STK39 / SPAK pSer311 antibody Ab
- Known as:
- STK39 / SPAK pSer311 (anti-) Antibody
- Catalog number:
- 1488171
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- STK39 / SPAK pSer311 antibody
Related genes to: STK39 / SPAK pSer311 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 pSer311 antibody Ab
Related articles to: STK39 / SPAK pSer311 antibody Ab
- Familial Parkinson's disease (PD) and vascular parkinsonism (VP) present overlapping features and may co-exist. To investigate whether PD and VP may share a potential pathogenic link and to what extent white matter hyperintensities may influence PD phenotype, we used the modified Scheltens scale and presented a descriptive and exploratory analysis of the classic neuroradiological features of cerebral small vessel disease (cSVD) in the axial T2-FLAIR MRI sequences in a cohort of 104 familial PD and PD prodromal patients and 48 age-matched controls from the PPMI publicly available database. We next performed whole exome sequencing to examine the protein coding variability in the main PD-causing and risk genes (VPS35, DJ1, PINK1, ATP13A2, PRKN, SNCA, LRRK2, GBA, MAPT, LAMP3, STK39) in a cohort of 96 patients with familial cSVD and 243 elderly healthy individuals (HEX database). In this cohort, patients with familial and prodromal PD present a moderate burden of superficial frontal white matter hyperintensities (p-value = 3.46e-06, Bonferroni-corrected), linked to a mild reduction of motor and cognitive function and an increased LRRK2 p.G2019S and p.R1441C variant penetrance, and bilateral basal ganglia periventricular enlarged spaces (p-value = 2.64e-03, Bonferroni-corrected). Moreover, one-third of familial PD patients displayed a burden of lacunar thalamic strokes (p-value = 0.058), associated with a moderate hypokinetic-rigid syndrome. Finally, we report no known pathogenic coding variant in the main PD causative genes and risk factors in a cohort of 96 early-onset cSVD Caucasian patients. Our study adds to the understanding of potential cSVD hallmarks within this familial LRRK2, GBA and SNCA PD-PD prodromal cohort. - Source: PubMed
Publication date: 2026/09/08
Mahat BigyanMalla BimalaFoddis MarcoBeule DieterBras JoseGuerreiro RitaKola VasilisSchmitt Hans-MichaelEndres MatthiasSassi Celeste - 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