Molekulargenetisches Labor
Zentrum für Nephrologie und Stoffwechsel

Hepatozyten-Wachstumsfaktor-Rezeptor

Das MET-Gen kodiert eine Tyrosinkinaserezeptor, der wenn an an Hepatozytenwachstumsfaktor gebunden eine wichtige Rolle beim Zellüberleben, Embryogenese, Migration und Invassion spielt. Mutationen werden bei verschiedenen Tumoren gesehen: papilläres Nierenzellkarzinom, hepatozelluläres Karzinom und verschiedene weitere Tumoren im Kopf- und Hals-Bereich.

Gentests:

Klinisch Untersuchungsmethoden Familienuntersuchung
Bearbeitungszeit 5 Tage
Probentyp genomische DNS
Forschung Untersuchungsmethoden Multiplex ligationsabhängige Amplifikation
Bearbeitungszeit 25 Tage
Probentyp genomische DNS
Klinisch Untersuchungsmethoden Direkte Sequenzierung der proteinkodierenden Bereiche eines Gens
Bearbeitungszeit 25 Tage
Probentyp genomische DNS
Klinisch Untersuchungsmethoden Hochdurchsatz-Sequenzierung
Bearbeitungszeit 25 Tage
Probentyp genomische DNS

Verknüpfte Erkrankungen:

Erbliche Schwerhörigkeit 97
MET
Hepatozelluläres Karzinom
MET
Hereditäres papilläres Nierenzellkarzinom 1
MET
Osteofibröse dysplasie
MET

Referenzen:

1.

Beals RK et. al. (1976) Familial congenital bowing of the tibia with pseudarthrosis and pectus excavatum: report of a kindred.

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2.

None (1992) The met oncogene: from detection by transfection to transmembrane receptor for hepatocyte growth factor.

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3.

Bottaro DP et. al. (1991) Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product.

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4.

Park M et. al. (1987) Sequence of MET protooncogene cDNA has features characteristic of the tyrosine kinase family of growth-factor receptors.

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5.

Dean M et. al. (1987) Chromosomal localization of the met proto-oncogene in the mouse and cat genome.

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6.

Dean M et. al. () The human met oncogene is related to the tyrosine kinase oncogenes.

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7.

Cooper CS et. al. () Molecular cloning of a new transforming gene from a chemically transformed human cell line.

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8.

Maina F et. al. (1996) Uncoupling of Grb2 from the Met receptor in vivo reveals complex roles in muscle development.

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9.

Schmidt L et. al. (1997) Germline and somatic mutations in the tyrosine kinase domain of the MET proto-oncogene in papillary renal carcinomas.

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10.

Sunkara UK et. al. (1997) Bilateral osteofibrous dysplasia: a report of two cases and review of the literature.

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11.

Jeffers M et. al. (1997) Activating mutations for the met tyrosine kinase receptor in human cancer.

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12.

Giordano S et. al. (1997) A point mutation in the MET oncogene abrogates metastasis without affecting transformation.

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13.

Schmidt L et. al. (1998) Two North American families with hereditary papillary renal carcinoma and identical novel mutations in the MET proto-oncogene.

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14.

Zhuang Z et. al. (1998) Trisomy 7-harbouring non-random duplication of the mutant MET allele in hereditary papillary renal carcinomas.

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15.

Jeffers M et. al. (1998) The mutationally activated Met receptor mediates motility and metastasis.

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16.

Park WS et. al. (1999) Somatic mutations in the kinase domain of the Met/hepatocyte growth factor receptor gene in childhood hepatocellular carcinomas.

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17.

Shen Y et. al. (2000) InIB-dependent internalization of Listeria is mediated by the Met receptor tyrosine kinase.

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18.

Powell EM et. al. (2001) Hepatocyte growth factor/scatter factor is a motogen for interneurons migrating from the ventral to dorsal telencephalon.

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19.

Maina F et. al. (2001) Coupling Met to specific pathways results in distinct developmental outcomes.

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20.

Giordano S et. al. (2002) The semaphorin 4D receptor controls invasive growth by coupling with Met.

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21.

Carrolo M et. al. (2003) Hepatocyte growth factor and its receptor are required for malaria infection.

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22.

Boccaccio C et. al. (2005) The MET oncogene drives a genetic programme linking cancer to haemostasis.

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23.

Veiga E et. al. (2005) Listeria hijacks the clathrin-dependent endocytic machinery to invade mammalian cells.

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24.

Karol LA et. al. (2005) Familial osteofibrous dysplasia. A case series.

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25.

Campbell DB et. al. (2006) A genetic variant that disrupts MET transcription is associated with autism.

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26.

Engelman JA et. al. (2007) MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

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27.

Zou C et. al. (2007) Lack of Fas antagonism by Met in human fatty liver disease.

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28.

Kaushansky A et. al. (2011) The crucial role of hepatocyte growth factor receptor during liver-stage infection is not conserved among Plasmodium species.

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29.

Rodgers JT et. al. (2014) mTORC1 controls the adaptive transition of quiescent stem cells from G0 to G(Alert).

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30.

Mujtaba G et. al. (2015) A mutation of MET, encoding hepatocyte growth factor receptor, is associated with human DFNB97 hearing loss.

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31.

Finisguerra V et. al. (2015) MET is required for the recruitment of anti-tumoural neutrophils.

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32.

Gray MJ et. al. (2015) Mutations Preventing Regulated Exon Skipping in MET Cause Osteofibrous Dysplasia.

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Update: 26. September 2018