mProX™ Human TRPC5 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Ion Channel Cell Lines
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Published Data
Fig.1 Comparison of the TRPC5 structure with other TRP channel structures.
Fluorescence microscopy and biotinylation accessibility revealed that mutant proteins trafficked to the plasma membrane even while deletion of cysteine residues led to greater intracellular retention of both TRPC4 and TRPC5.
Ref: Duan, Jingjing, et al. "Cryo-EM structure of TRPC5 at 2.8-Å resolution reveals unique and conserved structural elements essential for channel function." Science advances 5.7 (2019): eaaw7935.
Pubmed: 31355338
DOI: 10.1126/sciadv.aaw7935
Research Highlights
The exacerbation of joint inflammation and hyperalgesia is the consequence of either genetic deletion or pharmacological inhibition of TRPC5. In inflammatory joint situations, activation of TRPC5 may be linked to an endogenous analgesic/anti-inflammatory mechanism.
Alawi, Khadija M., et al. "Transient receptor potential canonical 5 (TRPC5) protects against pain and vascular inflammation in arthritis and joint inflammation." Annals of the Rheumatic Diseases 76.1 (2017): 252-260.
Pubmed:
27165180
DOI:
10.1136/annrheumdis-2015-208886
The plasma membrane experiences stress as a result of mechanical forces applied to cells. When cells perceive stress, a mechanoelectric transduction cascade is triggered, which sets off compensating mechanisms. The plasma membrane's mechanosensitive ion channels are in charge of converting mechanical signals into electrical signals.
Shen, Bing, et al. "Plasma membrane mechanical stress activates TRPC5 channels." PLoS One 10.4 (2015): e0122227.
Pubmed:
25849346
DOI:
10.1371/journal.pone.0122227