Polyclonal Rabbit MAP4K2 Antibody
- Known as:
- Polyclonal Rabbit MAP4K2 Antibody
- Catalog number:
- abx113854
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Polyclonal Rabbit MAP4K2 Antibody
Related genes to: Polyclonal Rabbit MAP4K2 Antibody
- Gene:
- MAP4K2 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase kinase 2
- Previous symbol:
- RAB8IP
- Synonyms:
- GCK, BL44
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-18
- Date modifiied:
- 2014-11-19
Related products to: Polyclonal Rabbit MAP4K2 Antibody
Related articles to: Polyclonal Rabbit MAP4K2 Antibody
- Abnormal expression of mammalian sterile 20-like kinase 4 (MST4) has been frequently linked to cancer development. This study explores the function of MST4 in non-small cell lung cancer (NSCLC) and delves into its functional mechanism. The expression and clinical indicative values of MST4 in NSCLC were analyzed using tissue microarrays. Gain- and loss-of-function experiments of MST4 were conducted in NSCLC cell lines to identify its effects on cell growth in vitro. Transfected NSCLC cells were co-cultured with natural killer (NK) cells to analyze immune resistance. Mouse NSCLC cells 3LL were transplanted into C57BL/6 mice to generate subcutaneous or orthotopic isograft tumor models. Upstream and downstream factors of MST4 were identified using bioinformatics. MST4 was under-expressed in NSCLC tissue microarrays and human NSCLC cells. MST4 overexpression suppressed growth activity of NSCLC cells in vitro, reduced expression of immune checkpoint genes, and reduced cell resistance to NK cell cytotoxicity. Reverse trends were observed in MST4-silenced cells. In vivo, MST4 overexpression inhibited tumorigenic activity of 3LL cells in mice and reduced immunosuppressive factors in tumor tissues. Regarding the mechanism, MST4 induced phosphorylation and cytoplasmic degradation of YAP1 by influencing the MAP4K2-LATS1/2 cascade. Protein phosphatase 4 catalytic subunit (PPP4C) was found to interact with MST4 and reduce its function, thus promoting growth and immunosuppression in NSCLC by activating YAP1. This study demonstrates that PPP4C-mediated MST4 degradation contributes to growth activity and immunosuppression in NSCLC by restoring YAP1 activity, suggesting PPP4C and MST4 as potential targets for NSCLC management. - Source: PubMed
Publication date: 2026/02/12
Xu ZhengshuiGao JianiYe ChangchunLi YuZhao DanwenLi LiangSun LiangzhangCheng YaoLi WendengJiang JiantaoLiu Shiyuan - Protein phosphorylation has pivotal roles in ABA and dehydration stress signaling in higher plants. However, little is known about MITOGEN-ACTIVATED PROTEIN KINASE KINASE KINASE KINASE (MAP4K) in dehydration tolerance. Here, we report MAP4K1 and MAP4K2 are involved in dehydration tolerance. Mutations in MAP4K1 or MAP4K2 did not show obvious phenotype whereas map4k1 map4k2 double mutant exhibited the dwarf phenotype and low dehydration tolerance with hyposensitivity to exogenous abscisic acid. MAP4K1 and MAP4K2 interacted with SnRK2.2, SnRK2.3, and OST1 in vitro and in vivo. OST1, but not SnRK2.2 or SnRK2.3, phosphorylated MAP4K1 and MAP4K2. Mass spectrometry and phosphorylation activity assay revealed that OST1 phosphorylated MAP4K1 on serine 487 and MAP4K2 on serine 488, respectively. MAP4K1 and MAP4K2 as well as OST1 act in the same dehydration stress pathway, with OST1 acting downstream of MAP4K1 and MAP4K2. Together, we identified MAP4K1 and MAP4K2 as new substrates of OST1, and MAP4K1 and MAP4K2 are redundant in dehydration tolerance. - Source: PubMed
Hu PengchengZheng LipengChen LanZhou YimingWang YuxinHuang TongtongZhang HeDing Yong - MAP kinase kinase kinase kinase (MAP4K) family kinases are key kinases for T cell-mediated immune responses; however, in vivo roles of MAP4K2 in immune regulation remain unclear. Using T cell-specific Map4k2 conditional knockout (T-Map4k2 cKO) mice, scRNA-seq, and mass spectrometry analysis, we found that MAP4K2 interacted with DDX39B, induced forkhead box protein P3 (FOXP3) gene expression, and promoted Treg differentiation. Mechanistically, MAP4K2 directly phosphorylated the DEAD box protein DDX39B, leading to DDX39B nuclear translocation and subsequent Foxp3 RNA splicing. MAP4K2-induced FOXP3 mRNA levels were abolished in DDX39B knockout T cells. Furthermore, T-Map4k2 cKO mice displayed the reduction of Treg population and the sustained inflammation during remission phase of EAE autoimmune disease model. Remarkably, the anti-PD-1 immunotherapeutic effect on pancreatic cancer was significantly improved in T-Map4k2 cKO mice, Treg-specific Map4k2-deficient mice, adoptively transferred chimeric mice, or MAP4K2-inhibitor-treated mice. Consistently, scRNA-seq analysis of patients with pancreatic cancer showed increased MAP4K2 levels in infiltrating Treg cells. Collectively, MAP4K2 promotes Treg differentiation by inducing DDX39B nuclear translocation, leading to the attenuation of antitumor immunity. - Source: PubMed
Publication date: 2026/01/29
Chuang Huai-ChiaWang Chia-WenHsueh Chia-HsinXiao Yu-ZhiTsai Ching-YiHsu Pu-MingTan Evelyn LChiu Hsien-YiTan Tse-Hua - Maturity-onset diabetes of the young (MODY), a common type of monogenic diabetes caused by a pathogenic variant in a single gene, is characterized by starting at an early age, autosomal dominant inheritance, and decreased secretion of insulin. Despite its clinical importance, its accurate diagnosis is challenging, and it is often misdiagnosed as other types of diabetes. Therefore, understanding the genetic basis of MODY can improve diagnostic accuracy. - Source: PubMed
Publication date: 2025/12/30
Sefid FatemeDehghan Tezerjani MasoudAsadollahi SamiraMadani Seyed AliPardal TayebehImani MaryamSalmani ZahraRahmanian MasoudHozhabri HosseinKalantar Seyed MehdiVahidi Mehrjardi Mohammad Yahya - Abscisic acid (ABA)-induced stomatal closure limits water loss from plants under drought stress. To investigate the signaling pathways involved in ABA-induced stomatal closure, we performed a phosphoproteomic analysis of ABA-treated guard cell protoplasts (GCPs). We found that ABA-responsive phosphorylation of MITOGEN-ACTIVATED PROTEIN 4 KINASE 1 (MAP4K1) was significantly down-regulated in SnRK2-disrupted mutants. Subsequent biochemical assays showed that Ser of MAP4K1 is directly phosphorylated by SRK2E/OST1, a central ABA kinase. Mutational analyses of MAP4K1 and MAP4K2 revealed that both kinases positively regulate ABA-induced stomatal closure and that Ser of MAP4K1 is required for this phenotype. In double mutants, stomatal closure was induced by applying exogenous Ca but not HO. Electrophysiological experiments showed that MAP4K1/2 is required for ABA-dependent activation of Ca-permeable channels in GCPs. Together, our results indicate that SnRK2 and MAP4K function as a signaling module to regulate the Ca-mediated pathway in ABA-induced stomatal closure. - Source: PubMed
Publication date: 2025/12/19
Yamashita KotaKatagiri SotaroTakase HinanoLi YangdanOishi AnzuOtoguro AiriKamiyama YoshiakiYamauchi ShotaWang Yuh-ShuhTakemiya AtsushiMori Izumi CKollist HannesUmezawa Taishi