Fosfatidyyli-inositidi ja THC?

Tästä hakusanasta tulen alueelle TRPV1 jonikanava, jota (PIP  ja  PIP2 säätelee.(inhiboiden ) (PIP3 ei vaikuta) ja THC vaikuttaa  aktivoiden käsittääkseni.  Tästä  jonikanavasta, joka  havainnoi pH.ta ja  liikalämpövaikutusta, en ole aiemmin  ollut tietoinen.
TRPV1  kanavasta on tuoretta  tietoa 2016.

TRPV1provided by HGNC

Official Full Name

transient receptor potential cation channel subfamily V member 1provided by HGNC

http://www.ncbi.nlm.nih.gov/gene/7442

Capsaicin, the main pungent ingredient in hot chili peppers, elicits a sensation of burning pain by selectively activating sensory neurons that convey information about noxious stimuli to the central nervous system. The protein encoded by this gene is a receptor for capsaicin and is a non-selective cation channel that is structurally related to members of the TRP family of ion channels.
 This receptor is also activated by increases in temperature in the noxious range, suggesting that it functions as a transducer of painful thermal stimuli in vivo.
 Four transcript variants encoding the same protein, but with different 5' UTR sequence, have been described for this gene. [provided by RefSeq, Jul 2008]

Related articles in PubMed

1. Expression and diagnosis of transient receptor potential vanilloid1 in urothelium of patients with overactive bladder. Zhang HY, et al. J Biol Regul Homeost Agents, 2015 Oct-Dec. PMID 26753651
2. TRPV1 on astrocytes rescues nigral dopamine neurons in Parkinson's disease via CNTF. Nam JH, et al. Brain, 2015 Dec. PMID 26490328,
3. Supraspinal Transient Receptor Potential Subfamily V Member 1 (TRPV1) in Pain and Psychiatric Disorders. Madasu MK, et al. Mod Trends Pharmacopsychiatri, 2015. PMID 26436415
4. Cannabinoid-based drugs targeting CB1 and TRPV1, the sympathetic nervous system, and arthritis. Lowin T, et al. Arthritis Res Ther, 2015 Sep 6. PMID 26343051, Free PMC Article
5. Interaction between the Linker, Pre-S1, and TRP Domains Determines Folding, Assembly, and Trafficking of TRPV Channels. Garcia-Elias A, et al. Structure, 2015 Aug 4. PMID 26146187

See all (268) citations in PubMed

See citations in PubMed for homologs of this gene provided by HomoloGene

GeneRIFs: Gene References Into FunctionsWhat's a GeneRIF

 

1. Studies indicate that crosstalk between cannabinoid receptor type 1 (CB1) and transient receptor potential vanilloid 1 (TRPV1) modulates pain and inflammation in arthritis.
2. Interaction between the linker, pre-S1, and TRP domains determines folding, assembly, and trafficking of TRPV1 and TRPV4 channels.
3. activation of astrocytic TRPV1 activates endogenous neuroprotective machinery in vivo and it is a novel therapeutic target for the treatment of Parkinson's disease
4. TRPV1 expression level, IL-4 level, and rs4790522 site mutation are the main risk factors inducing bronchial asthma in children
5. high expression of TRPV1 in urothelium of female overactive bladder(OAB) patients is closely correlated to OAB occurrence.
6. and TRPV1 have different sensitivities toward membrane phospholipids, such as PI(4)P, PI(4,5)P2, and AA, although they have common roles as proton sensors.  
7. This review focuses on the current knowledge of TRPV1 in improving VSMC function and attenuating hypertension. [review]
8. These findings suggested that the pathophysiology of heartburn sensation or esophageal hypersensitivity may be associated with the activation of PAR-2, TRPV1, and acid-sensing ion channels.
9. This study evaluated the presence of TRPV1 in human and canine mammary cancer cells and the role of TRPV1 in regulating cell proliferation.
10. Supraspinal/brain transient receptor potential subfamily V member 1 is known to modulate pain processing.

 (Kohta 3): Currently there is no neuroprotective or neurorestorative therapy for Parkinson's disease. Here we report that transient receptor potential vanilloid 1 (TRPV1) on astrocytes mediates endogenous production of ciliary neurotrophic factor (CNTF), which prevents the active degeneration of dopamine neurons and leads to behavioural recovery through CNTF receptor alpha (CNTFRα) on nigral dopamine neurons in both the MPP(+)-lesioned or adeno-associated virus α-synuclein rat models of Parkinson's disease. Western blot and immunohistochemical analysis of human post-mortem substantia nigra from Parkinson's disease suggests that this endogenous neuroprotective system (TRPV1 and CNTF on astrocytes, and CNTFRα on dopamine neurons) might have relevance to human Parkinson's disease. Our results suggest that activation of astrocytic TRPV1 activates endogenous neuroprotective machinery in vivo and that it is a novel therapeutic target for the treatment of Parkinson's disease.

(Kohta 6.)  Protons are released in pain-generating pathological conditions such as inflammation, ischemic stroke, infection, and cancer. During normal synaptic activities, protons are thought to play a role in neurotransmission processes. Acid-sensing ion channels (ASICs) are typical proton sensors in the central nervous system (CNS) and the peripheral nervous system (PNS). In addition to ASICs, capsaicin- and heat-activated transient receptor potential vanilloid 1 (TRPV1) channels can also mediate proton-mediated pain signaling. In spite of their importance in perception of pH fluctuations, the regulatory mechanisms of these proton-sensitive ion channels still need to be further investigated.

 Here, we compared regulation of ASICs and TRPV1 by membrane phosphoinositides, which are general cofactors of many receptors and ion channels. We observed that ASICs do not require membrane phosphatidylinositol 4-phosphate (PI(4)P) or phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) for their function. However, TRPV1 currents were inhibited by simultaneous breakdown of PI(4)P and PI(4,5)P2. By using a novel chimeric protein, CF-PTEN, that can specifically dephosphorylate at the D3 position of phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3), we also observed that neither ASICs nor TRPV1 activities were altered by depletion of PI(3,4,5)P3 in intact cells.

 Finally, we compared the effects of arachidonic acid (AA) on two proton-sensitive ion channels. We observed that AA potentiates the currents of both ASICs and TRPV1, but that they have different recovery aspects. In conclusion, ASICs and TRPV1 have different sensitivities toward membrane phospholipids, such as PI(4)P, PI(4,5)P2, and AA, although they have common roles as proton sensors. Further investigation about the complementary roles and respective contributions of ASICs and TRPV1 in proton-mediated signaling is necessary.