MEKK3 pAb
- Known as:
- MEKK3 pAb
- Catalog number:
- ASAKAS-MA013E
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- MEKK3 pAb
Related genes to: MEKK3 pAb
- 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 pAb
Related articles to: MEKK3 pAb
- 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 - Apoptosis plays a significant role in osteoporosis (OP), yet a causal relationship between apoptosis gene expressions and OP remains unexplored. This study applies an integrated multi-omics analysis to establish causality between them, offering clinical treatment and prediction insights. - Source: PubMed
Publication date: 2026/03/23
Wang YixiXia LintaoXiao YangWu MingxingZhang RuiRexiti PaerhatiZhang Hui - Visceral hypersensitivity is a hallmark feature of irritable bowel syndrome (IBS), yet its underlying mechanisms remain incompletely understood. In the present study, we found that miRNA-let7b5p was downregulated in the spinal cord of IBS model rats induced by neonatal colorectal distension. Concurrently, microglia exhibited a shift toward a pro-inflammatory M1 phenotype and selectively engulfed inhibitory synapses, resulting in impaired GABAergic neuronal function and disruption of the excitatory/inhibitory balance. Intrathecal administration of a miRNA-let7b5p agomir suppressed M1-type microglial activation in the spinal cord, reduced pro-inflammatory cytokine levels, and alleviated visceral hypersensitivity, whereas antagomir treatment induced visceral hypersensitivity in control rats. Mechanistically, MAP3K3 was identified as a direct target of miRNA-let7b5p, and its knockdown recapitulated the protective effects conferred by miRNA upregulation. Collectively, these findings demonstrate that miRNA-let7b5p attenuates IBS-associated visceral hypersensitivity by downregulating MAP3K3, thereby inhibiting spinal microglial activation and restoring GABAergic neuronal function. This study provides novel insights into the pathogenesis of IBS-related visceral hypersensitivity and highlights a potential therapeutic target for drug development. - Source: PubMed
Publication date: 2026/03/04
Wu XianheTang YingHe ZhengqingYang FanLiu YiqianZhang QianliChen AiqinChen YuLin Chun - Verrucous venous malformation (VVM) is frequently misdiagnosed. This individual demonstrates the value of genetic testing to inform correct diagnosis. Consent was provided for retrospective chart review and publication. At birth, the affected individual had a red flat patch with overgrowth of his right hand, arm, and shoulder. The overgrowth and red color persisted and began to cause pain, which prompted his initial evaluation at age 10 years, leading to a diagnosis of a capillary vascular malformation and overgrowth. Routine magnetic resonance imaging of the right arm showed no definitive vascular anomaly. At 12 years old, hyperkeratosis prompted a biopsy for diagnosis. Pathology from 2 skin biopsies was most consistent with a capillary malformation and showed mildly acanthotic epidermis with hyperkeratosis overlying dilated, thin-walled vascular channels. We performed a 34-gene somatic genetic testing panel on the biopsy tissue. Results showed a likely pathogenic variant in the gene c.674C>T, p.Ser225Phe at variant allele fraction of 4.2%-4.6% from sample 1 and 7.3%-8.0% from sample 2, confirming the diagnosis of VVM. Somatic genetic testing provided this affected individual with the diagnosis of VVM when radiology, pathology, and clinical findings were discrepant. This new genetic diagnosis influences treatment and prognosis. - Source: PubMed
Publication date: 2025/09/19
Britt AllisonBolli AmberTreat JamesCahill Anne MarieAdams DeniseGanguly ArupaQueenan MariaSurrey LeaLow DavidSheppard Sarah