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Titolo:
The collagen receptor DDR2 regulates proliferation and its elimination leads to dwarfism
Autore:
Labrador, JP; Azcoitia, V; Tuckermann, J; Lin, C; Olaso, E; Manes, S; Bruckner, K; Georgen, JL; Lemke, G; Yancopoulos, G; Angel, P; Martinez, C; Klein, R;
Indirizzi:
European Mol Biol Lab, D-69117 Heidelberg, Germany European Mol Biol Lab Heidelberg Germany D-69117 117 Heidelberg, Germany Consejo Super Invest Cient, Dept Immunol & Oncol, E-28049 Madrid, Spain Consejo Super Invest Cient Madrid Spain E-28049 l, E-28049 Madrid, Spain Deutsch Krebsforschungszentrum, D-69120 Heidelberg, Germany Deutsch Krebsforschungszentrum Heidelberg Germany D-69120 lberg, Germany Regeneron Pharmaceut Inc, Tarrytown, NY 10591 USA Regeneron Pharmaceut Inc Tarrytown NY USA 10591 , Tarrytown, NY 10591 USA CUNY Mt Sinai Sch Med, Div Liver Dis, New York, NY 10029 USA CUNY Mt SinaiSch Med New York NY USA 10029 r Dis, New York, NY 10029 USA CUNY Mt Sinai Sch Med, Dept Med, New York, NY 10029 USA CUNY Mt Sinai Sch Med New York NY USA 10029 t Med, New York, NY 10029 USA Salk Inst Biol Studies, Mol Neurobiol Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies La Jolla CA USA 92037 Lab, La Jolla, CA 92037 USA
Titolo Testata:
EMBO REPORTS
fascicolo: 5, volume: 2, anno: 2001,
pagine: 446 - 452
SICI:
1469-221X(200105)2:5<446:TCRDRP>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
DISCOIDIN DOMAIN RECEPTOR-1; TYROSINE KINASE; EXPRESSION; GROWTH; INTEGRIN; CANCER; FAMILY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Labrador, JP European Mol Biol Lab, Meyerhofstr 1, D-69117 Heidelberg, Germany European Mol Biol Lab Meyerhofstr 1 Heidelberg Germany D-69117
Citazione:
J.P. Labrador et al., "The collagen receptor DDR2 regulates proliferation and its elimination leads to dwarfism", EMBO REP, 2(5), 2001, pp. 446-452

Abstract

The discoidin domain receptor 2 (DDR2) is a member of a subfamily of receptor tyrosine kinases whose ligands are fibrillar collagens, and is widely expressed in postnatal tissues. We have generated DDR2-deficient mice to establish the in vivo functions of this receptor, which have remained obscure. These mice exhibit dwarfism and shortening of long bones. This phenotype appears to be caused by reduced chondrocyte proliferation, rather than aberrant differentiation or function. In a skin wound healing model, DDR2-/- mice exhibit a reduced proliferative response compared with wild-type littermates. In vitro, fibroblasts derived from DDR2-/- mutants proliferate more slowly than wild-type fibroblasts, a defect that is rescued by introduction of wild-type but not kinase-dead DDR2 receptor. Together our results suggestthat DDR2 acts as an extracellular matrix sensor to modulate cell proliferation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 15:08:48