Human ORAI1 blocking peptide (CDBP2122)

Synthetic Human ORAI1 blocking peptide for BL

Product Overview
Blocking peptide for anti-ORAI1 antibody
Target
ORAI1
Nature
Synthetic
Species Reactivity
Human
Tag/Conjugate
Unconjugated
Application Notes
For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not suitable for human or animal consumption.
Procedure
None
Format
Liquid
Concentration
200 μg/ml
Size
50 μg
Buffer
PBS containing 0.02% sodium azide
Preservative
0.02% Sodium Azide
Storage
Store at -20℃, stable for one year.
UniProt ID
Antigen Description
The protein encoded by this gene is a membrane calcium channel subunit that is activated by the calcium sensor STIM1 when calcium stores are depleted. This type of channel is the primary way for calcium influx into T-cells. Defects in this gene are a cause of immune dysfunction with T-cell inactivation due to calcium entry defect type 1 (IDTICED1). [provided by RefSeq, Sep 2011]
Function
ion channel activity; protein binding; store-operated calcium channel activity;
Synonyms
ORAI1; ORAI calcium release-activated calcium modulator 1; TMEM142A, transmembrane protein 142A; calcium release-activated calcium channel protein 1; calcium release activated calcium modulator 1; CRACM1; FLJ14466; protein orai-1; transmembrane protein 142A; calcium release-activated calcium modulator 1; ORAT1; TMEM142A;

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References


Unveiling some FDA-approved drugs as inhibitors of the store-operated Ca2+ entry pathway

SCIENTIFIC REPORTS

Authors: Rahman, Saifur; Rahman, Taufiq

The store-operated calcium entry (SOCE) pathway is an important route for generating cytosolic Ca2+ signals that regulate a diverse array of biological processes. Abnormal SOCE seem to underlie several diseases that notably include allergy, inflammation and cancer. Therefore, any modulator of this pathway is likely to have significant impact in cell biology under both normal and abnormal conditions. In this study, we screened the FDA-approved drug library for agents that share significant similarity in 3D shape and surface electrostatics with few, hitherto best known inhibitors of SOCE. This has led to the identification of five drugs that showed dose-dependent inhibition of SOCE in cell-based assay, probably through interacting with the Orai1 protein which effectively mediates SOCE. Of these drugs, leflunomide and teriflunomide could suppress SOCE significantly at clinically-relevant doses and this provides for an additional mechanism towards the therapeutic utility of these drugs as immunosuppressants. The other three drugs namely lansoprazole, tolvaptan and roflumilast, were less potent in suppressing SOCE but were more selective and thus they may serve as novel scaffolds for future development of new, more efficacious SOCE inhibitors.

Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

FRONTIERS IN PHYSIOLOGY

Authors: Dominguez-Rodriguez, Alejandro; Mayoral-Gonzalez, Isabel; Avila-Medina, Javier; de Rojas-de Pedro, Eva S.; Calderon-Sanchez, Eva; Diaz, Ignacio; Hmadcha, Abdelkrim; Castellano, Antonio; Rosado, Juan A.; Benitah, Jean-Pierre; Gomez, Ana M.; Ordonez, Antonio; Smani, Tarik

Aims: Urocortin-2 (Ucn-2) is a potent cardioprotector against Ischemia and Reperfusion (I/R) injuries. However, little is known about its role in the regulation of intracellular Ca2+ concentration ([Ca2+](i)) under I/R. Here, we examined whether the addition of Ucn-2 in reperfusion promotes cardioprotection focusing on {[Ca2+](i) handling. Methods and Results: Cardiac Wistar rat model of I/R was induced by transient ligation of the left coronary artery and experiments were conducted 1 week after surgery in tissue and adult cardiomyocytes isolated from risk and remote zones. We observed that I/R promoted significant alteration in cardiac contractility as well as an increase in hypertrophy and fibrosis in both zones. The study of confocal [Ca2+](i) imaging in adult cardiomyocytes revealed that I/R decreased the amplitude of [Ca2+](i) transient and cardiomyocytes contraction in risk and remote zones. Interestingly, intravenous infusion of Ucn-2 before heart's reperfusion recovered significantly cardiac contractility and prevented fibrosis, but it didn't affect cardiac hypertrophy. Moreover, Ucn-2 recovered the amplitude of [Ca2+](i) transient and modulated the expression of several proteins related to [Ca2+](i) homeostasis, such as TRPC5 and Orai1 channels. Using Neonatal Rat Ventricular Myocytes (NRVM) we demonstrated that Ucn-2 blunted I/R-induced Store Operated Ca2+ Entry (SOCE), decreased the expression of TRPC5 and Orai1 as well as their interaction in reperfusion. Conclusion: Our study provides the first evidences demonstrating that Ucn-2 addition at the onset of reperfusion attenuates I/R-induced adverse cardiac remodeling, involving the [Ca2+](i) handling and inhibiting the expression and interaction between TRPC5 and Orai1.

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