mProX™ Human ORAI1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
To download a Certificate of Analysis, please enter a lot number in the search box below. Note: Certificate of Analysis not available for kit components.
Lot Number
Made to Order Inquiry
InquiryProduct Information
Product Properties
Protocols
Please visit our protocols page.
Customer Reviews
There are currently no Customer reviews or questions for mProX™ Human ORAI1 Stable Cell Line (S01YF-1023-PY259). Click the button above to contact us or submit your feedback about this product.
Taylor Smith (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Jordan Miller (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 Knockdown of ORAI1 protects from GSH depletion.
Protection from GSH depletion was achieved through knockdown of ORAI1. HT22S cells were subjected to transfection with two independent siRNAs targeting ORAI1, or a non-targeting control siRNA, followed by a 48-hour interval for cell survival experiments. Verification of successful knockdown was performed through immunoblot analysis, wherein membranes were simultaneously probed with antibodies against ORAI1 and actin, serving as the loading control, and subsequently analyzed using the Licor infrared imaging system. Survival experiments were carried out on siRNA-transfected cells, with glutamate or BSO being added 48 hours post-transfection, and viability quantified using the CTB reagent 16 hours after the addition of glutamate or BSO. The graphs depict the mean fluorescence±S.E.M. of 15 replicates obtained in three independent experiments, plotted against the concentration of glutamate or BSO.
Ref: Henke, Nadine, et al. "The plasma membrane channel ORAI1 mediates detrimental calcium influx caused by endogenous oxidative stress." Cell death & disease 4.1 (2013): e470-e470.
Pubmed: 23348584
DOI: 10.1038/cddis.2012.216
Research Highlights
Tsujikawa, Shogo et al. "Regulation of neuropathic pain by microglial Orai1 channels." Science advances vol. 9,4 (2023): eade7002.
Microglial activity in neuroinflammation associated with neuropathic pain lacks a full understanding of molecular checkpoints. A study delved into Orai1 channels' impact on microglial-mediated neuroinflammation following nerve injury. The results revealed that Orai1 deletion in microglia reduced Ca2+ signaling and the release of inflammatory cytokines induced by proalgesic agents. This deletion also curbed microglial proliferation, spinal cytokine levels, and heightened excitatory neurotransmission post-peripheral nerve injury, ultimately alleviating pain hyperalgesia in male mice. Intriguingly, this protective effect was not observed in female mice, highlighting a sexual dimorphism in Orai1's role in microglial reactivity and hyperalgesia during neuroinflammation linked to neuropathic pain.
Tsujikawa, Shogo et al. "Regulation of neuropathic pain by microglial Orai1 channels." Science advances vol. 9,4 (2023): eade7002.
Pubmed:
36706180
DOI:
10.1126/sciadv.ade7002
N O'Connor, Thomas. et al. "Voluntary wheel running mitigates disease in an Orai1 gain-of-function mouse model of tubular aggregate myopathy." bioRxiv : the preprint server for biology, 2023.
Tubular aggregate myopathy (TAM) is a genetic muscle disorder characterized by gradual muscle weakness, cramps, and myalgia. TAs, which are highly organized arrays of densely packed SR straight-tubes in muscle tissue, are a distinctive feature of TAM observed in muscle biopsies. This condition is caused by mutations in proteins responsible for coordinating store-operated Ca2+ entry, resulting in abnormal accumulation of TAs. TAM is inherited and presents as a key histopathological manifestation in affected individuals.
N O'Connor, Thomas. et al. "Voluntary wheel running mitigates disease in an Orai1 gain-of-function mouse model of tubular aggregate myopathy." bioRxiv : the preprint server for biology, 2023.
Pubmed:
37808709
DOI:
10.1101/2023.09.29.559036
