Year: 2022

ACTIVE INTERACTIONS. "The new interactome map lends support to a long-held suspicion that proteins implicated in cancer participate in disproportionate numbers of interactions with other proteins. As scientists sequence tumor genomes, more extensive knowledge of these protein-protein interactions could help to distinguish “driver” mutations that cause cancer from “passenger” mutations that are simply along for the ride." https://lnkd.in/etGh98E View in LinkedIn

CLINICAL SIGNS AND MODULES. "Characterization of clinical signs in the human interactome. Many diseases are related by shared associated molecules and pathways, exhibiting comorbidities and common phenotypes, an indication of the continuous nature of the human pathological landscape. We found that clinical signs are reflected as modules at the molecular network level, to at least to the same extent as diseases." https://lnkd.in/ebPrQCK View in LinkedIn

CLINICAL SIGNS AND GENES. "Clinical signs are thought to be reflected at the molecular network level, possibly to an even greater extent than diseases. There are numerous examples of diseases or groups of diseases with similar phenotypes caused by functionally related genes." https://lnkd.in/ebPrQCK View in LinkedIn

SO ENDS this summary of the community of protein interactions. The various levels of cellular active agents, from gene to protein to protein clusters to giant modules with specific phenotypes, is an exemplar of the nuanced complexity that evolution has wrought. That it all hangs together at all, or is exquisitely regulated at cell cycle checkpoints is beyond remarkable. There are simply so many moving parts that can go wrong. View in LinkedIn

GIANT VIRUSES. "The prevalent view is that viruses were lucky combinations of self-replicating molecules - not living organisms - and per se not noble enough to deserve a genealogy. The identification of many large DNA viruses exhibiting more than two hundred, then three hundred genes over the last 14 years, was apparently not sufficient to change this view, outside of a small circle of specialists." https://lnkd.in/evsF7_x View in LinkedIn

MIMIVIRUSES BREAK DOGMAS. "The surprise in the mimivirus genome, was not only its record 1.2-Mb size, but the nature of its gene content itself. Lacking ribosomes, viruses are supposed to entirely hand over the synthesis of their own proteins to their host's machinery. Already weaken by the discovery of numerous tRNA in some phycodnavirus, this dogma is now further demolished by the finding of virus-encoded translation enzymes and factors." https://lnkd.in/evsF7_x View in LinkedIn

"A TRANSPOVIRON is a mobile genetic element found in the genomes of giant DNA viruses." https://lnkd.in/ef7GiPm View in LinkedIn

DIVERSE FREE CODE. "Recent advances of genomics and metagenomics reveal remarkable diversity of viruses and other selfish genetic elements." https://lnkd.in/eEM2HAP View in LinkedIn

MOBILOMES. "Giant viruses have been shown to possess their own mobilomes that include virophages, small viruses that parasitize on giant viruses of the Mimiviridae family, and transpovirons, distinct linear plasmids." Not mobile homes. https://lnkd.in/eEM2HAP View in LinkedIn

BIG FLEAS HAVE LITTLE FLEAS. "Much like bacteria, the giant viruses (sometimes called giruses) possess their own parasites and their own mobilomes, i.e. communities of associated mobile genetic elements." http://virologyj.biomedcentral.com/articles/10.1186/1743-422X-10-158 View in LinkedIn