ArticleScience signaling2009
Increased MKK4 abundance with replicative senescence is linked to the joint reduction of multiple microRNAs.
Article in Science signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
46 citing papers in PubMed, 77 citations in OpenAlex.
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- Non-coding RNAs as Regulators of Cellular Senescence in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease.Frontiers in medicine · 2020Review
- miR-15/107 microRNA Gene Group: Characteristics and Functional Implications in Cancer.Frontiers in cell and developmental biology · 2020Review
- Senescent dermal fibroblasts negatively influence fibroblast extracellular matrix-related gene expression partly via secretion of complement factor D.BioFactors (Oxford, England) · 2019Article
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- c-Myc inhibits myoblast differentiation and promotes myoblast proliferation and muscle fibre hypertrophy by regulating the expression of its target genes, miRNAs and lincRNAs.Cell death and differentiation · 2019Article
- MicroRNA controls of cellular senescence.BMB reports · 2018Article
- MicroRNAs and the metabolic hallmarks of aging.Molecular and cellular endocrinology · 2017Review
- Senescence-Associated MicroRNAs.International review of cell and molecular biology · 2017Review
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- Noncoding RNA in age-related cardiovascular diseases.Journal of molecular and cellular cardiology · 2015Review
- miR-15b induced by platelet-derived growth factor signaling is required for vascular smooth muscle cell proliferation.BMB reports · 2013Article
- Role of microRNA deregulation in the pathogenesis of diffuse large B-cell lymphoma (DLBCL).Leukemia research · 2013Review
- miR-30d, miR-181a and miR-199a-5p cooperatively suppress the endoplasmic reticulum chaperone and signaling regulator GRP78 in cancer.Oncogene · 2013Article
- The small GTPase RALA controls c-Jun N-terminal kinase-mediated FOXO activation by regulation of a JIP1 scaffold complex.The Journal of biological chemistry · 2013Article
- MicroRNA-92a negatively regulates Toll-like receptor (TLR)-triggered inflammatory response in macrophages by targeting MKK4 kinase.The Journal of biological chemistry · 2013Article
- Proteomics for understanding miRNA biology.Proteomics · 2013Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
MKK4 (mitogen-activated protein kinase kinase 4) is a pivotal upstream activator of c-Jun N-terminal kinase and p38. Here, we report that the abundance of MKK4 increases in senescent human diploid fibroblasts through enhanced translation. We identified four microRNAs (miR-15b, miR-24, miR-25, and miR-141) that target the MKK4 messenger RNA (mRNA); the abundance of these microRNAs decreased during replicative senescence. Individually modulating the amount of each microRNA did not modify MKK4 abundance, but their concomitant overexpression decreased and their joint reduction increased MKK4 abundance. Reporter analyses indicated that these microRNAs acted through the MKK4 5' and 3' untranslated regions. Elevated MKK4 abundance inhibited cell proliferation and increased the phosphorylation and activity of p38 and PRAK (p38-regulated/activated protein kinase). Thus, multiple microRNAs acting on a single target, the MKK4 mRNA, collectively influence MKK4 abundance during replicative senescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.