Title : Oncogenic activation of RET by two distinct FMTC mutations affecting the tyrosine kinase domain.

Pub. Date : 1997 Jul 24

PMID : 9242375






2 Functional Relationships(s)
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1 The majority of MEN2A and FMTC mutations are clustered in the extra-cellular cysteine-rich domain and result in constitutive activation of the tyrosine kinase through the formation of disulfide-bonded RET homodimers. Disulfides ret proto-oncogene Homo sapiens
2 The majority of MEN2A and FMTC mutations are clustered in the extra-cellular cysteine-rich domain and result in constitutive activation of the tyrosine kinase through the formation of disulfide-bonded RET homodimers. Disulfides ret proto-oncogene Homo sapiens