The MET tyrosine kinase receptor (also known as the HGF receptor) promotes tissue remodelling, which underlies developmental morphogenesis, wound repair, organ homeostasis and cancer metastasis, by integrating growth, survival and migration cues in response to environmental stimuli or cell-autonomous perturbations. The versatility of MET-mediated biological responses is sustained by qualitative and quantitative signal modulation. Qualitative mechanisms include the engagement of dedicated signal transducers and the subcellular compartmentalization of MET signalling pathways, whereas quantitative regulation involves MET partnering with adaptor amplifiers or being degraded through the shedding of its extracellular domain or through intracellular ubiquitylation. Controlled activation of MET signalling can be exploited in regenerative medicine, whereas MET inhibition might slow down tumour progression.

MET signalling: principles and functions in development, organ regeneration and cancer.

TRUSOLINO, Livio;BERTOTTI, Andrea;COMOGLIO, Paolo
2010-01-01

Abstract

The MET tyrosine kinase receptor (also known as the HGF receptor) promotes tissue remodelling, which underlies developmental morphogenesis, wound repair, organ homeostasis and cancer metastasis, by integrating growth, survival and migration cues in response to environmental stimuli or cell-autonomous perturbations. The versatility of MET-mediated biological responses is sustained by qualitative and quantitative signal modulation. Qualitative mechanisms include the engagement of dedicated signal transducers and the subcellular compartmentalization of MET signalling pathways, whereas quantitative regulation involves MET partnering with adaptor amplifiers or being degraded through the shedding of its extracellular domain or through intracellular ubiquitylation. Controlled activation of MET signalling can be exploited in regenerative medicine, whereas MET inhibition might slow down tumour progression.
2010
11
12
834
848
http://www.nature.com/nrm/journal/v11/n12/full/nrm3012.html
HEPATOCYTE GROWTH-FACTOR; RECEPTOR-TYROSINE KINASE; NF-KAPPA-B; EPITHELIAL-MESENCHYMAL TRANSITION; ANCHORAGE-INDEPENDENT GROWTH; DEPENDENT INVASIVE GROWTH; CARCINOMA-CELL-LINES; DOMAIN BINDING-SITE; C-MET; SCATTER-FACTOR
Trusolino L; Bertotti A; Comoglio PM
File in questo prodotto:
File Dimensione Formato  
Trusolino et al.pdf

Open Access dal 02/06/2011

Tipo di file: POSTPRINT (VERSIONE FINALE DELL’AUTORE)
Dimensione 744.28 kB
Formato Adobe PDF
744.28 kB Adobe PDF Visualizza/Apri
Trusolino, Bertotti, Comoglio_Nat Rev Mol Cell Biol 2010.pdf

Accesso riservato

Tipo di file: PDF EDITORIALE
Dimensione 856.28 kB
Formato Adobe PDF
856.28 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/78969
Citazioni
  • ???jsp.display-item.citation.pmc??? 516
  • Scopus 965
  • ???jsp.display-item.citation.isi??? 908
social impact