By Theodore Friedmann, Jay C. Dunlap, Stephen F. Goodwin
The booklet continuously publishes vital reports of the broadest curiosity to geneticists and their colleagues in affiliated disciplines, seriously studying destiny directions.
1. Genetics and Pharmacology of sturdiness: the line to Therapeutics for fit Aging
Jorge Iv?n Castillo-Quan, Kerri J. Kinghorn and Ivana Bjedov
2. MicroRNAs: instruments of Mechanistic Insights and organic Therapeutics Discovery for the infrequent Neurogenetic Syndrome Lesch-Nyhan ailment (LND)
3. Small RNAs in micro organism and Archaea: Who they're, What They Do, and the way They Do It
E. Gerhart H. Wagner and Pascale Romby
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26 Jorge Ivan Castillo-Quan et al. regimes with the gene/intervention of interest will reveal whether the nondietary intervention acts in the same molecular pathway. In a hypothetical scenario where the effect of overexpressing the transcription factor involved in lysosomal biogenesis (transcription factor EB (TF-EB) or mitochondrial biogenesis, PGC-1a, are tested to determine their roles in life span extension under DR in Drosophila, one of the three scenarios can occur (Figure 3). Firstly, a true DR mechanism would show a right-shifted DR tent, where the life span beneﬁts would only be observed at the higher end of the yeast concentration.
2014; Brooks-Wilson, 2013). , 2014). , 2014). This is an exciting ﬁnding given that these might point to an important regulatory function for noncoding genes in longevity (De Magalh~aes, 2014). In an interesting approach, Suh and colleagues showed that genetic variations in IGF1R (encoding for the IGF1 receptor) were enriched in Ashkenazi Jewish centenarians. One particular variant lead to increased IGF1 circulating levels, but this was found to be due to IGF1 insensitivity. , 2008). Technological advances now provide the opportunity for interrogating the genome for rare variants.
2011; Shaw & Cantley, 2006). This allows independent activation of mTOR by PI3K/Akt and Ras-Erk. Additionally other signaling kinases like GSK-3 can also modulate mTOR signaling. GSK-3 also phosphorylates TSC2, but in turn this phosphorylation activates the GAP activity of the complex, hence inhibiting signaling through mTOR. , 2006). Both Erk and GSK-3 can modulate mTOR independent of the TSC complex. , 2011). , 2011). , 2007). Given the central role of mTOR in the integration of multiple cellular inputs, its detailed and stratiﬁed interaction with other signaling pathways is not surprising.
Advances in Genetics by Theodore Friedmann, Jay C. Dunlap, Stephen F. Goodwin