Disease relevance of Yes1

• Disrupting the endothelial barrier directly with anti-VE-cadherin both amplifies metastasis in normal mice and overcomes the genetic resistance in Yes-deficient mice [1].

High impact information on Yes1

• In cells microinjected with a neutralizing antibody specific for Src, Fyn, and Yes (anti-cst.1) during G2, cell division was inhibited by 75 percent [2].
• However, transgenic mice expressing the PyV middle T antigen in the mammary epithelium of wild-type or Yes-deficient mice developed multifocal mammary tumors with comparable kinetics [3].
• At the molecular level, VEGF compromises the endothelial barrier by disrupting a VE-cadherin-beta-catenin complex in lung endothelium from wild-type, but not Yes-deficient, mice [1].
• Brain-blood barrier? Yes and no [4].
• Similar to Fyn deletion, simultaneous deletion of Fyn and Yes reduced Nephrin phosphorylating activity [5].

Biological context of Yes1

• Fyn and Yes, the other members of the Src family present in fibroblasts, were also found to be activated at mitosis [2].
• The reading frame encodes a protein of 541 amino acids with a calculated molecular mass of 60.63 kDa that is reactive with anti-Yes antisera and possesses protein kinase activity [6].
• Although Yes appears to effect the regulation of Nephrin phosphorylation, the mechanism by which this occurs requires investigation [5].

Anatomical context of Yes1

• Biochemical analysis of complexes between PymT and the Src-related kinases in these cell lines suggests that the Yes kinase is responsible for a significant amount of the PymT-associated kinase activity in transformed endothelial cells [7].

Associations of Yes1 with chemical compounds

• Activation of c-Yes tyrosine kinase correlated with the capacity of c-Yes to associate with Neu in vivo in lysates derived from primary tumor samples [8].
• The binding of Shiga toxin to globotriaosyl ceramide in raft microdomains of the human renal tubular cell line ACHN causes temporal activation of Src-kinase Yes [9].

Other interactions of Yes1

• We have generated mouse embryos harboring functional null mutations of the ubiquitously expressed SFKs Src, Yes and Fyn [10].
• These analyses revealed that c-Yes kinase activity was elevated in Neu-induced tumors by comparison to the adjacent tissue [8].
• Increased utilization of yes mRNA resulted in elevated expression of the protein product in cells transformed with eIF4E, and suggested that overexpression of Yes could contribute to eIF4E-mediated transformation [11].

Analytical, diagnostic and therapeutic context of Yes1

• Debate: is ICSI a genetic time bomb? Yes [12].

References