Ask about this productRelated genes to: MAPK12 antibody
- Gene:
- MAPK12 NIH gene
- Name:
- mitogen-activated protein kinase 12
- Previous symbol:
- SAPK3
- Synonyms:
- ERK6, PRKM12, p38gamma, SAPK-3
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2016-10-05
Related products to: MAPK12 antibody
Related articles to: MAPK12 antibody
- The cashmere fibers produced by the secondary hair follicles of cashmere goats are precious textile raw materials. The secondary hair follicles exhibit a distinct annual cyclical pattern, comprising anagen, catagen, and telogen phases. Although a large amount of skin transcriptome data is currently available for cashmere goats, this study aims to systematically investigate the regulatory factors controlling the cyclical dynamics of secondary hair follicles through re-analysis of these data. Skin transcriptome data of Inner Mongolian cashmere goats were downloaded from the Sequence Read Archive (SRA) database. Bioinformatics analyses, including quality control, read mapping, quantification, differential expression analysis, Gene Ontology (GO) enrichment analysis, and KEGG pathway analysis, were performed to identify key regulatory genes governing the secondary hair follicle cycle. The results revealed a total of 1232 differentially expressed genes (DEGs) from comparisons across different phases. KEGG pathway analysis identified three signaling pathways associated with cashmere development: the cAMP signaling pathway (chx04024), the relaxin signaling pathway (chx04926), and the estrogen signaling pathway (chx04915). GO analysis yielded 335 terms, of which 236 were statistically significant ( < 0.05). The DEGs were predominantly involved in biological processes such as regulation of transcription by RNA polymerase II, proteolysis, and positive regulation of transcription by RNA polymerase II. Significantly enriched cellular components included the plasma membrane, membrane, and extracellular space, and molecular functions were mainly related to protein binding, identical protein binding, and DNA-binding transcription factor activity, RNA polymerase II-specific. Based on their expression patterns, five key genes were selected: , , , , and . These genes displayed significantly distinct expression profiles across the hair follicle cycle. exhibited the highest expression in anagen, intermediate expression in catagen, and the lowest expression in telogen, with significant differences among all three phases. was specifically upregulated in telogen and was significantly more highly expressed than in both anagen and catagen. showed high expression in anagen and catagen but extremely low expression in telogen. displayed significantly higher expression in both anagen and catagen compared to telogen. reached its highest expression in catagen, which was significantly different from that in telogen, while its expression in anagen showed no significant difference from either telogen or catagen. This study characterized the regulatory genes of the secondary hair follicle cycle in cashmere goats at the transcriptional level and analyzed the association between their expression patterns and cycle regulation. - Source: PubMed
Publication date: 2026/07/11
Gong GaoTang YuekunZhao JianqingZhu MengtingQi AladaerBi ShijieSulaiman YimingZheng Wenxin - Lung adenocarcinoma (LUAD), the most common non-small cell lung cancer, often resists ferroptosis and autophagy-two tumor-suppressive, therapy-sensitive regulated cell death pathways. MAPK12 (a stress-responsive p38 MAPK kinase) boosts LUAD cell survival under oxidative stress, while USP32 (a LUAD-upregulated deubiquitinase) correlates with poor prognosis. However, the USP32-MAPK12 axis's regulatory role in LUAD ferroptosis and autophagy remains uninvestigated. USP32/MAPK12 expression in LUAD tissues/cell lines was detected via Western blotting and immunohistochemistry. Functional assays (colony formation, Transwell migration, ferroptosis/mitophagy tests) were performed after gene overexpression/knockdown. Protein interactions and ubiquitination were analyzed by co-immunoprecipitation, with in vivo validation using xenograft models. USP32 overexpression in LUAD correlated with reduced overall survival; it stabilized MAPK12 by removing K48-linked ubiquitin chains to block proteasomal degradation. USP32/MAPK12 knockdown activated autophagy/ferroptosis (elevated LC3B/ACSL4/Fe²⁺/MDA, reduced GPX4/p62), inhibited LUAD cell proliferation/migration in vitro and tumor growth in vivo. Thus, targeting the USP32-MAPK12 axis may restore cell death sensitivity, representing a promising LUAD therapeutic strategy. - Source: PubMed
Publication date: 2026/07/19
Zhang QiangSheng HongxuPing DongnanGao Jixiang - Stress MAPKp38γ () has established roles in promoting tumorigenesis; however, the mechanisms involved remain largely unclear. This paper will review recently published and unpublished studies of p38γ in programming immune evasion in breast cancer, pancreatic cancer, and colon cancer to promote tumorigenesis. First, we show that p38γ is an oncogene that transforms breast epithelial cells into triple-negative breast cancer (TNBC), is required for breast tumorigenesis in mice, and activates tumor-suppressive environments via a positive feedback signaling loop. Moreover, we show that epithelial p38γ is required for KRAS-oncogene-induced pancreatic cancer in two genetic murine models (KPC and KTC) by activating glycolytic pathways to provide metabolic support for cancer cells and by increasing chemokine CXCL5-dependent fibrosis and immune cell infiltrations. Lastly, we will delineate how p38γ is activated by the main risk factors for colon cancer and serves as a key integrator of oncogenic and inflammatory signaling to promote tumorigenesis by increasing Wnt proliferative signaling and programming immune evasion. These results indicate that p38γ MAPK can integrate common risk factors for colon cancer and amplify oncogenic signaling by phosphorylating its substrate, β-catenin, increasing transcription of Wnt and the chemokine CXCL13, and promoting PD-L1 expression. In each of these tumor models, we will present evidence supporting our hypothesis, followed by additional experiments for verification. Our studies suggest that targeting p38γ may be an innovative approach in cancer therapeutic intervention. - Source: PubMed
Publication date: 2026/07/07
Chandrashekar NaveenkumarQi Xiao-MeiChen Guan - Aortic dissection (AD) is a life-threatening vascular condition characterized by acute inflammation and structural deterioration of the aortic wall. This study aimed to delineate the immune landscape, particularly T cell-mediated responses, and identify conserved inflammatory mechanisms driving AD pathogenesis across human and murine models. - Source: PubMed
Publication date: 2026/07/11
Zhang ShenZhang YongguiSun YaodongZhu MinfangWu Naishi - This study sought to investigate the impact of MAPK12 on immune evasion in hepatocellular carcinoma (HCC) by modulating PD-L1 expression through the PI3K/AKT/mTOR pathway. Using GEPIA, Kaplan-Meier plotter, and TIMER databases, MAPK12 expression in HCC and its prognostic value were analyzed. MAPK12 expression was knocked down in HCC cells using shRNAs, and cell proliferation, migration, invasion, and EMT were evaluated. CD8 T cells were co-cultured with HCC cells. An orthotopic HCC mouse model was established to observe tumor growth, survival duration, CD8 T cell infiltration, and levels of cytokines and effector molecules. MAPK12 expression was higher in HCC tissues and cell lines. HCC patients with high MAPK12 exhibited shorter overall survival. MAPK12 knockdown reduced HCC cell growth and EMT progression, suppressed PD-L1 expression, and enhanced CD8 T cell killing activity. MAPK12 deficiency suppressed the PI3K/Akt/mTOR pathway activation, while the PI3K activator (740Y-P) reversed PD-L1 downregulation and immune killing effects. The immunosuppressive effect mediated by MAPK12 overexpression was blocked by the PI3K inhibitor LY294002. MAPK12 knockdown restricted tumor growth and extended survival in mice, accompanied by increased CD8 T cell infiltration. In summary, MAPK12 promotes HCC immune escape by upregulating PD-L1 via the PI3K/Akt/mTOR pathway. - Source: PubMed
Zhang QianLi Jun-JieWang Jin-HaiXu Yong-Jian