Induction of vanilloid receptor channel activity by protein kinase C
By L. Premkumar, G. Ahern. Nature, 2000
847 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology, Sensory Systems
View Paper: https://www.semanticscholar.org/paper/624856f1b8cdb38104e3bcb602455c7f4c6bc201
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Citations in the corpus
- Molecular mechanisms of nociception (2001, background): “, an effect that may be mediated through direct or indirect modification of VR1 by the e-isoform of PK”
- TRP channels and pain. (2013, background): “…of TRPV1 at two main intracellular sites (S502 and S800) located within the loop connecting TM3 and TM4 and the proximal region of the C-terminal tail, respectively (Bhave et al. 2003, Cesare & McNaughton 1996, Numazaki et al. 2002, Premkumar & Ahern 2000, Vellani et al. 2001) (Figure 4a).”
- TRPA1 mediates the inflammatory actions of environmental irritants and proalgesic agents. (2006, positive): “Genetic and electrophysiological studies suggest that bradykinin-evoked thermal hypersensitivity is produced through PLC-mediated potentiation of TRPV1 (Cesare et al., 1999; Chuang et al., 2001; Premkumar and Ahern, 2000).”
- The transient receptor potential family of ion channels (2011, background): “PKCdependent phosphorylation might be a direct activatory mechanism or might sensitize the channel for other stimuli (for example, it sensitizes TRPV1 to heat or capsaicin) [73,74].”
- Anandamide and vanilloid TRPV1 receptors (2003, background): “Premkumar & Ahern (2000) report that the repeated application of anandamide evokes progressively larger TRPV1 currents in oocytes and that anandamide treatment enhances proton-evoked currents.”
- NGF rapidly increases membrane expression of TRPV1 heat‐gated ion channels (2005, background): “This process, called sensitization or hyperalgesia, is mediated by a variety of proinflammatory factors, including bradykinin, ATP and NGF, which cause sensitization to noxious heat stimuli by enhancing the membrane current carried by the heat- and capsaicingated ion channel, TRPV1.”
- An introduction to TRP channels. (2006, background): “0 antagonist (56, 75, 126) I HEK, SCG 2-APB TRPV1 114-249μM 1.”
- Bradykinin and nerve growth factor release the capsaicin receptor from PtdIns(4,5)P2-mediated inhibition (2001, background): “, and that PKC potentiates capsaicin-evoked responses in VR1-expressing oocyte”
- Identification of a cold receptor reveals a general role for TRP channels in thermosensation (2002, background): “Indeed, several TRP channels are regulated by receptors that couple to phospholipase C (PLC), and the thermal activation threshold for VR1 can be markedly shifted to lower temperatures by inflammatory agents (for example, bradykinin and nerve growth factor) that activate this pathwa”