We are analyzing https://link.springer.com/article/10.1007/s11357-020-00183-3.

Title:
Regulation of senescence traits by MAPKs | GeroScience
Description:
A phenotype of indefinite growth arrest acquired in response to sublethal damage, cellular senescence affects normal aging and age-related disease. Mitogen-activated protein kinases (MAPKs) are capable of sensing changes in cellular conditions, and in turn elicit adaptive responses including cell senescence. MAPKs modulate the levels and function of many proteins, including proinflammatory factors and factors in the p21/p53 and p16/RB pathways, the main senescence-regulatory axes. Through these actions, MAPKs implement key traits of senescence—growth arrest, cell survival, and the senescence-associated secretory phenotype (SASP). In this review, we summarize and discuss our current knowledge of the impact of MAPKs in senescence. In addition, given that eliminating or suppressing senescent cells can improve health span, we discuss the function and possible exploitation of MAPKs in the elimination (senolysis) or suppression (senostasis) of senescent cells.
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Keywords {🔍}

pubmed, article, google, scholar, cas, central, cell, senescence, biol, cells, cellular, kinase, protein, cancer, mol, aging, signaling, nat, kim, activation, disease, senescent, zhang, senescenceassociated, factor, res, chem, wang, growth, rev, dna, expression, regulation, phenotype, pathways, secretory, human, erk, lee, genes, pathway, mitogenactivated, mrna, mapk, mapks, response, dev, med, liu, regulates,

Topics {✒️}

mek-extracellular signal-regulated kinase platelet-derived growth factor single-cell rna-seq identifies mitogen-activated protein kinases month download article/chapter mitogen-activated protein kinase stress-activated protein kinase-1 transforming growth factor-beta src-family tyrosine kinases mapk-activated protein kinases rna-binding protein immunoprecipitation dna double-strand breaks ras-induced premature senescence oligomeric amyloid beta-peptide mitogen-activated protein retinoblastoma protein signalling p85/p110-phosphatidylinositol 3-kinase kotb abdelmohsen & myriam gorospe src family kinases dna damage-mediated formation l-dopa-induced dyskinesia human ras-transformed cells histone methylation-dependent pathways tgf-beta/smad pkbalpha/akt1 acts downstream p38 map kinase atm-dependent erk signaling h2o2-mediated erk activation main senescence-regulatory axes gc-rich promoter elements ros-generating oxidases nox1 sanchez-arevalo lobo vj cell cycle-related events tgf-beta type nf-kappab p65 subunit beta/smad signaling rb-mediated heterochromatin formation ras-erk signaling ras-dependent pathway ephrin-eph signalling article geroscience aims aging cells-connecting metabolism full article pdf dna damage independently transcription factor hbp1 receptor tyrosine kinases stress kinase p38alpha receptor tyrosine kinase phosphorylated map kinase ras-induced senescence

Questions {❓}

How ERK1/2 activation controls cell proliferation and cell death: is subcellular localization the answer?
Senescence and apoptosis: dueling or complementary cell fates?
To clear, or not to clear (senescent cells)?

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