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Crk proteins activate the Rap1 guanine nucleotide exchange factor C3G by segregated adaptor-dependent and -independent mechanisms.

Antonio Rodríguez-BlázquezArturo CarabiasAlba Morán-VaqueroSergio de CimaJuan Román Luque-OrtegaCarlos AlfonsoPeter W SchuckJosé António MansoSandra Macedo-RibeiroCarmen GuerreroJosé María de Pereda
Published in: Cell communication and signaling : CCS (2023)
Our study revealed that phosphorylation of C3G by Src and Crk-binding form a two-factor mechanism that ensures tight control of C3G activation. Additionally, the simultaneous SH2 and SH3N interaction of CrkL with C3G, required for the activation, reveals a novel adaptor-independent function of Crk proteins relevant to understanding their role in physiological signaling and their deregulation in diseases. Video abstract.
Keyphrases
  • blood brain barrier
  • tyrosine kinase
  • single cell
  • protein kinase