Passive-aggressive antagonist Jon Lieff is again attempting to sneak up from behind on FB via his 11/26/19 regurgitation of this report on Cell signalling breakthrough opens up new avenues for research 11/4/19
The study results were published as Strong anion exchange-mediated phosphoproteomics reveals extensive human non-canonical phosphorylation 8/21/19
The authors revealed that energy-dependent cell signaling biophysically constrains viral latency via microRNA-mediated autophagy.
See: Autophagy: Biology and Diseases Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1206)
Epigenetic Regulation of Autophagy Pages 221-236
The role of non-coding RNAs such as microRNA in autophagy regulation will be covered in other chapters.
The other chapters from AEMB, volume 1206, include”
Many researchers are actively exploring the relationship between non-selective and selective autophagy and various pathophysiological states in humans, and are studying the molecular mechanisms underlying autophagy regulation in various biological conditions, including cancer, neurodegenerative diseases, cardiovascular diseases, immune responses, development and ageing.
Claims about evolutionarily conserved processes that fail to consider Pheromonal Regulation of Genetic Processes: Research on the House Mouse (Mus musculus L.) exemplify human idiocy. They fail to link the Creation of anti-entropic virucidal light and the Creation of water to all oxygen-dependent ecological adaptations. The adaptations are manifested in species from microbes to humans via the physiology of pheromone-controlled reproduction.
For instance, the food energy-dependent physiology of reproduction biophysically constrains viral latency via the energy-dependent regulation of autophagy. In the absence of biophysically contrained autophagy/viral latency, you get constraint-breaking mutations and the mutation-driven evolution of all pathology.
See also: Part II Regulation of Autophagy
The mammalian autophagy complex-ULK1 complex is composed of ULK1, FIP200, ATG13 and ATG101, and the yeast autophagy initiation complex-ATG1 complex is composed of ATG1, ATG13, ATG17, ATG29 and ATG31. After this complex is activated, it binds and phosphorylates ATG9 on the vesicles.
Many studies have shown that a number of signal transduction pathways are involved in the regulation of autophagy.
All signal transduction pathways are energy-dependent.
AMPK is an evolutionarily conserved serine/threonine-protein kinase that acts as an energy sensor in cells and plays a key role in the upregulation of catabolism and inactivation of anabolism.
How could this serine/threonine-protein kinase create itself so that it could act as an evolutionarily conserved energy sensor?
…this landmark protein is essential for autophagy. By investigating the interaction between Bcl-2 and Beclin 1, key molecular mechanisms of mammalian autophagy regulation have been discovered.
It is foolish to link a protein to autophagy when autophagy is required for the energy-dependent biophysically constrained creation of the protein. Simply put, organisms that do not eat, do not create proteins.
…Tp53 actions are highly context dependent. Tp53 target genes also play key opposing roles in autophagy induction or inhibition such as DRAM and TIGAR, respectively. Finally, the role of Tp53 mutants in autophagy regulation are discussed.
Failed autophagy regulation links the virus-driven degradation of messenger RNA to mutations and pathology.
It seems to be still a long way to thoroughly understand the truth of Ca(2+) and autophagy.
The truth is that oxidative phosphorylation links the Creation of sunlight and water to oxygen-dependent ecological adaptations in all living genera via autophagy and the physiology of reproduction in all living genera.
See MicroRNAs biophysically constrain Virus-driven pathology (5) in prep