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
- Bladder cancer (BC) is a highly prevalent malignant tumor. The traditional Chinese medicine formula Guo Lou Qu Mai Wan (GLQMW), when used in conjunction with chemotherapy, has been shown to reduce adverse reactions and prolong survival time, although its specific mechanisms remain unclear. This study aims to investigate whether GLQMW exerts its therapeutic effects on bladder cancer by modulating the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/04/15
Teng QiliangCheng ShuminChen JiaZhu HongyaHu KaiSun LinglingZhao JinYuan ZhenboWang WenjingZhang LiLiu TaoliFeng Jiahao - To develop a telomere-related prognostic signature for esophageal carcinoma (ESCA), we integrated bioinformatics and machine learning approaches. Hub genes were identified from overlapping differentially expressed genes (DEGs). A prognostic model was constructed using LASSO and multivariate Cox regression, validated in independent GEO datasets, and further verified through cytological experiments. We also elucidated the mechanism by which MAPK12 promotes ESCA migration. The model robustly predicted survival of patients with ESCA, supported by both high-throughput data and experimental evidence. Our findings highlight MAPK12 as a promising biomarker and provide a theoretical basis for understanding ESCA pathogenesis and developing targeted therapies. - Source: PubMed
Publication date: 2025/12/29
Gu ShuyuanYan XinyangChen ShihuiDong ZepengLi XiaopengYe ChangchunZhao ChenyeYuan HangSun XuejunZhao WeiZhang Peng - Prurigo nodularis (PN) is a chronic, neuroimmune-driven skin disease characterized by intensely pruritic nodules and marked impairment in QOL. Although PN shares inflammatory features with atopic dermatitis and psoriasis, its underlying pathogenesis remains poorly defined. In this study, we performed NanoString-based transcriptomic profiling on lesional skin biopsies from patients with PN (n = 26), those with atopic dermatitis (n = 25), those with psoriasis (n = 15), and healthy controls (n = 12) using a custom neuroinflammation-focused panel. PN demonstrated a unique molecular signature involving neuroimmune activation (, ), extracellular matrix remodeling (matrix metalloproteinase 14 gene , ), and fibrotic signaling (, ), with IL-6 and MAPK12 as key inflammatory mediators. Compared with atopic dermatitis, PN displayed reduced T helper 2 signaling but greater neuroinflammatory and fibrotic activity. Relative to psoriasis, PN lacked T helper 17-driven hyperproliferation but showed macrophage and extracellular matrix activation. STRING network analysis also revealed IL-6 and TGF-β signaling as central hubs linking neuroinflammation and fibrosis. These findings establish PN as a distinct inflammatory skin disease at the intersection of neuroimmune dysregulation and tissue remodeling. Our results highlight key pathways that may guide precision therapies beyond current T helper 2-targeted treatments, supporting the development of IL-6, TGF-β, and Jak/signal transducer and activator of transcription-directed strategies in PN. This transcriptomic analysis establishes a framework to guide mechanistic and therapeutic investigations in PN. - Source: PubMed
Publication date: 2025/10/17
Akiska Yagiz MatthewBhatt ShreyVats KavitaYossef Selina MGage DaviesShahsavari ShahinBorn Louis JBhagchandani PeryaFayyad DeenaCornman HannahPritchard ThomasTeague Jessica EClark Rachael AKwatra Madan MKwatra Shawn G - Neuroblastoma (NB) is a devastating childhood cancer where most tumours have no clear oncogenic driver. We aimed to define whether HMMR, an oncogene-like protein in several cancers, harbors similar potential in neuroblastoma cells. HMMR is a hyaluronic acid (HA) receptor and a mitotic microtubule regulator. We show that high HMMR expression does not correlate well with MYCN driver expression and moreover statistically HMMR is an independent prognostic indicator of poor survival in NB patients. In cultured KELLY neuroblastoma cells, removal of the HMMR protein suppresses proliferation, motility and clonogenic capacity, while xenografts of HMMR-deficient cells imparted longer animal survival compared to wild type cells. Loss of motility in culture was compensated by addition of exogenous HA, suggesting that HMMR signaling is at least partly under HA control. Through an unbiased phosphoproteomic analysis, we also found that signaling downstream of MAPK1/2 was disrupted after loss of HMMR. In addition, RPS6 and p70S6 kinase were hypophosphorylated, while the DNA damage response (DDR) proteins such as CHK2 and TP53BP1 were significantly hyperphosphorylated. We thus provide, for the first time, evidence that HMMR does have oncoprotein-like properties in neuroblastoma cells and that HMMR expression has potential as a prognostic marker. Moreover, initial biochemical analyses highlight a potential influence for HMMR in MTOR and DDR pathway regulation. - Source: PubMed
Publication date: 2025/11/18
Karapouliou ChristinaFaizul Elisyazaviera MRajeeve VinothiniCutillas Pedro RStoker Andrew W - Cancer remains a leading cause of mortality globally, driven by complex molecular mechanisms and characterized by significant biological heterogeneity across cancer types. We aimed to discover mitogen-activated protein kinases (MAPKs) family members as both biomarkers and therapeutic targets in different cancer types. MAPKs are key signaling molecules regulating cell proliferation, differentiation, stress response, and apoptosis. Dysregulation of MAPK pathways has been implicated in the onset and progression of multiple cancers, contributing to tumor growth, metastasis, and therapeutic resistance. Given their diverse roles across cancer types, systematic analysis of MAPK gene expression, mutations, and interactions with tumor microenvironment is essential. - Source: PubMed
Sulaimani Md NayabSingh PrithviSaeed Mohammad UmarZaidi SobiaHussain AfzalAlajmi Mohamed FShamsi AnasDohare RavinsHassan Md Imtaiyaz