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Defective downregulation of receptor tyrosine kinases in cancer
Author(s) -
Bache Kristi G,
Slagsvold Thomas,
Stenmark Harald
Publication year - 2004
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7600292
Subject(s) - biology , downregulation and upregulation , receptor tyrosine kinase , receptor protein tyrosine kinases , tyrosine kinase , kinase , cancer research , proto oncogene tyrosine protein kinase src , cancer , receptor , microbiology and biotechnology , ror1 , tyrosine , protein tyrosine phosphatase , signal transduction , genetics , biochemistry , platelet derived growth factor receptor , gene , growth factor
Most growth factors control cellular functions by activating specific receptor tyrosine kinases (RTKs). While overactivation of RTK signalling pathways is strongly associated with carcinogenesis, it is becoming increasingly clear that impaired deactivation of RTKs may also be a mechanism in cancer. A major deactivation pathway, receptor downregulation, involves ligand‐induced endocytosis of the RTK and subsequent degradation in lysosomes. A complex molecular machinery that uses the small protein ubiquitin as a key regulator assures proper endocytosis and degradation of RTKs. Here we discuss evidence that implicates deregulation of this machinery in cancer.