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
- 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 - The development of BCR::ABL1 tyrosine kinase inhibitors (TKIs) has transformed chronic myeloid leukemia into a chronic disease with near-normal life expectancy. More recently, treatment-free remission (TFR), defined as sustained molecular remission even after TKI discontinuation, has emerged as a realistic therapeutic goal and a type of functional cure. Landmark studies, including STIM1, A-STIM, EURO-SKI, ENESTfreedom, DADI, and J-SKI, have established the feasibility and safety of TFR. Their results showed that approximately half of eligible patients can successfully discontinue therapy. However, the reliable prediction of TFR success remains a major challenge. Accumulating evidence indicates that durable TFR reflects a dynamic equilibrium between residual leukemic stem cells (LSCs) and host immune surveillance. Natural killer cells and T-cell immunity contribute to maintaining remission after TKI discontinuation. Conversely, immune exhaustion and the persistence of LSCs are associated with molecular relapse. Emerging biomarkers, including immune profiling, immunogenetic markers, and minimal residual disease kinetics, may improve relapse-risk stratification. To increase the proportion of patients who achieve durable TFR, future efforts should focus on the development of risk-adapted consolidation strategies incorporating optimized TKI therapy, immune modulation, and LSC-targeted approaches. - Source: PubMed
Publication date: 2026/09/11
Ureshino Hiroshi - Crosslinking of the high affinity IgE receptor (FcεRI) by multivalent antigen increases intracellular Ca concentration ([Ca]) through two sequential steps: (i) Ca release from the endoplasmic reticulum (ER) and (ii) store-operated Ca entry (SOCE) mediated by stromal interaction molecule 1 (STIM1)-Orai1 interaction. This process is essential for basophil and mast cell activation. We previously showed that FcεRI disaggregation by monomeric hapten rapidly and persistently inhibited [Ca] increase although upstream signal disruption was transient in rat basophilic leukemia cells. However, the underlying inhibitory mechanisms remain unclear. In this study, we found that monomeric hapten dissociates STIM1-Orai1 interaction by promoting Orai1 re-phosphorylation. Although Ca release from ER, the first step in [Ca] increase, was blocked by monomeric hapten addition, phosphorylation of phospholipase Cγ1, a critical step for Ca release from the ER, was inhibited only when the monomeric hapten was added immediately after multivalent antigen stimulation, but not when added several minutes later. However, STIM1-Orai1 interaction was dissociated by the monomeric hapten, regardless of the timing of its addition. Multivalent antigen induced Orai1 dephosphorylation, which is necessary for SOCE. In contrast, monomeric hapten addition promoted its re-phosphorylation. These results suggest that cessation of [Ca] increase following FcεRI disaggregation primarily arises from immediate suppression of SOCE via STIM1-Orai1 dissociation. - Source: PubMed
Publication date: 2026/09/04
Suzuki RurikoOgawa RinkaFuruno Tadahide