

Figure 2. LncRNA TUG1 may promote weight loss, insulin sensitivity, motor function and extend lifespan through induction of ATG5 and other longevity-promoting genes

Figure 3 LncRNA TUG1 functions as a longevity-promoter through induction of ATG5.

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Thus, pharmacological formulations encompassing Ursolic acid, Maresin, DIM, Ursolic acid  Lutein, Maresin, Cholecalciferol, Catalpol, Isoliquiritigenin (UMDULMCCI) and/or LncRNA TUG1 or their analogs/activators, either alone or in combination with drugs” may be used to increase the lifespan of an individual (Fig.1).


Details of the research findings: 

Idea Proposed/Formulated by Dr L Boominathan PhD

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

Amount: $500#

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

# Research cooperation

Undisclosed mechanistic information: How does a therapeutic mix encompassing UMDULMCCI and/or LncRNA TUG1 increase the expression of ATG5 and promote longevity?


References: 

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

Courtesy: When you cite us, just drop us a line at info@genomediscovery.org

Citation: Boominathan, L., Ribonucleic acid-based Lifespan extension therapy: A therapeutic mix encompassing lncRNA-TUG1 and/or Ursolic acid, Maresin, DIM, Ursolic acid  Lutein, Maresin, Cholecalciferol, Catalpol, Isoliquiritigenin (UMDULMCCI activates autophagy, promotes leanness, increases insulin sensitivity, improves motor function, alleviates ageing feature and extends lifespan via upregulation of its target gene ATG5 (Autophagy-related 5), 14/March/2018, 11.01 pm

 

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