Title : Galectin-3 mediates cross-talk between K-Ras and Let-7c tumor suppressor microRNA.

Pub. Date : 2011

PMID : 22102901






4 Functional Relationships(s)
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1 BACKGROUND: Galectin-3 (Gal-3) and active (GTP-bound) K-Ras contribute to the malignant phenotype of many human tumors by increasing the rate of cell proliferation, survival, and migration. Guanosine Triphosphate KRAS proto-oncogene, GTPase Homo sapiens
2 These Gal-3-mediated effects result from a selective binding to K-Ras.GTP, causing increased nanoclustering in the cell membrane and leading to robust Ras signaling. Guanosine Triphosphate KRAS proto-oncogene, GTPase Homo sapiens
3 We found that knockout of Gal-3 induced strong downregulation (~60%) of K-Ras and K-Ras.GTP. Guanosine Triphosphate KRAS proto-oncogene, GTPase Homo sapiens
4 These additional effects are probably attributable to inhibition of the weak interactions of K-Ras.GTP with Gal-1. Guanosine Triphosphate KRAS proto-oncogene, GTPase Homo sapiens