MEKK3 Polyclonal Antibody
- Known as:
- MEKK3 Polyclonal Antibody
- Catalog number:
- a-0474-100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Epigentek inc
- Gene target:
- MEKK3 Polyclonal Antibody
Related genes to: MEKK3 Polyclonal Antibody
- Gene:
- MAP3K3 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase 3
- Previous symbol:
- MEKK3
- Synonyms:
- MAPKKK3
- Chromosome:
- 17q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-14
- Date modifiied:
- 2016-01-15
Related products to: MEKK3 Polyclonal Antibody
Related articles to: MEKK3 Polyclonal Antibody
- Cerebral cavernous malformations (CCMs) are vascular lesions caused by the loss-of-function mutations in one of three CCM genes, CCM1 (KRIT1), CCM2, and CCM3 (PDCD10), or gain-of-function mutation in MAP3K3, which encodes MEKK3. Loss of function in CCM genes leads to pathological activation of MEKK3 signaling. Genetic reduction of MAP3K3 gene dosage or pharmacological inhibition of MEKK3 suppresses CCM formation in mouse models, establishing MEKK3 as a promising therapeutic target for CCM. - Source: PubMed
Publication date: 2026/07/28
Zhao QianqianZheng MinWan XiaoboLi BingjieYang XiGao CaixiaHan ZhimingSun HuabingFu YuanZheng Xiangjian - Chronic primary pain conditions (CPPCs), such as fibromyalgia and vestibulodynia, affect over 100 million Americans, predominantly women, and pose a substantial healthcare challenge. CPPCs arise from genetic and environmental factors that enhance catecholamine tone, potentially through miRNA dysregulation following catecholamine activation of β-adrenergic receptors. Here, we identified miR-133a-3p as a biomarker of CPPC status and investigated its functions using in vivo and in vitro approaches. Plasma levels of miR-133a-3p were consistently downregulated in humans with ≥ 1 CPPC and in rat and mouse models of primary pain. Our data suggest that miR-133a-3p is packaged in extracellular vesicles that are secreted by adipocytes and trafficked to the spinal cord. Activation of adrenergic receptors on white adipocytes resulted in downregulation of miR-133a-3p, negatively regulating pain-related genes in the spinal cord, such as MAP3K3, which is critical for sensory neuron activation. Adipose-specific overexpression of miR-133a-3p in a mouse model of primary pain reversed mechanical hypersensitivity in both sexes. These findings implicate miR-133a-3p dysregulation in primary pain across conditions and species and establish its role in multisite mechanical hypersensitivity. Furthermore, miR-133a-3p overexpression shows therapeutic potential for the millions of individuals with CPPCs. - Source: PubMed
Publication date: 2026/07/21
Hernandez Nathaniel PChen JiegenQian YilingZhang XinWang YaominCiszek Brittney PGao XianglongKlein Marguerita EPai Yun-LingKaraky MohamadMeloto Carolina BeraldoMontagna FrancescaKanke MattCrewe ClairDiatchenko LudaSethupathy PraveenNackley Andrea G - Myxomas are benign soft tissue neoplasms typically driven by activating GNAS mutations. However, a subset lacks this alteration and remains molecularly undefined. Recent reports have implicated MAP3K family gene fusions in rare myxoid neoplasms sharing features with myxoma. - Source: PubMed
Publication date: 2026/07/05
Macagno NicolasFrankel DianeMeurgey AlexandraPissaloux DanielBuisson AdrienBaltrès AlineGouin FrançoisVaz GualterBrahmi MehdiDufresne ArmelleDecouvelaere Anne-ValérieMaran-Gonzales AurélieRochaix PhilippeLeroux AgnèsWeinbreck Nicolasde la Fouchardière ArnaudBlay Jean-YvesTirode FranckKaranian Marie - Cisplatin-based chemotherapy is first-line for muscle-invasive bladder cancer (BLCA), but chemoresistance remains the primary barrier to clinical efficacy. RNA-binding proteins (RBPs) orchestrate post-transcriptional gene regulation and are increasingly implicated in cancer chemoresistance; however, the role and regulatory mechanism of the splicing factor RBP SLU7 in BLCA cisplatin resistance remain completely unknown. - Source: PubMed
Publication date: 2026/05/18
Wang BenlinZheng XianchongHua QingshengZou FengHuang TaoChen Jiawei - Cerebral cavernous malformations (CCMs) are vascular lesions in the central nervous system that can cause strokes and seizures. Aggressive CCM growth follows an endothelial cell two-hit mechanism in which enhanced MEKK3-KLF2/4 signaling stimulates PI3K signaling, but how these pathways are linked has been undefined. Here, we use human CCM specimens, two mouse models of CCM disease, and primary human endothelial cells to examine the roles of the major endothelial growth factor receptors, VEGFR2 and TIE2. We find no evidence of augmented VEGFR2 signaling in CCM lesions, and neither genetic nor pharmacologic blockade of VEGFR2 reduced CCM formation in mouse models. Instead, we observe markedly increased phospho-TIE2 levels in human and mouse CCM lesions, MEKK3-KLF2/4-driven induction of TIE2 receptor expression, and almost complete rescue of CCM formation following genetic or pharmacologic TIE2 blockade in mouse models. Our studies identify TIE2 as the molecular link between the MEKK3-KLF2/4 and PI3K signaling pathways during CCM formation and suggest that targeting TIE2 may be an effective means to treat human CCM disease. - Source: PubMed
Publication date: 2026/03/27
Li LunCastro MarcoHongo HirokiRen JianShenkar RobertJabarkheel RashadGao SiqiNarayan SwetaFrankfurter MaxwellTang Alan TYang JishengChen MeiBockman JennaMericko-Ishizuka PatriciaAlcazar RobertoSader GeorgioIqbal JavedKinkade SerenaLightle RhondaRessler Andrew KQu XianghuBaldwin H ScottMarchuk Douglas AAwad Issam ABurkhardt Jan-KarlPotente MichaelKahn Mark L