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
- Triple-negative breast cancer (TNBC) remains a major cause of cancer mortality due to its aggressive behavior, metabolic adaptability, and high therapeutic resistance. Extracellular vesicles (EVs) within the tumor microenvironment contribute to tumor progression and metastasis by transferring pro-tumorigenic cargo. While conventional Tumor Treating Fields use high-frequency alternating fields to disrupt mitosis, low-energy triple-frequency bioelectromagnetic approaches remain poorly characterized. We evaluated a device-drug strategy combining triple-frequency low-intensity electromagnetic stimulation (EMS2: 396 Hz, 285 Hz, 528 Hz) with the pleiotropic drug Fingolimod (FTY720). Treatments were tested in MDA-MB-231 and ARM-G breast cancer cells, with Paclitaxel as a positive control. Cell proliferation was assessed by MTS assay, and extracellular vesicles were isolated following individual and combination treatments. Quantitative LC-MS/MS proteomics was used to characterize treatment-induced changes in EVs cargo. EMS2 reduced proliferation in both cell lines and produced morphological changes consistent with altered cell-cycle progression. EMS2 alone triggered adaptive metabolic responses, whereas combination with Fingolimod suppressed these compensatory signatures. EVs proteomics revealed combination-specific alterations associated with mitochondrial stress, ER stress, NF-κB suppression, and autophagy-associated pathways. The combination also reduced levels of metastasis- and stroma-associated proteins, including Mitogen-Activated Protein Kinase 12 (MAPK12) and collagen-associated ECM components (Collagen Type I Alpha 1 Chain (COL1A1), Collagen Type VI Alpha 1 Chain (COL6A1), Collagen Type VI Alpha 3 Chain (COL6A3), and Matrilin 3 (MATN3)) in EVs. Bliss independence analysis identified a subset of metastasis-associated proteins suppressed in EVs beyond the level predicted by an additive model, an exploratory finding that will require further validation with dose-response and functional assays. Combined triple-frequency EMS2 and Fingolimod treatment altered the extracellular vesicle proteome, inducing signatures consistent with mitochondrial and endoplasmic reticulum stress, metabolic disruption, and reduced levels of metastasis-associated and stromal/ECM remodeling proteins, along with reduced proliferation. These findings suggest a coordinated anti-cancer effect of this tunable device-drug strategy, warranting further functional and in vivo validation to confirm therapeutic potential. - Source: PubMed
Publication date: 2026/09/04
Haroutunian GregDaniels LawrenceTsaghikian AshotZhao CaifengZavras PhaedonMarukian SvetlanaZheng HaiyanMosoian Arevik - 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