STIM1 Mouse Monoclonal Antibody
- Known as:
- STIM1 Mouse Monoclonal Antibody
- Catalog number:
- ENZ-006786-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- STIM1 Mouse Monoclonal Antibody
Related genes to: STIM1 Mouse Monoclonal Antibody
- Gene:
- STIM1 NIH gene
- Name:
- stromal interaction molecule 1
- Previous symbol:
- -
- Synonyms:
- GOK, D11S4896E
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-05
- Date modifiied:
- 2019-04-23
Related products to: STIM1 Mouse Monoclonal Antibody
Related articles to: STIM1 Mouse Monoclonal Antibody
- Autosomal recessive polycystic kidney disease (ARPKD) is a severe ciliopathy caused by mutations in Polycystic kidney and hepatic disease 1 gene (PKHD1), resulting in progressive renal and hepatobiliary disease for which effective targeted therapies are lacking. Although reduced cystic fibrosis transmembrane conductance regulator (CFTR) expression has been implicated in hepatic cystogenesis, whether pharmacological restoration of CFTR is associated with improvement of the underlying cellular abnormalities remains unclear. We investigated the effects of the CFTR correctors VX-809 and VX-445, and compared them with the CFTR inhibitor CFTRinh-172, in cholangiocytes isolated from Pkhd1 mice. FPC-deficient cholangiocytes exhibited enhanced cyst growth and proliferation together with marked reductions in CFTR, polycystin-1 (PC1), and polycystin-2 (PC2) protein expression. These changes were accompanied by profound remodeling of intracellular signaling, including elevated resting cytosolic Ca²⁺, an increased thapsigargin-releasable endoplasmic reticulum Ca²⁺ pool, increased STIM1 expression, reduced IP₃ receptor expression, a marked increase in intracellular cAMP, and a switch in adenylyl cyclase isoform expression characterized by increased AC3 and reduced AC6. CFTR localization was also altered, with redistribution toward the apical membrane. Treatment with either VX-809 or VX-445 improved many of these abnormalities by increasing CFTR expression, partially restoring PC1 and PC2 expression, attenuating abnormal Ca²⁺ and cAMP signaling, reducing cholangiocyte proliferation and cyst growth, and shifting CFTR membrane distribution toward the WT pattern. In contrast, CFTRinh-172 failed to reproduce many of the same effects, indicating that inhibition of chloride conductance alone does not account for the broader cellular effects of the CFTR correctors. These findings identify coordinated remodeling of Ca²⁺- and cAMP-dependent signaling as a central feature of ARPKD cholangiocytes and show that CFTR correctors are associated with improvement of multiple disease-associated pathways. Our results support further evaluation of clinically available CFTR correctors as a potential therapeutic strategy for hepatobiliary disease in ARPKD. - Source: PubMed
Publication date: 2026/09/19
Sharma AbhishekAfshani MasoudSharma TanviCebotaru Liudmila - The mechanisms that cause hypertension remain elusive despite more than a century of investigation. Some of its triggers include aging, sex, salt, diet, stress, experience with adversity, socio-cultural-economic disparities, and poor-quality sleep. The renin-angiotensin-aldosterone and the endothelin systems and other hormones contribute to varying degrees to the rise in BP and target organ damage. It has become increasingly recognized that inflammation and the innate and adaptive immune systems play a role in the etiopathogenesis of hypertension. We review here the participation of different cellular and molecular (genetic and epigenetic) mechanisms that play a role in hypertension via the immune system, including neutrophil extracellular traps, memory T cells, and aldosterone-modulated trained immunity mediated by monocytes/macrophages. Molecular mechanisms, including the effects of neutrophil gelatinase-associated lipocalin as an immunomodulator, and the role of isolevoglandins in mediating oxidative stress-induced activation of the adaptive immune system are analysed. We conclude by summarizing potential therapeutic avenues to address inflammation in hypertension. - Source: PubMed
Publication date: 2026/09/18
Fields EviatarBerillo OlgaSchiffrin Ernesto L - The Ca release-activated Ca (CRAC) channel, triggered by the interaction between the Ca sensor STIM1 and Orai1, is the primary mediator of store-operated calcium entry (SOCE). Dysregulation of this process drives numerous human pathologies, particularly immune disorders and cancer hallmarks. Due to its role, Orai1 has emerged as an attractive target for precision therapeutics. - Source: PubMed
Publication date: 2026/09/21
Jardín IsaacMacias-Díaz AlvaroJimenez-Velarde VanesaFuentes-Mateos ManuelSmani TarikRosado Juan A - Exposure to fine particulate matter (PM) is a major environmental risk factor for pulmonary fibrosis, yet the involvement of calcium dyshomeostasis and its upstream Wnt signaling regulators in this process remains incompletely understood. This study investigated whether the dietary antioxidant β-carotene (BC) alleviates PM-induced pulmonary fibrosis by modulating the Wnt5a/Ca pathway and, if so, to identify the receptor mediating this effect. We employed a C57BL/6 murine model of intratracheal PM instillation, alongside BEAS-2B human bronchial epithelial cells subjected to Fzd5 overexpression. In vivo, PM exposure induced significant fibrosis, oxidative stress, and calcium homeostasis disruption, characterized by increased mitochondria-associated ER membranes (MAMs), aberrant expression of calcium-handling proteins (IPR, STIM1, ORAI1, SERCA2), and activation of the Wnt5a/Fzd5/Ca axis. BC treatment effectively reversed these pathological changes. In vitro, Fzd5 overexpression not only exacerbated PM-evoked activation of the Wnt5a/Ca pathway, calcium overload, oxidative stress, and EMT, but also, crucially, abrogated the protective effects of BC against these fibrotic changes. These results identify Fzd5 as a critical mediator through which BC acts. Our findings demonstrate that BC ameliorates PM-induced pulmonary fibrosis by suppressing the Fzd5-mediated Wnt5a/Ca pathway, thereby restoring calcium homeostasis. This study reveals a novel mechanistic axis in PM pathogenesis and suggests that BC may hold promise as a dietary supplement for mitigating environment-related pulmonary fibrosis. - Source: PubMed
Publication date: 2026/09/18
Wu WenboLiu LanhaoZhou JianWu ChunyueLiu YumeiLuan MengxiaoTan FengjiaoHan XiaolinTu LuxiWu MeinaMa YunyunZou YingjieWang QinLi XiaohongLi Wanwei - Hepatitis-hydropericardium syndrome (HHS), caused by fowl adenovirus serotype 4 (FAdV-4), is an acute and highly fatal disease that poses a major threat to the global poultry industry. Calcium ions serve as critical second messengers that regulate multiple stages of the viral life cycle, including entry, replication, and assembly. However, whether FAdV-4 exploits intracellular calcium signaling to facilitate its own replication remains largely unexplored. Here, we demonstrate that FAdV-4 infection significantly elevates intracellular calcium levels in LMH cells in a time- and dose-dependent manner. Mechanistically, FAdV-4 induces endoplasmic reticulum (ER) stress, which in turn upregulates the expression of STIM1 and ORAI1 and promotes the translocation of STIM1 to the plasma membrane, thereby activating the store-operated calcium entry (SOCE) channel and driving sustained intracellular calcium elevation. Functionally, elevation of intracellular calcium enhances viral protein expression and increases viral titers, whereas calcium depletion markedly suppresses FAdV-4 replication. Collectively, our findings uncover a previously unrecognized mechanism by which FAdV-4 hijacks intracellular calcium homeostasis to promote viral replication, offering new potential targets for antiviral therapy. - Source: PubMed
Publication date: 2026/08/27
Li WeiWang ChenyangShao JintianHan YanchunLiu MengyuanWang HongnuanSun ZilongZhang DingYang Bo