Overview
- Peptide (C)NSLPMESTPHK(S)RGS, corresponding to amino acid residues 605-619 of rat TRPV1 (Accession O35433). 3rd extracellular loop.
Won't recognize TRPV1 from human samples.
- Rat dorsal root ganglion (DRG) lysate (1:200).
- Western blot analysis of TRPV1 in rat DRG:1. Anti-TRPV1 (VR1) (extracellular) Antibody (#ACC-029), (1:200).
2. Anti-TRPV1 (VR1) (extracellular) Antibody, preincubated with TRPV1/VR1 (extracellular) Blocking Peptide (#BLP-CC029).
- Rat dorsal root ganglion (DRG) frozen section (1:100).
- Cell surface detection of TRPV1 by indirect flow cytometry in live intact mouse BV-2 microglia cell line:___ Cells.
___ Cells + goat-anti-rabbit-FITC.
___ Cells + Anti-TRPV1 (VR1) (extracellular) Antibody (#ACC-029), (2.5μg) + goat-anti-rabbit-FITC.
- F11, rat DRG cell line (1:1000) (Goswami, C. et al. (2010) J. Cell Sci. 123, 2045.).
TRP channels are a large family (about 28 genes) of plasma membrane, non-selective cationic channels that are either specifically or ubiquitously expressed in excitable and non-excitable cells.1
According to IUPHAR the TRP family comprises of three main subfamilies on the basis of sequence homology; TRPC, TRPM and TRPV (to date, three extra subfamilies are considered to belong to the TRP family; the TRPA, TRPML, and TRPP).1-4 The TRPV subfamily consists of six members, TRPV1-6.5
TRPV1 channel has many activators among them heat, protons, vanilloids like capsaicin, reiniferatoxin (RTX), and lipids. This channel is associated with tissue injury and inflammation.6,7
TRPV1 is expressed predominantly in nociceptors and in sensory neurons.
Recent studies demonstrated involvement of TRPV1 in apoptosis where inhibition of the receptor prevented apoptosis.8,9
Application key:
Species reactivity key:
Expression of TRPV1 in rat TGNs.Immunocytochemical staining of living rat trigeminal ganglia neurons (TGNs). Extracellular staining of cells using Anti-TRPV1 (VR1) (extracellular) Antibody (#ACC-029). Adapted from Meng, J. et al. (2016) Sci. Rep. 6, 21226. with permission of Nature Publishing Group.