Aquaporin 3: Difference between revisions
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'''Aquaporin 3''' is found in the basolateral cell membrane of principal [[collecting duct]] cells and | '''Aquaporin 3''' is found in the basolateral cell membrane of principal [[collecting duct]] cells and provides a pathway for water to exit these cells.<ref name="pmid9558461">{{cite journal |vauthors=Sasaki S, Ishibashi K, Marumo F | title = Aquaporin-2 and -3: representatives of two subgroups of the aquaporin family colocalized in the kidney collecting duct |journal=Annu. Rev. Physiol. | volume = 60 | issue = | pages = 199–220 | year = 1998 | pmid = 9558461 |doi=10.1146/annurev.physiol.60.1.199}}</ref> In the kidney, AQP3 is regulated by [[vasopressin]] (ADH).<ref name="pmid9824541">{{cite journal |year=2014|title=Medical Biochemistry |url=https://www.elsevier.com/books/medical-biochemistry/baynes/978-1-4557-4580-7 |journal=Medical Biochemistry |type=Textbook |edition=4 |volume= |issue= |page=346 |pages=|doi=|issn=|pmid=|via=Elsevier |vauthors=Baynes JW, Dominiczak MH}}</ref> This protein is also a determinant for the GIL blood group system.<ref name="pmid12239222">{{cite journal |vauthors=Roudier N, Ripoche P, Gane P, Le Pennec PY, Daniels G, Cartron JP, Bailly P | title = AQP3 deficiency in humans and the molecular basis of a novel blood group system, GIL | journal = J. Biol. Chem. | volume = 277 | issue = 48 | pages = 45854–9 | year = 2002 | pmid = 12239222 | doi = 10.1074/jbc.M208999200}}</ref> | ||
[[Suberoylanilide hydroxamic acid]] (SAHA) (a [[HDAC inhibitor]]) increases expression of aquaporin-3 in normal skin cells ([[keratinocyte]]s).<ref name=MCG2017>[https://medicalxpress.com/news/2017-05-cancer-therapy-psoriasis-treatment.html Cancer therapy shows promise for psoriasis treatment]</ref> | [[Suberoylanilide hydroxamic acid]] (SAHA) (a [[HDAC inhibitor]]) increases expression of aquaporin-3 in normal skin cells ([[keratinocyte]]s).<ref name=MCG2017>[https://medicalxpress.com/news/2017-05-cancer-therapy-psoriasis-treatment.html Cancer therapy shows promise for psoriasis treatment]</ref> | ||
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==External links== | ==External links== | ||
* [https://www.ncbi.nlm.nih.gov/projects/mhc/xslcgi. | * [https://www.ncbi.nlm.nih.gov/projects/gv/mhc/xslcgi.cgi?cmd=bgmut/systems_info&system=gil GIL blood group system] at [[BGMUT]] Blood Group Antigen Gene Mutation Database at [[National Center for Biotechnology Information|NCBI]], [[NIH]] | ||
* {{UCSC gene info|AQP3}} | * {{UCSC gene info|AQP3}} | ||
Latest revision as of 07:44, 10 January 2019
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Aquaporin 3 is found in the basolateral cell membrane of principal collecting duct cells and provides a pathway for water to exit these cells.[1] In the kidney, AQP3 is regulated by vasopressin (ADH).[2] This protein is also a determinant for the GIL blood group system.[3]
Suberoylanilide hydroxamic acid (SAHA) (a HDAC inhibitor) increases expression of aquaporin-3 in normal skin cells (keratinocytes).[4]
Clinical significance
AQP3 levels are often lower in psoriasis than in healthy skin.[4]
AQP3 is expressed more in atopic eczema.[5]
See also
References
- ↑ Sasaki S, Ishibashi K, Marumo F (1998). "Aquaporin-2 and -3: representatives of two subgroups of the aquaporin family colocalized in the kidney collecting duct". Annu. Rev. Physiol. 60: 199–220. doi:10.1146/annurev.physiol.60.1.199. PMID 9558461.
- ↑ Baynes JW, Dominiczak MH (2014). "Medical Biochemistry". Medical Biochemistry (Textbook) (4 ed.): 346 – via Elsevier.
- ↑ Roudier N, Ripoche P, Gane P, Le Pennec PY, Daniels G, Cartron JP, Bailly P (2002). "AQP3 deficiency in humans and the molecular basis of a novel blood group system, GIL". J. Biol. Chem. 277 (48): 45854–9. doi:10.1074/jbc.M208999200. PMID 12239222.
- ↑ 4.0 4.1 Cancer therapy shows promise for psoriasis treatment
- ↑ Olsson M, Broberg A, Jernãs M, et al. (2006). "Increased expression of aquaporin 3 in atopic eczema". Allergy. 61 (9): 1132–7. doi:10.1111/j.1398-9995.2006.01151.x. PMID 16918518.
Further reading
- Bietz S, Montilla I, Külzer S, et al. (2009). "Recruitment of human aquaporin 3 to internal membranes in the Plasmodium falciparum infected erythrocyte". Mol. Biochem. Parasitol. 167 (1): 48–53. doi:10.1016/j.molbiopara.2009.04.006. PMID 19393693.
- Bahamontes-Rosa N, Tena-Tomás C, Wolkow J, et al. (2008). "Genetic conservation of the GIL blood group determining aquaporin 3 gene in African and Caucasian populations". Transfusion. 48 (6): 1164–8. doi:10.1111/j.1537-2995.2008.01683.x. PMID 18435676.
- Wang S, Amidi F, Beall M, et al. (2006). "Aquaporin 3 expression in human fetal membranes and its up-regulation by cyclic adenosine monophosphate in amnion epithelial cell culture". J. Soc. Gynecol. Investig. 13 (3): 181–5. doi:10.1016/j.jsgi.2006.02.002. PMID 16638588.
- Ben Y, Chen J, Zhu R, et al. (2008). "Upregulation of AQP3 and AQP5 induced by dexamethasone and ambroxol in A549 cells". Respiratory physiology & neurobiology. 161 (2): 111–8. doi:10.1016/j.resp.2007.12.007. PMID 18280225.
- Yasui H, Kubota M, Iguchi K, et al. (2008). "Membrane trafficking of aquaporin 3 induced by epinephrine". Biochem. Biophys. Res. Commun. 373 (4): 613–7. doi:10.1016/j.bbrc.2008.06.086. PMID 18601899.
- Horie I, Maeda M, Yokoyama S, et al. (2009). "Tumor necrosis factor-alpha decreases aquaporin-3 expression in DJM-1 keratinocytes". Biochem. Biophys. Res. Commun. 387 (3): 564–8. doi:10.1016/j.bbrc.2009.07.077. PMID 19619514.
- Bellemère G, Von Stetten O, Oddos T (2008). "Retinoic acid increases aquaporin 3 expression in normal human skin". J. Invest. Dermatol. 128 (3): 542–8. doi:10.1038/sj.jid.5701047. PMID 17943189.
- Cohly HH, Isokpehi R, Rajnarayanan RV (2008). "Compartmentalization of aquaporins in the human intestine". Int J Environ Res Public Health. 5 (2): 115–9. doi:10.3390/ijerph5020115. PMC 2694936. PMID 18678926.
- Lee TC, Ho IC, Lu WJ, Huang JD (2006). "Enhanced expression of multidrug resistance-associated protein 2 and reduced expression of aquaglyceroporin 3 in an arsenic-resistant human cell line". J. Biol. Chem. 281 (27): 18401–7. doi:10.1074/jbc.M601266200. PMID 16672223.
- Hara-Chikuma M, Verkman AS (2008). "Aquaporin-3 facilitates epidermal cell migration and proliferation during wound healing". J. Mol. Med. 86 (2): 221–31. doi:10.1007/s00109-007-0272-4. PMID 17968524.
- Hara-Chikuma M, Takahashi K, Chikuma S, et al. (2009). "The expression of differentiation markers in aquaporin-3 deficient epidermis". Arch. Dermatol. Res. 301 (3): 245–52. doi:10.1007/s00403-009-0927-9. PMC 3582396. PMID 19184071.
- Wang J, Tanji N, Kikugawa T, et al. (2007). "Expression of aquaporin 3 in the human prostate". Int. J. Urol. 14 (12): 1088–92, discussion 1092. doi:10.1111/j.1442-2042.2007.01901.x. PMID 18036046.
- Higuchi S, Kubota M, Iguchi K, et al. (2007). "Transcriptional regulation of aquaporin 3 by insulin". J. Cell. Biochem. 102 (4): 1051–8. doi:10.1002/jcb.21350. PMID 17471492.
- Tancharoen S, Matsuyama T, Abeyama K, et al. (2008). "The role of water channel aquaporin 3 in the mechanism of TNF-alpha-mediated proinflammatory events: Implication in periodontal inflammation". J. Cell. Physiol. 217 (2): 338–49. doi:10.1002/jcp.21506. PMID 18543247.
- Richardson SM, Knowles R, Marples D, et al. (2008). "Aquaporin expression in the human intervertebral disc". J. Mol. Histol. 39 (3): 303–9. doi:10.1007/s10735-008-9166-1. PMID 18247144.
- Avril-Delplanque A, Casal I, Castillon N, et al. (2005). "Aquaporin-3 expression in human fetal airway epithelial progenitor cells". Stem Cells. 23 (7): 992–1001. doi:10.1634/stemcells.2004-0197. PMID 16043462.
- Kida H, Miyoshi T, Manabe K, et al. (2005). "Roles of aquaporin-3 water channels in volume-regulatory water flow in a human epithelial cell line". J. Membr. Biol. 208 (1): 55–64. doi:10.1007/s00232-005-0819-7. PMID 16596446.
- Liu YL, Matsuzaki T, Nakazawa T, et al. (2007). "Expression of aquaporin 3 (AQP3) in normal and neoplastic lung tissues". Hum. Pathol. 38 (1): 171–8. doi:10.1016/j.humpath.2006.07.015. PMID 17056099.
External links
- GIL blood group system at BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH
- Human AQP3 genome location and AQP3 gene details page in the UCSC Genome Browser.