transient receptor potential cation channel subfamily V member 1; osm-9-like TRP channel 1; vanilloid receptor 1; VR1 capsaicin receptor (TRPV1, OTRPC1)
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Function
- receptor-activated non-selective Ca+ channel
- detection of noxious chemical & thermal stimuli
- mediates proton influx
- intracellular acidosis in nociceptive neurons
- mediation of inflammatory pain & hyperalgesia
- sensitized by phosphatidylinositol second messenger system activated by receptor tyrosine kinases involving PKC & PLC
- may form heteromeric channel with TRPV3
- interacts with calmodulin, PRKCM, CSK, PRKCG, NTRK1
- phosphorylation by PKA reverses capsaicin-induced
- dephosphorylation at multiple sites, probably including Ser-117 (major phosphorylation site)
- phosphorylation by CAMK2 regulates binding to vanilloids
- phosphorylated & modulated by PKCM & PKCZ
- dephosphorylation by calcineurin desensitizatizes receptor; phosphorylation by CAMKII recovers activity
- responses evoked by low pH & heat, & capsaicin, antagonized by capsazepine
Structure
self-associates, homotetramer
Compartment
Alternative splicing
named isoforms=2
Expression
- widely expressed at low levels
- expressed in nerves & joints
- expression is elevated in dorsal root ganglia
- in skin, expressed in cutaneous sensory nerve fibers, mast cells, epidermal keratinocytes, dermal blood vessels, the inner root sheet & infundibulum of hair follicles, differentiated sebocytes, sweat gland ducts, secretory portion of eccrine sweat glands
- vagal Npy2r(+) neurons largely co-express Trpv1 & respond to capsaicin
Pharmacology
- potent agonist of TRPV1 resiniferatoxin is an experimental non-opiate analgesic for treatment of patients with refractory cancer pain[4]
Comparative biology
More general terms
- transient receptor potential cation channel subfamily V (TRPV)
- Ca+2 channel
- transmembrane 6 protein
- phosphoprotein
- glycoprotein
References
- ↑ UniProt http://www.uniprot.org/uniprot/Q8NER1.html
- ↑ 2.0 2.1 Mishra SK, Hoon MA. The cells and circuitry for itch responses in mice. Science 2013 May 24; 340:968 PMID: https://pubmed.ncbi.nlm.nih.gov/23704570
- ↑ 3.0 3.1 Steven Coles cites Dillin et al at UC Berkeley & The Salk Institute for Biological Studies to appear in the journal Cell. GRG bulletin board May 22, 2014 & May 27, 2014
- ↑ 4.0 4.1 Mannes AJ, Heiss JD, Berger A et al Treatment of Intractable Cancer Pain with Resiniferatoxin - An Interim Study. NEJM Evid. 2025 Jun;4(6):EVIDoa2400423. PMID: https://pubmed.ncbi.nlm.nih.gov/40423401 Clinical Trial.
- ↑ Chen E How tumours trick the brain into shutting down cancer-fighting cells. Lung cancer in mice hijacks neurons to send a signal that subdues the immune system, study finds. Nature News. 2026. Feb 4 https://www.nature.com/articles/d41586-026-00338-w
Wei HK, Yu CD, Hu B Tumour-brain crosstalk restrains cancer immunity via a sensory-sympathetic axis. Nature. 2026 Feb 4. doi:http://dx.doi.org/ 10.1038/s41586-025-10028-8. PMID: https://pubmed.ncbi.nlm.nih.gov/41639447