2024年12月25日 · MAP3K2 (Mitogen-Activated Protein Kinase Kinase Kinase 2) is a Protein Coding gene. Diseases associated with MAP3K2 include Lung Cancer and Prostate Cancer. Among its related pathways are NGF Pathway and NF-KappaB Family Pathway.

Mitogen-Activated Protein Kinase Kinase Kinase 2 also known as MEKK2 (MEK/ERK Kinase 2) is an enzyme that in humans is encoded by the MAP3K2 gene. [5][6][7] The protein encoded by this gene is a member of serine/threonine protein kinase family. This kinase preferentially activates other kinases involved in the MAP kinase signaling pathway.

2021年3月8日 · map3k2 是一个多器官组成性表达的丝 / 苏氨酸蛋白激酶。 在分子机制上研究人员发现 Map3k2 通过响应 DSS 诱导的损伤信号上调 R-spondin1 的表达，介导 MAPK 信号与 Wnt 信号之间的互作；并确认肠道间质细胞是肠道炎症损伤信号上调 R-spondin1 表达的关键细胞。

2021年3月3日 · A subset of intestinal stromal cells that is regulated by the kinase MAP3K2 protects intestinal stem cells against injury by producing the WNT agonist R-spondin 1.

2014年5月21日 · Here we show that methylation of MAP3K2 by SMYD3 increases MAP kinase signalling and promotes the formation of Ras-driven carcinomas. Using mouse models for pancreatic ductal adenocarcinoma and...

2025年2月8日 · MEKK2 is a potent activator of the c-Jun N-terminal kinase pathway in fibroblast-like synoviocytes in rheumatoid arthritis. The protein encoded by this gene is a member of serine/threonine protein kinase family.

2023年6月7日 · MAP3K2 phosphorylates IRF3 at Ser173 without involving extracellular-signal-regulated kinase 5 (ERK5) or c-Jun N-terminal kinase (JNK), increases polyubiquitination via the K33-linkage, and inhibits virus-induced IRF3 dimerization and nuclear translation, which further reduces the production of IFN-β and IFN-stimulated genes.

Ubiquitous expression in bone marrow (RPKM 11.2), thyroid (RPKM 10.3) and 25 other tissues. 该基因编码的蛋白质是丝氨酸/苏氨酸蛋白激酶家族的成员。 该激酶优先激活其他参与 MAP …

2020年7月31日 · map3k2通过il-18-jnk信号通路在肠道t细胞免疫中的新型调节作用，可为临床干预t细胞介导的肠炎提供新的潜在靶点。 图1.MAP3K2促进肠道T细胞介导的肠炎。 A .

Here we describe a subset of intestinal stromal cells, named MAP3K2-regulated intestinal stromal cells (MRISCs), and show that they are the primary cellular source of the WNT agonist R-spondin 1 following intestinal injury in mice.