MAP2K3 & MAP2K6 Protein Protein Interaction Antibody Pair
- Known as:
- MAP2K3 & MAP2K6 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0532
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MAP2K3 & MAP2K6 Protein Interaction Antibody Pair
Related genes to: MAP2K3 & MAP2K6 Protein Protein Interaction Antibody Pair
- Gene:
- MAP2K3 NIH gene
- Name:
- mitogen-activated protein kinase kinase 3
- Previous symbol:
- PRKMK3
- Synonyms:
- MEK3, MKK3, MAPKK3
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-11
- Date modifiied:
- 2016-10-05
- Gene:
- MAP2K6 NIH gene
- Name:
- mitogen-activated protein kinase kinase 6
- Previous symbol:
- PRKMK6
- Synonyms:
- MEK6, MKK6, SAPKK3, MAPKK6
- Chromosome:
- 17q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-11
- Date modifiied:
- 2016-01-15
Related products to: MAP2K3 & MAP2K6 Protein Protein Interaction Antibody Pair
Related articles to: MAP2K3 & MAP2K6 Protein Protein Interaction Antibody Pair
- Cell division cycle protein 42 (Cdc42) is a member of the Rho GTPase subfamily that serves as a signal mediating factor in cell cycle division, cytoskeleton arrangement, cell polarization, membrane trafficking and signal transduction. However, the role of Cdc42 in cardiac remodeling, including hypertrophy and fibrosis, remains controversial. This study aimed to clarify the role and underlying mechanism of Cdc42 in cardiac remodeling. Cardiac Cdc42 knockout (Cdc42) mice were generated by crossing Cdc42 mice with MLC2v-Cre mice. Mouse cardiac remodeling models were induced by subcutaneous administration of AngII (1500 ng/kg/min) for 7 days or transverse aortic constriction (TAC) for 2 or 8 weeks. Our results showed that cardiac Cdc42 deletion significantly suppressed AngII- or TAC-induced cardiac hypertrophy and fibrosis and improved cardiac function in mice. Cdc42 or specific inhibition of Cdc42, markedly inhibited Ang II-mediated activation of the MKK3/6-p38 cascade in the heart and in isolated newborn/adult mouse cardiomyocytes or H9c2 cells. Furthermore, Cdc42 overexpression increased the surface area and hypertrophic gene expression in myocytes, whereas ML141 (a Cdc42 inhibitor) and SB203580 (a p38 inhibitor) specifically decreased p38 activation and hypertrophy in Cdc42-overexpressing or AngII-induced hypertrophic cardiomyocytes, indicating that p38 is a downstream effector of Cdc42 in cardiac hypertrophy. Taken together, our results demonstrated that Cdc42 is a key driver of cardiac remodeling via activation of the p38 signaling pathway. - Source: PubMed
Publication date: 2025/07/03
Wen KeXie LinLiu Quan-WenYu Guan-HuiQiao Xu-HuiHuang Yu-ChunWang LuLi XinWen Li-DanWang Xiao-LeiHe JingXiao Xin-YuZhao Xiao-XiaoWang Ling-FangXin Hong-BoDeng Ke-Yu - Liver hepatocellular carcinoma (LIHC) is a common cancer worldwide. Mitogen-activated protein kinase kinase (MAP2Ks) are related to the occurrence and development of a variety of tumors. However, the expression pattern, role, and prognostic value of the 7 MAP2K family members in LIHC have not yet been elucidated. We used the Oncomine, UALCAN, Human Protein Atlas, GeneMANIA, Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, TIMER, and Kaplan-Meier Plotter databases. On August 7, 2021, we searched these databases for the terms MAP2K1, MAP2K2, MAP2K3, MAP2K4, MAP2K5, MAP2K6, MAP2K7, and "liver cancer." The exposure group comprised LIHC patients, and the control group comprised normal patients (those with noncancerous liver tissue). All patients shown in the retrieval language search were included. We compared the mRNA expression of these proteins in LIHC and control patients to examine the potential role of MAP2K1 to 7 in LIHC. Relative to the normal liver tissue, mRNA expression of MAP2K1/3 was significantly downregulated (P < .001), MAP2K4 was downregulated (P < .05), and that of MAP2K2/5/6/7 significantly upregulated (P < .001), in LIHC. MAP2K mRNA expression varied with gender (P < .0001), cancer stage (P < .05), tumor grade (P < .05), and with node metastasis status (P < .05), except for MAP2K4. Based on Kyoto Encyclopedia of Genes and Genomes enrichment analysis, these genes were associated with the following pathways: MAPK signaling pathway, GnRH signaling pathway, Fc epsilon RI signaling pathway (P < .05). The MAP2Ks were significantly associated with purity (P < .05), except for MAP2K1/2, with B cell (P < .05), except for MAP2K3, and that all significantly associated withCD8+ T cell, CD4+ T cell, macrophage, neutrophil, and dendritic cell infiltration (P < .05). High mRNA expression of MAP2K1/3/4/5 (P < .05) and low expression of MAP2K6 (P < .05) indicated overall survival, the high expression of MAP2K3/4/5 were related to relapse free survival and progression free survival; the high expression of MAP2K3/5/7 were related to disease free survival. We identified MAP2K1 to 7 as potential diagnostic markers, and MAP2K2 to 7 as prognostic markers, of LIHC. Our future work will promote the use of MAP2Ks in the diagnosis and treatment of LIHC. - Source: PubMed
Dong ShenJing ShenQinshun JiaoHuaning WangRong Zhu - Scar formation is a process that occurs due to increased collagen deposition and uncontrolled inflammation. Previous studies have demonstrated that Pirfenidone (Pf), an FDA approved anti-inflammatory and antifibrotic drug can reduce inflammation as well as regulate activation of LPS-stimulated neutrophils. However, the molecular level mechanism of Pf's action is not well understood. Here, we used neural networks to identify new targets and molecular modeling methods to investigate the Pf's action pathways at the molecular level that are related to its ability to reduce both the inflammatory and remodeling phases of the wound healing process. Out of all the potential targets identified, both molecular docking and molecular dynamics results suggest that Pf has a noteworthy binding preference towards the active conformation of the p38 mitogen activated protein kinase-14 (MAPK14) and it is potentially a type I inhibitor-like molecule. In addition to p38 MAPK (MAPK14), additional potential targets of Pf include AKT1, MAP3K4, MAP2K3, MAP2K6, MSK2, MAP2K2, ERK1, ERK2, and PDK1. We conclude that several proteins/kinases, rather than a single target, are involved in Pf's wound healing ability to regulate signaling, inflammation, and proliferation. - Source: PubMed
Publication date: 2024/03/25
Wijewardhane Prageeth RWells AdrienneMuhoberac MatthewLeung Kai PChopra Gaurav - Stress-activated p38 kinases control a plethora of functions, and their dysregulation has been linked to the development of steatosis, obesity, immune disorders, and cancer. Therefore, they have been identified as potential targets for novel therapeutic strategies. There are four p38 family members (p38α, p38β, p38γ, and p38δ) that are activated by MKK3 and MKK6. Here, we demonstrate that lack of MKK6 reduces the lifespan in mice. Longitudinal study of cardiac function in MKK6 KO mice showed that young mice develop cardiac hypertrophy which progresses to cardiac dilatation and fibrosis with age. Mechanistically, lack of MKK6 blunts p38α activation while causing MKK3-p38γ/δ hyperphosphorylation and increased mammalian target of rapamycin (mTOR) signaling, resulting in cardiac hypertrophy. Cardiac hypertrophy in MKK6 KO mice is reverted by knocking out either p38γ or p38δ or by inhibiting the mTOR pathway with rapamycin. In conclusion, we have identified a key role for the MKK3/6-p38γ/δ pathway in the development of cardiac hypertrophy, which has important implications for the clinical use of p38α inhibitors in the long-term treatment since they might result in cardiotoxicity. - Source: PubMed
Publication date: 2022/08/16
Romero-Becerra RafaelMora AlfonsoManieri ElisaNikolic IvanaSantamans Ayelén MelinaMontalvo-Romeral ValleCruz Francisco MiguelRodríguez ElenaLeón MartaLeiva-Vega LuisSanz LauraBondía VíctorFilgueiras-Rama DavidJiménez-Borreguero Luis JesúsJalife JoséGonzalez-Teran BarbaraSabio Guadalupe - Gamma synuclein (SNCG) is a neuronal protein that is also aberrantly overexpressed in various types of human cancer. SNCG overexpression promotes cancer invasion and metastasis. However, the mechanisms that drive cancer metastasis upon SNCG expression remain elusive. Elucidation of the mechanisms underlying the promotion of cancer metastasis by SNCG may help discover therapeutic avenues for SNCG-overexpressed cancer. Here, we show that SNCG promotes transforming growth factor-β (TGF-β)-induced p38 mitogen-activated protein kinase (MAPK) phosphorylation. Mechanistically, SNCG promotes p38MAPK phosphorylation by interacting with the MAPK kinase 3/6 (MKK3/6) and prevents their degradation. SNCG knockdown leads to a decrease in TGF-β-induced phosphorylation of MKK3/6; and abrogates the induction of matrix metalloproteinase (MMP)-9 expression by TGF-β and its target gene Twist1. Furthermore, p38MAPK inhibition abrogates the promotion of MMP-9 expression and cancer cell invasion by SNCG. Both p38MAPK and MMP inhibitors can suppress the promotion of cancer cell invasion by SNCG. Finally, overexpression of SNCG in liver cancer cells promotes lung metastasis, which can be suppressed by the p38MAPK inhibitor. Together, our data uncover a previously unknown role of SNCG in promoting TGF-β-MKK3/6-p38MAPK signaling. This study highlights the critical role of p38MAPK in the promotion of cancer metastasis by SNCG, and indicates that p38MAPK inhibitor may serve as a potential therapeutic for SNCG-overexpressed cancer. - Source: PubMed
Publication date: 2022/05/01
Liu JieyaShao TingZhang JinLiu QianyiHua HuiZhang HongyingWang JiaoLuo TingShi Yuenian EricJiang Yangfu