Ask about this productRelated genes to: MAPK15 Blocking Peptide
- Gene:
- MAPK15 NIH gene
- Name:
- mitogen-activated protein kinase 15
- Previous symbol:
- -
- Synonyms:
- ERK8, ERK7
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-04-05
- Date modifiied:
- 2014-11-18
Related products to: MAPK15 Blocking Peptide
Related articles to: MAPK15 Blocking Peptide
- Environmental stressors in commercial poultry systems can negatively affect bird welfare, although individuals vary considerably in their responses. Neuroplasticity within the hippocampus, measured through the density of doublecortin-positive (DCX) neurons, provides a potential biomarker of stress experience in laying hens. However, the genetic basis underlying variation in this biomarker remains poorly understood. A total of 42 H&N and Hy-Line Brown hens housed in a multitier free range and enriched cage system, respectively, were genotyped using Genotyping by Sequencing, yielding over 200 000 SNP markers after initial filtering. Hippocampal tissue sections were immunostained for DCX to quantify the density of highly plastic neurons. A genome-wide association analysis identified 19 genomic regions across eight chromosomes within the top 1% of windows explaining the greatest proportion of genetic variance in the neuroplasticity phenotype. Within ±100 kb of these regions, 39 annotated genes were identified, several of which are involved in cellular regulation and genetic information processing pathways. Notably, PIK3R6, VPS37D, STX1A, BAZ1B, HGH1, MAF1, MAPK15, and PIT54 emerged as positional candidate genes potentially contributing to variation in stress responsiveness. These findings provide preliminary insight into the genetic architecture of hippocampal neuroplasticity in laying hens and highlight candidate genes that may contribute to individual differences in stress response, with potential implications for breeding strategies aimed at improving poultry welfare. - Source: PubMed
Neuert LindsayOsborne VernArmstrong Elena APértille FábioBosagna Carlos GuerreroBoswell TimothySmulders Tom VBaes Christine FMakanjuola Bayode O - Due to intensifying global climate change and coastal eutrophication, dissolved oxygen (DO) and temperature constitute crucial environmental factors modulating physiological and biochemical processes of echinoderms. Strongylocentrotus intermedius, a commercially valuable mariculture sea urchin, is increasingly threatened by high temperature and hypoxia. This study established four groups: control (NC), high temperature (HT), hypoxia (LO), and high temperature - hypoxia combined stress (OT), followed by 48-h temperature recovery and reoxygenation. We assayed time to first death (TFD) and median lethal time (LT50), conducted transcriptome sequencing of tube feet, and validated dynamic expression of genes after stress exposure and during the recovery phase via real-time quantitative polymerase chain reaction (RT-qPCR). Survival time under combined stress was significantly shorter than under individual stress. A total of 2391, 21552, and 2973 differentially expressed genes (DEGs) were identified in hypoxia, high temperature and combined stress groups, respectively. DEGs in LO group were enriched in hypoxia-inducible factor-1 (HIF-1) signal pathway and glycolysis/gluconeogenesis; DEGs in HT group were mainly enriched in antigen processing and presentation, and protein processing in endoplasmic reticulum; the apoptosis pathway was uniquely enriched in OT group. Genes such as L-lactate dehydrogenase gene (ldh), mitogen-activated protein kinase 15 gene (mapk15) and phosphatidate phosphatase gene (plpp1_2_3) were selected as key DEGs. Key DEGs were significantly upregulated under stress and reversibly downregulated during recovery. These findings clarify the molecular mechanisms of S. intermedius responding to complex stresses, providing potential molecular targets for breeding stress-resistant sea urchin strains. - Source: PubMed
Publication date: 2026/08/20
Dong JialiangSong ZheCong LinYan YuehanGuan YuQin ZilingZheng YiYu Wenchao - The senescence of intestinal epithelial cells (IECs) is closely associated with the development of ulcerative colitis (UC), but the underlying regulatory mechanism remains unclear. Although mitogen activated protein kinase 15 (MAPK15) has been shown to inhibit cellular senescence, its specific role in UC has not yet been clarified. This study investigates the role of MAPK15 in modulating IEC senescence during UC and explores the molecular mechanisms involved in this regulatory process. The senescence phenotype and MAPK15 expression in colon tissues from UC patients, dextran sodium sulfate (DSS)-induced UC mice, and DSS-induced NCM460 cells were detected by SA-β-Gal staining, immunohistochemistry (IHC) staining, and Western blot analysis. To further determine the molecular mechanism of the MAPK15/Suz12/Drp1 axis in UC, MAPK15 was overexpressed and Suz12 was silenced, and the underlying regulatory interactions were assessed using techniques including Co-immunoprecipitation (Co-IP), RIP-qPCR, and RNA pull-down. The results showed that the expressions of senescence-associated markers (p53, p16, and p21) and senescence-associated secretory phenotype (SASP) factors (IL-6, IL-8, and MMP-3) in IECs from UC patients and DSS-induced mice were upregulated, whereas the expression of MAPK15 was downregulated. Functional experiments further demonstrated that overexpression of MAPK15 alleviated DSS-induced intestinal inflammation, reduced cellular senescence-like phenotype, and suppressed Drp1-dependent mitochondrial fission. Mechanistically, MAPK15 enhanced the binding of Suz12 to Drp1 mRNA through phosphorylation of Suz12, which reduced the stability of Drp1 mRNA, and thereby inhibited Drp1-mediated mitochondrial fission damage. However, silencing of Suz12 reversed the protective effect induced by MAPK15 overexpression. In conclusion, these findings indicated that MAPK15 contributed to the inhibition of mitochondrial fission through regulation of the Suz12/Drp1 axis, thereby mitigating IEC senescence-like phenotype and suppressing the progression of UC. These results suggested that MAPK15 might serve as a potential therapeutic target for UC.Clinical Trial Number: Not applicable. - Source: PubMed
Publication date: 2026/04/24
Li JuanChen GangBao Xinyi - Liangshan Meigu Yanying chicken is an indigenous high-altitude breed in Sichuan, China, but its population genetic structure and the genetic basis of key growth and meat-quality traits remain unclear. In this study, 211 Meigu Yanying chickens were whole-genome resequenced, and leg muscle weight, liver weight, leg muscle total protein content and leg muscle total cholesterol content were recorded at slaughter. After quality control, high-confidence single-nucleotide polymorphisms were used to analyze linkage disequilibrium, population structure and genome-wide associations. Linkage disequilibrium decayed rapidly with distance, and multivariate analyses indicated an overall homogeneous genetic background with only mild substructure and few closely related individuals. Genome-wide association studies for the four traits detected several significant or suggestive regions harboring biologically plausible candidate genes, including CPNE4, PLXNB2, SMAP1, SDHAF4, FAM135A, LCP1, MAPK15 and SCRIB. Gene Ontology enrichment showed that candidate genes for leg muscle weight and liver weight were mainly involved in cellular processes and tissue development, whereas those for leg muscle total cholesterol content were enriched in phosphorus metabolism and phosphate-containing compound metabolism. These results provide a genome-wide resource for Meigu Yanying chickens and lay a basis for conservation and genomic breeding aimed at improved growth performance, meat quality and nutritional value. - Source: PubMed
Publication date: 2026/02/09
Hu YaodongCai BinjianLi TianyuTang ShiWang SiluSun CaiyunChen BinlongRen Peng - Accumulation of lipids in the liver characterizes metabolic dysfunction-associated steatotic liver disease (MASLD), the most prevalent chronic liver disease worldwide. - Source: PubMed
Publication date: 2026/01/29
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