Diferenzas entre revisións de «Factor de crecemento de hepatocitos»

 
== Estrutura ==
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It is secreted as a single inactive polypeptide and is cleaved by serine proteases into a 69-kDa alpha-chain and 34-kDa beta-chain. A disulfide bond between the alpha and beta chains produces the active, heterodimeric molecule. The protein belongs to the [[plasminogen]] subfamily of S1 peptidases but has no detectable [[protease]] activity.<ref name = "entrez" >{{cite web | title = Entrez Gene: HGF hepatocyte growth factor (hepapoietin A; scatter factor)| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3082| accessdate = }}</ref>
 
ItSegrégase isen secretedforma asdun a singlepolipéptido inactiveinactivo polypeptidee anddespois isé cleavedclivado bypor serine[[serina proteasesprotease]]s intodando aunha cadea alfa de 69- kDa alpha-chaine andoutra beta de 34-kDa beta-chainkDa. AUnha disulfide[[ponte bonddisulfuro]] betweenentre as thecadeas alphaalfa ande beta chainsúneas producesdando thelugar active,ao heterodimericproduto moleculeactivo heterodimérico. TheA proteinproteína belongspertence to theá subfamilia do [[plasminogenplasminóxeno]] subfamilyde of[[peptidase]]s S1, peptidasespero butnon hasten noactividade detectable de [[protease]] activity.<ref name = "entrez" >{{cite web | title = Entrez Gene: HGF hepatocyte growth factor (hepapoietin A; scatter factor)| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=3082| accessdate = }}</ref>
== Importncia clínica ==
 
== ImportnciaImportancia clínica ==
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[[Human HGF plasmid DNA therapy]] of [[cardiomyocytes]] is being examined as a potential treatment for [[coronary artery disease]] as well as treatment for the damage that occurs to the heart after [[myocardial infarction]].<ref name=YangZhang2008>{{cite journal | vauthors = Yang ZJ, Zhang YR, Chen B, Zhang SL, Jia EZ, Wang LS, Zhu TB, Li CJ, Wang H, Huang J, Cao KJ, Ma WZ, Wu B, Wang LS, Wu CT | title = Phase I clinical trial on intracoronary administration of Ad-hHGF treating severe coronary artery disease | journal = Molecular Biology Reports | volume = 36 | issue = 6 | pages = 1323–9 | date = July 2009 | pmid = 18649012 | pmc = | doi = 10.1007/s11033-008-9315-3 }}</ref><ref name=HahnPyun2011>{{cite journal | vauthors = Hahn W, Pyun WB, Kim DS, Yoo WS, Lee SD, Won JH, Shin GJ, Kim JM, Kim S | title = Enhanced cardioprotective effects by coexpression of two isoforms of hepatocyte growth factor from naked plasmid DNA in a rat ischemic heart disease model | journal = The Journal of Gene Medicine | volume = 13 | issue = 10 | pages = 549–55 | date = October 2011 | pmid = 21898720 | pmc = | doi = 10.1002/jgm.1603 }}</ref>
As well as the well-characterised effects of HGF on [[epithelial cell]]s, [[endothelial cell]]s and [[haemopoietic progenitor cell]]s, HGF also regulates the chemotaxis of T cells into heart tissue. Binding of HGF by c-Met, expressed on T cells, causes the upregulation of c-Met, [[CXCR3]], and [[CCR4]] which in turn imbues them with the ability to migrate into heart tissue.<ref name="pmid26070483">{{cite journal | vauthors = Komarowska I, Coe D, Wang G, Haas R, Mauro C, Kishore M, Cooper D, Nadkarni S, Fu H, Steinbruchel DA, Pitzalis C, Anderson G, Bucy P, Lombardi G, Breckenridge R, Marelli-Berg FM | title = Hepatocyte Growth Factor Receptor c-Met Instructs T Cell Cardiotropism and Promotes T Cell Migration to the Heart via Autocrine Chemokine Release | journal = Immunity | volume = 42 | issue = 6 | pages = 1087–99 | date = September 2016 | pmid = 26070483 | pmc = 4510150 | doi = 10.1016/j.immuni.2015.05.014 }}</ref> HGF also promotes angiogenesis in ischemia injury. <ref>{{cite journal | vauthors = Chang HK, Kim PH, Cho, HM, Yum, SY, Choi, YJ, Lee D, Kang I, Kang KS, Jang G, Cho JY| title = Inducible HGF-secreting Human Umbilical Cord Blood-derived MSCs Produced via TALEN-mediated Genome Editing Promoted Angiogenesis | journal = Molecular Therapy | volume = 24 | issue = 9 | pages = 1644-54 | date = Sep 2016 | pmid = 27434585 | pmc = 5113099 | doi = 10.1038/mt.2016.120 }}</ref>
Hepatocyte growth factor interacts with the sulfated glycosaminoglycans heparan sulfate and dermatan sulfate.<ref name="ReferenceA">{{cite journal | vauthors = Lyon M, Deakin JA, Gallagher JT | title = The mode of action of heparan and dermatan sulfates in the regulation of hepatocyte growth factor/scatter factor | journal = The Journal of Biological Chemistry | volume = 277 | issue = 2 | pages = 1040–6 | date = January 2002 | pmid = 11689562 | doi = 10.1074/jbc.M107506200 }}</ref><ref>{{cite journal | vauthors = Lyon M, Deakin JA, Rahmoune H, Fernig DG, Nakamura T, Gallagher JT | title = Hepatocyte growth factor/scatter factor binds with high affinity to dermatan sulfate | journal = J Biol Chem | volume = 273 | issue = 1 | pages = 271–8. | date = Jan 1998 | PMID = 9417075 | doi = 10.1074/jbc.273.1.271 | url = http://www.jbc.org/content/273/1/271.long}}</ref> The interaction with heparan suflate allows hepatocyte growth factor to form a complex with c-Met that is able to transduce intracellular signals leading to cell division and cell migration.<ref name="ReferenceA"/><ref>{{cite journal | vauthors = Sergeant N, Lyon M, Rudland PS, Fernig DG, Delehedde M | title = Stimulation of DNA synthesis and cell proliferation of human mammary myoepithelial-like cells by hepatocyte growth factor/scatter factor depends on heparan sulfate proteoglycans and sustained phosphorylation of mitogen-activated protein kinases p42/44 | journal = The Journal of Biological Chemistry | volume = 275 | issue = 22 | pages = 17094–9 | date = June 2000 | pmid = 10747885 | doi = 10.1074/jbc.M000237200 }}</ref>
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== Notas ==
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