MEK_2 (Ab_394) Antibody
- Known as:
- MEK_2 (Ab_394) Antibody
- Catalog number:
- E021008-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- MEK_2 (Ab_394) Antibody
Related genes to: MEK_2 (Ab_394) Antibody
- Gene:
- MAP2K2 NIH gene
- Name:
- mitogen-activated protein kinase kinase 2
- Previous symbol:
- PRKMK2
- Synonyms:
- MEK2
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2019-04-23
- Gene:
- PPP4R3B NIH gene
- Name:
- protein phosphatase 4 regulatory subunit 3B
- Previous symbol:
- SMEK2
- Synonyms:
- PSY2, FLFL2, KIAA1387, FLJ31474
- Chromosome:
- 2p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-10-12
- Date modifiied:
- 2015-11-17
Related products to: MEK_2 (Ab_394) Antibody
Related articles to: MEK_2 (Ab_394) Antibody
- ObjectiveTo identify susceptibility genes associated with varicose veins (VVs) using a cross-tissue transcriptome-wide association study (TWAS) framework.MethodsWe performed a cross-tissue TWAS by integrating GWAS data from the FinnGen R12 dataset (38,467 VVs cases and 432,223 controls of European ancestry) with eQTL data from GTEx V8. The initial analysis was conducted using the Unified Test for Molecular Signatures (UTMOST), and subsequent validation incorporated multiple complementary methods, including Functional Summary-based Imputation (FUSION), Conditional and Joint Association Analysis (COJO), Fine-mapping Of CaUsal gene Sets (FOCUS), and Multi-marker Analysis of Genomic Annotation (MAGMA). Mendelian randomization (MR) and colocalization analyses were performed to explore potential genetically supported associations between candidate genes and VVs. Finally, Western blotting (WB) was conducted in venous tissue samples collected from patients undergoing surgery for VVs to provide preliminary experimental validation.ResultsThis cross-tissue TWAS analysis identified four genes (MAP3K2, PDK1, TMEM87B, and POLR1B) as susceptibility genes associated with VVs risk. MR indicated that PDK1, TMEM87B, and POLR1B may be associated with the development of VVs. Colocalization analysis suggested that POLR1B was the primary candidate gene, showing strong colocalization with VVs in whole blood (PPH4 = 0.987), and preliminary WB results suggested that the protein level of POLR1B was significantly elevated in varicose tissue.ConclusionOur findings identify POLR1B as a promising candidate susceptibility gene potentially associated with VVs risk, providing a basis for future mechanistic and translational studies. - Source: PubMed
Publication date: 2026/06/23
Kuang QuanxingZhu QingfengLi XiaochengYang HanJiang WenhongWang YoufuQin Xiao - Most Spitz tumors exhibit recurrent gene fusions involving receptor tyrosine kinase or MAPK pathway genes. Here, we describe a Spitz tumor with a novel fusion involving MAP3K2. The lesion occurred on the penile shaft of an 18-year-old. Histopathologically, tumor cells were predominantly dermal, arranged in irregularly shaped nests and cords showing minimal maturation with dermal descent, and accompanied by pseudoepitheliomatous epidermal hyperplasia. Melanocytes displayed abundant eosinophilic to amphophilic cytoplasm, variably enlarged rounded nuclei, fine chromatin, and scattered nucleoli or chromocenters. There were occasional dermal mitotic figures (1/mm). The lesion involved the deep aspect of the biopsy specimen. SOX10, S100 protein, and MITF immunohistochemical stains were diffusely positive, while Melan-A and HMB45 staining was only focal. PRAME was negative. FISH showed copy number gains at 6p25 (RREB1) and 11q13 (CCND1) narrowly exceeding cutoff values. Next-generation sequencing revealed a CPEB2::MAP3K2 fusion and a low tumor mutation burden (2.1/Mb). To our knowledge, this fusion has not been previously reported in melanocytic lesions or other human tumors. A conservative re-excision was performed, and a PET/CT scan showed no evidence of dissemination. With 16 months of follow-up available, longer-term monitoring will be required to determine the clinical behavior and biologic potential of this tumor. - Source: PubMed
Publication date: 2026/04/02
McAfee John LRicotti Claudia MRonen ShiraBillings Steven Dde la Fouchardiere ArnaudKo Jennifer S - - Source: PubMed
Publication date: 2026/02/24
Meng FantingHan XianlongGe LingxiaGuan Nan - BACKGROUND: Esophageal cancer remains a highly lethal malignancy with limited therapeutic options. Although MAP3K family members regulate proliferation and differentiation, their clinical significance and functional roles in esophageal cancer remain poorly understood. METHODS: We performed integrated multi-omics analyses including transcriptomic profiling, DNA methylation assessment, and single-cell RNA sequencing to systematically characterize MAP3K family members in esophageal cancer. WGCNA and regulatory network analyses identified downstream targets of MAP3K11. Functional studies were conducted in esophageal cancer cell lines to validate findings. RESULTS: We identified MAP3K2, MAP3K11, and MAP3K13 as significantly upregulated in esophageal cancer tissues and found that elevated MAP3K11 expression independently predicted poorer prognosis and associated with advanced metastatic disease. Single-cell analysis revealed preferential MAP3K11 enrichment in endothelial cells and uncovered a distinct MAP3K11-high malignant subpopulation exhibiting substantially enhanced communication with cancer-associated fibroblasts. MAP3K11 regulated an extensive gene network involved in apoptosis and cell junction regulation, with Rad21 emerging as a critical downstream effector. Functional studies demonstrated that MAP3K11 suppression markedly inhibited cancer cell proliferation and migration while promoting apoptosis, effects that were substantially reversed by Rad21 restoration. CONCLUSION: MAP3K11 functions as a key driver of esophageal cancer progression through the Rad21 axis and represents a promising candidate biomarker for diagnosis and prognosis. The identification of MAP3K11-mediated tumor-stromal crosstalk provides novel mechanistic insights into esophageal cancer microenvironmental dynamics. - Source: PubMed
Publication date: 2026/02/15
Zhu XiaokangZhu GongjianGuo TaoMin WeirunLi Xiangqian - Psoriasis is a chronic autoimmune disorder characterized by immune dysregulation and excessive keratinocyte proliferation. The mitogen-activated protein kinase (MAPK) signaling pathway plays a key role in driving inflammation in psoriatic skin. - Source: PubMed
Publication date: 2026/01/07
Plata-Babula AleksandraWójcik MichałGłowaczewska AmeliaZmarzły NikolaChalcarz MichałKaminiow KonradMitka-Krysiak ElżbietaKuraszewska BernadetaWieczorek WeronikaGrabarek Beniamin Oskar