Kindlin-3 interacts with the ribosome and regulates c-Myc expression required for proliferation of chronic myeloid leukemia cells

• المؤلفون الرئيسيون: Qu, J, Ero, R, Feng, C, Ong, L.-T, Tan, H.-F, Lee, H.-S, Ismail, M.H, Bu, W.-T, Nama, S, Sampath, P, Gao, Y.-G, Tan, S.-M
• مؤلفون آخرون: BIOCHEMISTRY
• التنسيق: مقال
• منشور في: Nature Publishing Group 2020
• الموضوعات: antineoplastic antibiotic; beta3 integrin; cell surface receptor; GNB2L1 protein, human; guanine nucleotide binding protein; membrane protein; MIG2B protein, human; Myc protein; protein binding; rapamycin; recombinant protein; target of rapamycin kinase; tumor protein; animal; antagonists and inhibitors; Bagg albino mouse; biosynthesis; cell proliferation; chemistry; chronic myeloid leukemia; drug effects; genetics; HEK293 cell line; human; isolation and purification; K-562 cell line; knockout mouse; metabolism; mouse; pathology; ribosome; RNA interference; signal transduction; umbilical vein endothelial cell; Animals; Antibiotics, Antineoplastic; Cell Proliferation; GTP-Binding Proteins; HEK293 Cells; Human Umbilical Vein Endothelial Cells; Humans; Integrin beta3; K562 Cells; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Membrane Proteins; Mice; Mice, Inbred BALB C; Mice, Knockout; Neoplasm Proteins; Protein Binding; Proto-Oncogene Proteins c-myc; Receptors, Cell Surface; Recombinant Proteins; Ribosomes; RNA Interference; Signal Transduction; Sirolimus; TOR Serine-Threonine Kinases
• الوصول للمادة أونلاين: https://scholarbank.nus.edu.sg/handle/10635/180401
• المؤسسة: National University of Singapore

10.1038/srep18491