Ask about this productRelated genes to: ORAI2 Blocking Peptide
- Gene:
- ORAI2 NIH gene
- Name:
- ORAI calcium release-activated calcium modulator 2
- Previous symbol:
- C7orf19, TMEM142B
- Synonyms:
- CBCIP2, FLJ12474, FLJ14733, H_NH0514P08.8
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-09
- Date modifiied:
- 2016-07-18
Related products to: ORAI2 Blocking Peptide
Related articles to: ORAI2 Blocking Peptide
- Circular RNAs (circRNAs) play a crucial role in the progression of malignant tumors such as breast cancer. - Source: PubMed
Publication date: 2026/04/22
Yang HaojieTan ZicongLiu ZihaoChen KangLiufu NingJi Fengtao - Store-operated calcium entry (SOCE), mediated by ORAI1-3 calcium channels and stromal interaction molecules STIM1 and STIM2, is increasingly recognized as a regulator of cancer progression. However, its role in head and neck squamous cell carcinoma (HNSCC) and its relationship with major oncogenic pathways remain poorly defined. Transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) were analyzed to profile isoform-specific ORAI1-3 and STIM1-2 expression across HNSCC subtypes and oncogenic contexts. In parallel, the effects of pharmacologic SOCE inhibition with 2-aminoethoxydiphenyl borate (2-APB) were evaluated in FaDu (epidermal growth factor receptor [EGFR]-high, PIK3CA-wild-type) and Detroit-562 (metastatic, PIK3CA-mutant) cells by assessing viability, migration, and clonogenic survival. TCGA analysis revealed a context-dependent SOCE expression profile. ORAI1-3 and STIM2 were broadly upregulated in tumors, while STIM1 was significantly downregulated, particularly in advanced and basaloid subtypes. PIK3CA mutations, especially the H1047R hotspot, were associated with higher STIM1 expression, whereas EGFR expression correlated positively with STIM1/2 but negatively with ORAI1/3. In vitro, Detroit-562 cells expressed higher levels of SOCE components and showed greater sensitivity to SOCE inhibition, with marked reductions in viability, migration, and clonogenic capacity. FaDu cells, despite higher EGFR expression, exhibited lower SOCE gene expression and relative resistance to 2-APB, which suggests reduced dependence on SOCE-mediated signaling. These findings suggest that SOCE components are transcriptionally dysregulated in HNSCC and may represent a context-dependent therapeutic vulnerability, particularly in PIK3CA-mutant tumors. Validation in additional preclinical models, patient-derived xenografts, and clinical specimens is required to establish SOCE as a biomarker and therapeutic target in HNSCC. - Source: PubMed
Publication date: 2026/03/09
Ghozlan HebaAl-Malahmeh SajaAl-Shboul OthmanMistareehi Anas JElsalem Lina - Post-inflammatory hyperpigmentation (PIH) is a common pigmentary disorder characterized by excessive melanin production following skin inflammation. Histamine, a key inflammatory mediator, is known to stimulate melanogenesis via H receptors; however, the underlying calcium (Ca) signaling mechanisms remain largely unexplored. In this study, we investigated the role of the ORAI1-STIM1 complex in histamine-induced melanogenesis using B16F10 melanoma cells and normal human epidermal melanocytes (NHEMs). Histamine (10-30 μM) significantly increased melanin content (2.5-2.8-fold), an effect specifically abolished by the H antagonist famotidine. Notably, while acute histamine application failed to trigger immediate Ca influx, chronic exposure significantly enhanced store-operated Ca entry (SOCE) capacity by approximately 2.8-fold, providing evidence for a functional remodeling of the Ca signaling machinery. Histamine-induced melanogenesis was significantly suppressed by intracellular Ca chelation, pharmacological inhibition of ORAI1 (BTP-2 or Synta-66), and siRNA-mediated silencing of ORAI1 or STIM1, but not ORAI2, ORAI3, or STIM2. Our findings demonstrate that chronic histamine exposure drives hyperpigmentation through ORAI1-STIM1-mediated SOCE remodeling, establishing this complex as a promising therapeutic target for the treatment of PIH and related inflammatory pigmentary disorders. - Source: PubMed
Publication date: 2026/02/22
Van Nhung Thi HongPhan Hong Thi LamNguyen Minh TuanKim Woo KyungKim Hyun JongNam Joo Hyun - Acute myeloid leukemia (AML) remains a high-risk hematologic malignancy due to frequent relapse and therapeutic resistance. Although induction therapy can achieve cytological remission, a fraction of leukemic cells (minimal residual disease, MRD) persists within the protective bone marrow (BM) microenvironment. MRD is heterogeneous and may include subclones with intrinsic survival features present before therapy. Among these, rare BM-resident leukemic cells (BMresLC) may represent pre-adapted precursors of MRD, maintained in a low-proliferative (Ki67) or quiescent state. We previously showed that calcium signaling through ORAI1-dependent store-operated calcium entry (SOCE) contributes not only to AML stemness and drug resistance but also to the regulation of the G0-G1 cell-cycle transition and the emergence of slow-cycling leukemic cells. With this study, we have characterized the stemness and calcium signature of BMresLC before any therapeutic intervention. Our results, beyond further characterizing a population of cells rarely studied, could thus pave the way to new therapeutic opportunities combining current treatments with the targeting of relevant pathways highlighted by our work. - Source: PubMed
Publication date: 2026/01/09
Titah SofiaGuillemette AurélieLewuillon ClaraShaik Faruk AzamBerthon CélineGoursaud LaureTardivel MeryemBongiovanni AntoninoChauvet PaulJouy NathaliePeyrouze PaulineCheok MeylingBrinster CarineManier SalomonTarhan Mehmet ÇagatayLemonnier LoïcQuesnel BrunoTouil Yasmine - Store-operated Ca entry (SOCE) is a key regulator of cytosolic Ca (Ca). Presynaptic SOCE can be activated by ligands like α-latrotoxin, which acts through the presynaptic G-protein-coupled receptor latrophilin-1 (LPHN1), inducing Ca influx and neurotransmitter release. To understand how SOCE-associated proteins contribute to LPHN1 signaling in neurons, we used mouse neuroblastoma NB2a cells as a genetically tractable neuronal model. The cells were stably transfected with exogenous LPHN1 or its non-signaling mutant and stimulated with the non-pore-forming α-latrotoxin mutant LTX, a known trigger of neurotransmitter release. LPHN1 expression increased the proportion of neuron-like cells and upregulated the voltage-gated Ca channels Ca1.2 and Ca2.1. LPHN1 stimulation by LTX induced a small Ca release sensitive to thapsigargin, and a strong, gradual influx of Ca, which was insensitive to thapsigargin. Single-cell imaging revealed that this influx consisted of desynchronized high-amplitude Ca oscillations in individual cells. This response was reduced by Orai2 knockdown and completely blocked by the Ca2.1/2.2 inhibitor ω-conotoxin MVIIC. We conclude that LPHN1 activation by LTX primes Ca stores and induces the opening of Ca2.1/2.2 channels. These channels mediate an initial Ca influx that triggers Ca-induced Ca release and SOCE. This mechanism, elucidated in model cells, can explain how LTX stimulates neurotransmitter release. - Source: PubMed
Publication date: 2025/11/19
Blackburn Jennifer KSilva John-PaulPetitto EvelinaCholewa DietmarFasler-Kan ElizavetaVolynski Kirill EUshkaryov Yuri A