Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 2.7.10.2 extracted from

  • Sancier, F.; Dumont, A.; Sirvent, A.; Paquay de Plater, L.; Edmonds, T.; David, G.; Jan, M.; de Montrion, C.; Coge, F.; Leonce, S.; Burbridge, M.; Bruno, A.; Boutin, J.A.; Lockhart, B.; Roche, S.; Cruzalegui, F.
    Specific oncogenic activity of the Src-family tyrosine kinase c-Yes in colon carcinoma cells (2011), PLoS ONE, 6, e17237.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine in HT29 colon carcinoma cells, silencing of tyrosine kinase c-Yes, but not of kinase c-Src, selectively leads to an increase of cell clustering associated with a localisation of beta-catenin at cell membranes and a reduction of expression of beta-catenin target genes. c-Yes silencing induces an increase in apoptosis, inhibition of growth in soft-agar and in mouse xenografts, inhibition of cell migration and loss of the capacity to generate liver metastases in mice. Reintroduction of c-Yes, but not c -Src, restores transforming properties of c-Yes depleted cells. c-Yes kinase activity is required for its role in beta-catenin localisation and growth in soft agar, whereas kinase activity is dispensable for its role in cell migration. c-Yes regulates specific oncogenic signalling pathways important for colon cancer progression that are not shared with c-Src Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P07947 YES1
-

Source Tissue

Source Tissue Comment Organism Textmining
HT-29 cell
-
Homo sapiens
-

Synonyms

Synonyms Comment Organism
Yes
-
Homo sapiens
YES1
-
Homo sapiens

General Information

General Information Comment Organism
physiological function in HT29 colon carcinoma cells, silencing of tyrosine kinase c-Yes, but not of kinase c-Src, selectively leads to an increase of cell clustering associated with a localisation of beta-catenin at cell membranes and a reduction of expression of beta-catenin target genes. c-Yes silencing induces an increase in apoptosis, inhibition of growth in soft-agar and in mouse xenografts, inhibition of cell migration and loss of the capacity to generate liver metastases in mice. Reintroduction of c-Yes, but not c -Src, restores transforming properties of c-Yes depleted cells. c-Yes kinase activity is required for its role in beta-catenin localisation and growth in soft agar, whereas kinase activity is dispensable for its role in cell migration. c-Yes regulates specific oncogenic signalling pathways important for colon cancer progression that are not shared with c-Src Homo sapiens