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{{Infobox_gene}}
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'''Transient receptor potential cation channel subfamily V member 4''' is an ion channel protein that in humans is encoded by the ''TRPV4'' [[gene]].
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<!-- The GNF_Protein_box is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
The ''TRPV4'' gene encodes TRPV4, initially named "vanilloid-receptor related osmotically activated channel" (VR-OAC) and "OSM9-like [[transient receptor potential]] [[ion channel|channel]], member 4 (OTRPC4)",<ref name="pmid11081638"/><ref name="pmid11025659"/> a member of the vanilloid subfamily in the [[transient receptor potential]] (TRP) superfamily of [[ion channel]]s.<ref name="pmid16382100">{{cite journal | vauthors = Clapham DE, Julius D, Montell C, Schultz G | title = International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels | journal = Pharmacol. Rev. | volume = 57 | issue = 4 | pages = 427–50  | date = Dec 2005 | pmid = 16382100 | pmc = | doi = 10.1124/pr.57.4.6 }}</ref><ref name="pmid10717675">{{cite journal | vauthors = Harteneck C, Plant TD, Schultz G | title = From worm to man: three subfamilies of TRP channels | journal = Trends Neurosci. | volume = 23 | issue = 4 | pages = 159–66 | date = April 2000 | pmid = 10717675 | doi = 10.1016/S0166-2236(99)01532-5 }}</ref><ref name="pmid17217058">{{cite journal | vauthors = Plant TD, Strotmann R | title = TRPV4 | journal = Handb Exp Pharmacol | volume = 179 | issue = 179 | pages = 189–205 | year = 2007 | pmid = 17217058 | doi = 10.1007/978-3-540-34891-7_11 }}</ref> The encoded protein is a Ca<sup>2+</sup>-permeable, nonselective cation channel that has been found involved in multiple physiologic functions, dysfunctions and also disease. It functions in the regulation of systemic osmotic pressure by the brain, in vascular function, in liver, intestinal, renal and bladder function, in skin barrier function and response of the skin to ultraviolet-B radiation, in growth and structural integrity of the skeleton, in function of joints, in airway- and lung function, in retinal and inner ear function, and in pain. The channel is activated by osmotic, mechanical and chemical cues. It also responds to thermal changes (warmth). Channel activation can be sensitized by inflammation and injury.
{{GNF_Protein_box
| image = 
| image_source = 
| PDB =
| Name = Transient receptor potential cation channel, subfamily V, member 4
| HGNCid = 18083
| Symbol = TRPV4
| AltSymbols =; OTRPC4; TRP12; VR-OAC; VRL-2; VRL2; VROAC
| OMIM = 605427
| ECnumber =
| Homologene = 11003
| MGIid = 1926945
| GeneAtlas_image1 = 219516_at
| GeneAtlas_image2 = 61963_at
<!-- The Following entry is a time stamp of the last bot update.  It is typically hidden data -->
| DateOfBotUpdate = 03:25, 2 October 2007 (UTC)
| Function = {{GNF_GO|id=GO:0004872 |text = receptor activity}} {{GNF_GO|id=GO:0005034 |text = osmosensor activity}} {{GNF_GO|id=GO:0005216 |text = ion channel activity}} {{GNF_GO|id=GO:0005262 |text = calcium channel activity}} {{GNF_GO|id=GO:0005509 |text = calcium ion binding}} {{GNF_GO|id=GO:0005516 |text = calmodulin binding}} {{GNF_GO|id=GO:0015281 |text = cation channel activity}} {{GNF_GO|id=GO:0042802 |text = identical protein binding}}
| Component = {{GNF_GO|id=GO:0005886 |text = plasma membrane}} {{GNF_GO|id=GO:0016020 |text = membrane}} {{GNF_GO|id=GO:0016021 |text = integral to membrane}}
  | Process = {{GNF_GO|id=GO:0006811 |text = ion transport}} {{GNF_GO|id=GO:0006816 |text = calcium ion transport}} {{GNF_GO|id=GO:0006874 |text = cellular calcium ion homeostasis}} {{GNF_GO|id=GO:0006884 |text = regulation of cell volume}} {{GNF_GO|id=GO:0007231 |text = osmosensory signaling pathway}} {{GNF_GO|id=GO:0009612 |text = response to mechanical stimulus}} {{GNF_GO|id=GO:0030103 |text = vasopressin secretion}} {{GNF_GO|id=GO:0042538 |text = hyperosmotic salinity response}} {{GNF_GO|id=GO:0047484 |text = regulation of response to osmotic stress}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 59341
    | Hs_Ensembl = ENSG00000111199
    | Hs_RefseqProtein = NP_067638
    | Hs_RefseqmRNA = NM_021625
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 12
    | Hs_GenLoc_start = 108705277
    | Hs_GenLoc_end = 108755595
    | Hs_Uniprot = Q9HBA0
    | Mm_EntrezGene = 63873
    | Mm_Ensembl = ENSMUSG00000014158
    | Mm_RefseqmRNA = NM_022017
    | Mm_RefseqProtein = NP_071300
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 5
    | Mm_GenLoc_start = 114883154
    | Mm_GenLoc_end = 114919404
    | Mm_Uniprot = A0JNY0
  }}
}}
'''Transient receptor potential cation channel, subfamily V, member 4''', also known as '''TRPV4''', is a human [[gene]].


<!-- The PBB_Summary template is automatically maintained by Protein Box Bot. See Template:PBB_Controls to Stop updates. -->
The ''TRPV4'' gene has been co-discovered by W. Liedtke et al.<ref name="pmid11081638">{{cite journal | vauthors = Liedtke W, Choe Y, Martí-Renom MA, Bell AM, Denis CS, Sali A, Hudspeth AJ, Friedman JM, Heller S | title = Vanilloid receptor-related osmotically activated channel (VR-OAC), a candidate vertebrate osmoreceptor | journal = Cell | volume = 103 | issue = 3 | pages = 525–35  | date = October 2000 | pmid = 11081638 | pmc = 2211528 | doi = 10.1016/S0092-8674(00)00143-4 }}</ref> and R. Strotmann et al.<ref name="pmid11025659">{{cite journal | vauthors = Strotmann R, Harteneck C, Nunnenmacher K, Schultz G, Plant TD | title = OTRPC4, a nonselective cation channel that confers sensitivity to extracellular osmolarity | journal = Nat. Cell Biol. | volume = 2 | issue = 10 | pages = 695–702  | date = October 2000 | pmid = 11025659 | doi = 10.1038/35036318 }}</ref>
{{PBB_Summary
| section_title =  
| summary_text = This gene encodes a member of the OSM9-like transient receptor potential channel (OTRPC) subfamily in the transient receptor potential (TRP) superfamily of ion channels. The encoded protein is a Ca2+-permeable, nonselective cation channel that is thought to be involved in the regulation of systemic osmotic pressure. Two transcript variants encoding different isoforms have been found for this gene.<ref>{{cite web | title = Entrez Gene: TRPV4 transient receptor potential cation channel, subfamily V, member 4| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=59341| accessdate = }}</ref>
}}


==References==
== Clinical significance ==
{{reflist|2}}
==Further reading==
{{refbegin | 2}}
{{PBB_Further_reading
| citations =
*{{cite journal  | author=Harteneck C, Plant TD, Schultz G |title=From worm to man: three subfamilies of TRP channels. |journal=Trends Neurosci. |volume=23 |issue= 4 |pages= 159-66 |year= 2000 |pmid= 10717675 |doi=  }}
*{{cite journal  | author=Clapham DE, Julius D, Montell C, Schultz G |title=International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels. |journal=Pharmacol. Rev. |volume=57 |issue= 4 |pages= 427-50 |year= 2006 |pmid= 16382100 |doi= 10.1124/pr.57.4.6 }}
*{{cite journal  | author=Plant TD, Strotmann R |title=TRPV4. |journal=Handb Exp Pharmacol |volume= |issue= 179 |pages= 189-205 |year= 2007 |pmid= 17217058 |doi= 10.1007/978-3-540-34891-7_11 }}
*{{cite journal  | author=Harteneck C, Reiter B |title=TRP channels activated by extracellular hypo-osmoticity in epithelia. |journal=Biochem. Soc. Trans. |volume=35 |issue= Pt 1 |pages= 91-5 |year= 2007 |pmid= 17233610 |doi= 10.1042/BST0350091 }}
}}
{{refend}}


{{protein-stub}}
Channelopathy [[mutation]]s in the ''TRPV4'' gene lead to skeletal dysplasias, premature osteoarthritis, and neurological motor function disorders and are associated with a range of disorders, including [[brachyolmia]] type 3, [[congenital distal spinal muscular atrophy]], [[scapuloperoneal spinal muscular atrophy]], and subtype 2C of [[Charcot–Marie–Tooth disease]].<ref>{{OMIM|605427}}</ref>
{{WikiDoc Sources}}
 
== Pharmacology ==
 
A number of TRPV4 agonists and antagonists have been identified since its discovery.<ref>{{cite journal | vauthors = Vincent F, Duncton MA | title = TRPV4 agonists and antagonists | journal = Curr Top Med Chem | volume = 11 | issue = 17 | pages = 2216–26 | year = 2011 | pmid = 21671873 | doi =  10.2174/156802611796904861}}</ref> The discovery of unselective modulators (e.g. antagonist Ruthenium Red) was followed by the apparition of more potent (agonist 4aPDD)<ref>{{cite journal | vauthors = Watanabe H, Davis JB, Smart D, Jerman JC, Smith GD, Hayes P, Vriens J, Cairns W, Wissenbach U, Prenen J, Flockerzi V, Droogmans G, Benham CD, Nilius B | title = Activation of TRPV4 channels (hVRL-2/mTRP12) by phorbol derivatives | journal = J. Biol. Chem. | volume = 277 | issue = 16 | pages = 13569–77  | date = April 2002 | pmid = 11827975 | doi = 10.1074/jbc.M200062200 }}</ref> or selective (antagonist RN-1734)<ref>{{cite journal | vauthors = Vincent F, Acevedo A, Nguyen MT, Dourado M, DeFalco J, Gustafson A, Spiro P, Emerling DE, Kelly MG, Duncton MA | title = Identification and characterization of novel TRPV4 modulators | journal = Biochem. Biophys. Res. Commun. | volume = 389 | issue = 3 | pages = 490–4  | date = November 2009 | pmid = 19737537 | doi = 10.1016/j.bbrc.2009.09.007 }}</ref> compounds, including some with bioavailability suitable for in vivo pharmacology studies such as agonist GSK1016790A<ref>{{cite journal | vauthors = Thorneloe KS, Sulpizio AC, Lin Z, Figueroa DJ, Clouse AK, McCafferty GP, Chendrimada TP, Lashinger ES, Gordon E, Evans L, Misajet BA, Demarini DJ, Nation JH, Casillas LN, Marquis RW, Votta BJ, Sheardown SA, Xu X, Brooks DP, Laping NJ, Westfall TD | title = N-((1S)-1-<nowiki/>{[4-((2S)-2-<nowiki/>{[(2,4-dichlorophenyl)sulfonyl]amino}-3-hydroxypropanoyl)-1-piperazinyl]carbonyl}-3-methylbutyl)-1-benzothiophene-2-carboxamide (GSK1016790A), a novel and potent transient receptor potential vanilloid 4 channel agonist induces urinary bladder contraction and hyperactivity: Part I | journal = J. Pharmacol. Exp. Ther. | volume = 326 | issue = 2 | pages = 432–42 | date = August 2008 | pmid = 18499743 | doi = 10.1124/jpet.108.139295 }}</ref> (with ~10 fold selectivity vs TRPV1), and antagonists HC-067047<ref>{{cite journal | vauthors = Everaerts W, Zhen X, Ghosh D, Vriens J, Gevaert T, Gilbert JP, Hayward NJ, McNamara CR, Xue F, Moran MM, Strassmaier T, Uykal E, Owsianik G, Vennekens R, De Ridder D, Nilius B, Fanger CM, Voets T | title = Inhibition of the cation channel TRPV4 improves bladder function in mice and rats with cyclophosphamide-induced cystitis | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 107 | issue = 44 | pages = 19084–9  | date = November 2010 | pmid = 20956320 | pmc = 2973867 | doi = 10.1073/pnas.1005333107 }}</ref> (with ~5 fold selectivity vs hERG and ~10 fold selectivity vs TRPM8) and RN-9893<ref>{{cite journal | vauthors = Wei ZL, Nguyen MT, O'Mahony DJ, Acevedo A, Zipfel S, Zhang Q, Liu L, Dourado M, Chi C, Yip V, DeFalco J, Gustafson A, Emerling DE, Kelly MG, Kincaid J, Vincent F, Duncton MA | title = Identification of orally-bioavailable antagonists of the TRPV4 ion-channel | journal = Bioorg. Med. Chem. Lett. | volume = 25 | issue = 18 | pages = 4011–5 | date = 2015 | pmid=26235950 | doi=10.1016/j.bmcl.2015.06.098}}</ref> (with ~50 fold selectivity vs TRPM8 and ~10 fold selectivity vs M1).
 
Resolvin D1 (RvD1), a metabolite of the [[omega 3 fatty acid]], [[docosahexaenoic acid]], is a member of the [[specialized proresolving mediators]] (SPMs) class of metabolites that function to resolve diverse inflammatory reactions and diseases in animal models and, it is proposed, humans. This SPM also dampens pain perception arising from various inflammation-based causes in animal models. The mechanism behind this pain-dampening effect involves the inhibition of TRPV4, probably (in at least certain cases) by an indirect effect wherein it activates another receptor located on neruons or nearby [[microglia]] or [[astrocyte]]s. [[CMKLR1]], [[GPR32]], [[FPR2]], and [[NMDA receptor]]s have been proposed to be the receptors through which a SPM may operate to [[down-regulate]] TRPs and thereby pain perception.<ref name="pmid25052386">{{cite journal | vauthors = Qu Q, Xuan W, Fan GH | title = Roles of resolvins in the resolution of acute inflammation | journal = Cell Biology International | volume = 39 | issue = 1 | pages = 3–22 | year = 2015 | pmid = 25052386 | doi = 10.1002/cbin.10345 | url = }}</ref><ref name="pmid25359497">{{cite journal | vauthors = Serhan CN, Chiang N, Dalli J, Levy BD | title = Lipid mediators in the resolution of inflammation | journal = Cold Spring Harbor Perspectives in Biology | volume = 7 | issue = 2 | pages = a016311 | year = 2015 | pmid = 25359497 | doi = 10.1101/cshperspect.a016311 | url = }}</ref><ref name="pmid26339646">{{cite journal | vauthors = Lim JY, Park CK, Hwang SW | title = Biological Roles of Resolvins and Related Substances in the Resolution of Pain | journal = BioMed Research International | volume = 2015 | issue = | pages = 830930 | year = 2015 | pmid = 26339646 | pmc = 4538417 | doi = 10.1155/2015/830930 | url = }}</ref><ref name="pmid21963090">{{cite journal | vauthors = Ji RR, Xu ZZ, Strichartz G, Serhan CN | title = Emerging roles of resolvins in the resolution of inflammation and pain | journal = Trends in Neurosciences | volume = 34 | issue = 11 | pages = 599–609 | year = 2011 | pmid = 21963090 | pmc = 3200462 | doi = 10.1016/j.tins.2011.08.005 | url = }}</ref><ref name="pmid25857211">{{cite journal | vauthors = Serhan CN, Chiang N, Dalli J | title = The resolution code of acute inflammation: Novel pro-resolving lipid mediators in resolution | journal = Seminars in Immunology | volume = 27 | issue = 3 | pages = 200–15 | year = 2015 | pmid = 25857211 | pmc = 4515371 | doi = 10.1016/j.smim.2015.03.004 | url = }}</ref>
 
== Interactions ==
 
TRPV4 has been shown to [[Protein-protein interaction|interact]] with [[MAP7]]<ref name="pmid14517216">{{cite journal | vauthors = Suzuki M, Hirao A, Mizuno A | title = Microtubule-associated [corrected] protein 7 increases the membrane expression of transient receptor potential vanilloid 4 (TRPV4) | journal = J. Biol. Chem. | volume = 278 | issue = 51 | pages = 51448–53  | date = December 2003 | pmid = 14517216 | doi = 10.1074/jbc.M308212200 }}</ref> and [[LYN]].<ref name=pmid12538589>{{cite journal | vauthors = Xu H, Zhao H, Tian W, Yoshida K, Roullet JB, Cohen DM | title = Regulation of a transient receptor potential (TRP) channel by tyrosine phosphorylation. SRC family kinase-dependent tyrosine phosphorylation of TRPV4 on TYR-253 mediates its response to hypotonic stress | journal = J. Biol. Chem. | volume = 278 | issue = 13 | pages = 11520–7  | date = Mar 2003 | pmid = 12538589 | doi = 10.1074/jbc.M211061200 }}</ref>
 
== See also ==
* [[TRPV]]
 
== References ==
{{Reflist|30em}}
 
== External links ==
* [https://www.ncbi.nlm.nih.gov/books/NBK1285/  GeneReviews/NCBI/NIH/UW entry on Charcot-Marie-Tooth Neuropathy Type 2]
* {{MeshName|TRPV4+protein,+human}}
 
{{NLM content}}
{{Ion channels|g4}}
{{Transient receptor potential channel modulators}}
 
[[Category:Ion channels]]

Revision as of 15:18, 3 November 2017

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External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
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Ensembl

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UniProt

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RefSeq (mRNA)

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RefSeq (protein)

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Transient receptor potential cation channel subfamily V member 4 is an ion channel protein that in humans is encoded by the TRPV4 gene.

The TRPV4 gene encodes TRPV4, initially named "vanilloid-receptor related osmotically activated channel" (VR-OAC) and "OSM9-like transient receptor potential channel, member 4 (OTRPC4)",[1][2] a member of the vanilloid subfamily in the transient receptor potential (TRP) superfamily of ion channels.[3][4][5] The encoded protein is a Ca2+-permeable, nonselective cation channel that has been found involved in multiple physiologic functions, dysfunctions and also disease. It functions in the regulation of systemic osmotic pressure by the brain, in vascular function, in liver, intestinal, renal and bladder function, in skin barrier function and response of the skin to ultraviolet-B radiation, in growth and structural integrity of the skeleton, in function of joints, in airway- and lung function, in retinal and inner ear function, and in pain. The channel is activated by osmotic, mechanical and chemical cues. It also responds to thermal changes (warmth). Channel activation can be sensitized by inflammation and injury.

The TRPV4 gene has been co-discovered by W. Liedtke et al.[1] and R. Strotmann et al.[2]

Clinical significance

Channelopathy mutations in the TRPV4 gene lead to skeletal dysplasias, premature osteoarthritis, and neurological motor function disorders and are associated with a range of disorders, including brachyolmia type 3, congenital distal spinal muscular atrophy, scapuloperoneal spinal muscular atrophy, and subtype 2C of Charcot–Marie–Tooth disease.[6]

Pharmacology

A number of TRPV4 agonists and antagonists have been identified since its discovery.[7] The discovery of unselective modulators (e.g. antagonist Ruthenium Red) was followed by the apparition of more potent (agonist 4aPDD)[8] or selective (antagonist RN-1734)[9] compounds, including some with bioavailability suitable for in vivo pharmacology studies such as agonist GSK1016790A[10] (with ~10 fold selectivity vs TRPV1), and antagonists HC-067047[11] (with ~5 fold selectivity vs hERG and ~10 fold selectivity vs TRPM8) and RN-9893[12] (with ~50 fold selectivity vs TRPM8 and ~10 fold selectivity vs M1).

Resolvin D1 (RvD1), a metabolite of the omega 3 fatty acid, docosahexaenoic acid, is a member of the specialized proresolving mediators (SPMs) class of metabolites that function to resolve diverse inflammatory reactions and diseases in animal models and, it is proposed, humans. This SPM also dampens pain perception arising from various inflammation-based causes in animal models. The mechanism behind this pain-dampening effect involves the inhibition of TRPV4, probably (in at least certain cases) by an indirect effect wherein it activates another receptor located on neruons or nearby microglia or astrocytes. CMKLR1, GPR32, FPR2, and NMDA receptors have been proposed to be the receptors through which a SPM may operate to down-regulate TRPs and thereby pain perception.[13][14][15][16][17]

Interactions

TRPV4 has been shown to interact with MAP7[18] and LYN.[19]

See also

References

  1. ↑ 1.0 1.1 Liedtke W, Choe Y, Martí-Renom MA, Bell AM, Denis CS, Sali A, Hudspeth AJ, Friedman JM, Heller S (October 2000). "Vanilloid receptor-related osmotically activated channel (VR-OAC), a candidate vertebrate osmoreceptor". Cell. 103 (3): 525–35. doi:10.1016/S0092-8674(00)00143-4. PMC 2211528. PMID 11081638.
  2. ↑ 2.0 2.1 Strotmann R, Harteneck C, Nunnenmacher K, Schultz G, Plant TD (October 2000). "OTRPC4, a nonselective cation channel that confers sensitivity to extracellular osmolarity". Nat. Cell Biol. 2 (10): 695–702. doi:10.1038/35036318. PMID 11025659.
  3. ↑ Clapham DE, Julius D, Montell C, Schultz G (Dec 2005). "International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels". Pharmacol. Rev. 57 (4): 427–50. doi:10.1124/pr.57.4.6. PMID 16382100.
  4. ↑ Harteneck C, Plant TD, Schultz G (April 2000). "From worm to man: three subfamilies of TRP channels". Trends Neurosci. 23 (4): 159–66. doi:10.1016/S0166-2236(99)01532-5. PMID 10717675.
  5. ↑ Plant TD, Strotmann R (2007). "TRPV4". Handb Exp Pharmacol. 179 (179): 189–205. doi:10.1007/978-3-540-34891-7_11. PMID 17217058.
  6. ↑ Online Mendelian Inheritance in Man (OMIM) 605427
  7. ↑ Vincent F, Duncton MA (2011). "TRPV4 agonists and antagonists". Curr Top Med Chem. 11 (17): 2216–26. doi:10.2174/156802611796904861. PMID 21671873.
  8. ↑ Watanabe H, Davis JB, Smart D, Jerman JC, Smith GD, Hayes P, Vriens J, Cairns W, Wissenbach U, Prenen J, Flockerzi V, Droogmans G, Benham CD, Nilius B (April 2002). "Activation of TRPV4 channels (hVRL-2/mTRP12) by phorbol derivatives". J. Biol. Chem. 277 (16): 13569–77. doi:10.1074/jbc.M200062200. PMID 11827975.
  9. ↑ Vincent F, Acevedo A, Nguyen MT, Dourado M, DeFalco J, Gustafson A, Spiro P, Emerling DE, Kelly MG, Duncton MA (November 2009). "Identification and characterization of novel TRPV4 modulators". Biochem. Biophys. Res. Commun. 389 (3): 490–4. doi:10.1016/j.bbrc.2009.09.007. PMID 19737537.
  10. ↑ Thorneloe KS, Sulpizio AC, Lin Z, Figueroa DJ, Clouse AK, McCafferty GP, Chendrimada TP, Lashinger ES, Gordon E, Evans L, Misajet BA, Demarini DJ, Nation JH, Casillas LN, Marquis RW, Votta BJ, Sheardown SA, Xu X, Brooks DP, Laping NJ, Westfall TD (August 2008). "N-((1S)-1-{[4-((2S)-2-{[(2,4-dichlorophenyl)sulfonyl]amino}-3-hydroxypropanoyl)-1-piperazinyl]carbonyl}-3-methylbutyl)-1-benzothiophene-2-carboxamide (GSK1016790A), a novel and potent transient receptor potential vanilloid 4 channel agonist induces urinary bladder contraction and hyperactivity: Part I". J. Pharmacol. Exp. Ther. 326 (2): 432–42. doi:10.1124/jpet.108.139295. PMID 18499743.
  11. ↑ Everaerts W, Zhen X, Ghosh D, Vriens J, Gevaert T, Gilbert JP, Hayward NJ, McNamara CR, Xue F, Moran MM, Strassmaier T, Uykal E, Owsianik G, Vennekens R, De Ridder D, Nilius B, Fanger CM, Voets T (November 2010). "Inhibition of the cation channel TRPV4 improves bladder function in mice and rats with cyclophosphamide-induced cystitis". Proc. Natl. Acad. Sci. U.S.A. 107 (44): 19084–9. doi:10.1073/pnas.1005333107. PMC 2973867. PMID 20956320.
  12. ↑ Wei ZL, Nguyen MT, O'Mahony DJ, Acevedo A, Zipfel S, Zhang Q, Liu L, Dourado M, Chi C, Yip V, DeFalco J, Gustafson A, Emerling DE, Kelly MG, Kincaid J, Vincent F, Duncton MA (2015). "Identification of orally-bioavailable antagonists of the TRPV4 ion-channel". Bioorg. Med. Chem. Lett. 25 (18): 4011–5. doi:10.1016/j.bmcl.2015.06.098. PMID 26235950.
  13. ↑ Qu Q, Xuan W, Fan GH (2015). "Roles of resolvins in the resolution of acute inflammation". Cell Biology International. 39 (1): 3–22. doi:10.1002/cbin.10345. PMID 25052386.
  14. ↑ Serhan CN, Chiang N, Dalli J, Levy BD (2015). "Lipid mediators in the resolution of inflammation". Cold Spring Harbor Perspectives in Biology. 7 (2): a016311. doi:10.1101/cshperspect.a016311. PMID 25359497.
  15. ↑ Lim JY, Park CK, Hwang SW (2015). "Biological Roles of Resolvins and Related Substances in the Resolution of Pain". BioMed Research International. 2015: 830930. doi:10.1155/2015/830930. PMC 4538417. PMID 26339646.
  16. ↑ Ji RR, Xu ZZ, Strichartz G, Serhan CN (2011). "Emerging roles of resolvins in the resolution of inflammation and pain". Trends in Neurosciences. 34 (11): 599–609. doi:10.1016/j.tins.2011.08.005. PMC 3200462. PMID 21963090.
  17. ↑ Serhan CN, Chiang N, Dalli J (2015). "The resolution code of acute inflammation: Novel pro-resolving lipid mediators in resolution". Seminars in Immunology. 27 (3): 200–15. doi:10.1016/j.smim.2015.03.004. PMC 4515371. PMID 25857211.
  18. ↑ Suzuki M, Hirao A, Mizuno A (December 2003). "Microtubule-associated [corrected] protein 7 increases the membrane expression of transient receptor potential vanilloid 4 (TRPV4)". J. Biol. Chem. 278 (51): 51448–53. doi:10.1074/jbc.M308212200. PMID 14517216.
  19. ↑ Xu H, Zhao H, Tian W, Yoshida K, Roullet JB, Cohen DM (Mar 2003). "Regulation of a transient receptor potential (TRP) channel by tyrosine phosphorylation. SRC family kinase-dependent tyrosine phosphorylation of TRPV4 on TYR-253 mediates its response to hypotonic stress". J. Biol. Chem. 278 (13): 11520–7. doi:10.1074/jbc.M211061200. PMID 12538589.

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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