STK39 / SPAK pSer325 antibody Ab
- Known as:
- STK39 / SPAK pSer325 (anti-) Antibody
- Catalog number:
- 1488168
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- STK39 / SPAK pSer325 antibody
Related genes to: STK39 / SPAK pSer325 antibody Ab
- Gene:
- STK39 NIH gene
- Name:
- serine/threonine kinase 39
- Previous symbol:
- -
- Synonyms:
- DCHT, SPAK
- Chromosome:
- 2q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-14
- Date modifiied:
- 2015-11-19
Related products to: STK39 / SPAK pSer325 antibody Ab
Related articles to: STK39 / SPAK pSer325 antibody Ab
- Septic cardiomyopathy (SCM) is a severe manifestation of sepsis characterized by myocardial dysfunction and systemic inflammation. The NLRP3 inflammasome-driven pyroptosis plays a pivotal role in SCM pathogenesis. This study aimed to elucidate the upstream molecular regulators of pyroptosis in SCM and investigate the functional role of serine/threonine kinase 39 (STK39) in modulating NLRP3 inflammasome activation. - Source: PubMed
Publication date: 2026/08/14
Dong WeiLiu WenYin YanWeng JunfeiZuo YingbingLi MenghuanXie FeiTao YuZhang LiupingXu YuemeiZhang QinPeng Xiaoping - Alzheimer's disease (AD), Parkinson's disease (PD) and Lewy body dementia (LBD) overlap clinically, pathologically and genetically, complicating interpretation of cross-disorder genome-wide association study (GWAS) signals. - Source: PubMed
Publication date: 2026/07/02
Zhang YingZhang ZhishuaiQiu ShizhengHu Yang - Transient Receptor Potential Melastatin 7 (TRPM7) is a 'chanzyme' with dual functions, acting both as a channel for divalent ions and as a serine/threonine kinase. Overexpression of TRPM7 has been linked to the development of various diseases, particularly cancers, making it a promising molecular target. Despite its relevance in oncogenesis, the phospho-regulatory network of TRPM7 remains largely unexplored, with limited evidence on its upstream kinases, downstream substrates, and site-specific phospho-regulated functions. - Source: PubMed
Publication date: 2026/06/01
Palollathil AkhinaMahin AlthafGopalakrishnan Athira PerunellySambreena AlimathShivamurthy Prathik BasthikoppaRaju Rajesh - 'Liver injury-liver fibrosis/cirrhosis-liver cancer' is the key evolution pathway of hepatocellular carcinoma (HCC), chronic inflammation serving as a major driving force in this process. However, the regulatory mechanisms underlying this process require further clarification. Here, the carcinogen-induced liver injury, liver fibrosis, and HCC models were investigated in the wild-type and STK39-knockout mice. Mass spectrometry analysis and immunoprecipitation assays were used to identify the interaction factors of STK39. QPCR, ELISA, and immunofluorescence were applied for the expression of inflammatory factors. In this study, we report that STK39 is gradually upregulated during the evolution of HCC (liver injury-liver fibrosis-liver cancer). Consequently, overexpression of STK39 further encouraged the evolution of HCC by facilitating a macrophage inflammatory response, as demonstrated in carcinogen-induced liver injury, liver fibrosis, and HCC models. Pharmacological inhibition of STK39 significantly slows the progression of HCC; however, this effect was considerably diminished after macrophage clearance. Mechanistically, mass spectrometry analysis and immunoprecipitation assays identified that STK39 interacted with PKR and promoted the activation of the PKR/NF-κB axis. Which, in turn, enhanced the macrophage inflammatory response and accelerated the evolution of HCC. The inflammatory factor TNF-α further induces the expression of STK39, suggesting a positive feedback regulation process exists. More notably, STK39 inhibition improves the efficacy of sorafenib and anti-PD1 therapy. In conclusions, our study reveals that STK39 holds significant potential for the early diagnosis and treatment of HCC. - Source: PubMed
Publication date: 2026/06/13
Zhang ChengfeiChen XinYao HongChen YiyingShe JunjunZha YongShi RuoyuChen BohaoSang YimengLei LeiZhou YangchunCheng ZhangjunXu FangguiXia Hongping - ATP2B1 and STK39 loci influence blood pressure in genome-wide association studies. We tested whether ATP2B1 rs2681472 and STK39 rs35929607 are associated with essential hypertension and blood pressure. - Source: PubMed
Akgün EgemenKaragöz AhmetMutlu İçduygu FadimeAlp Ebru