Fhit modulation of the Akt-survivin pathway in lung cancer cells: Fhit-tyrosine 114 (Y114) is essential
暂无分享,去创建一个
D. Iliopoulos | Y. Pekarsky | C. Croce | M. Fabbri | S. Volinia | H. Ishii | K. Huebner | P. Garrison | S. Semba | F. Trapasso | M. Fabbri | T. Druck | K. A. McCorkell | L. Barnes | K A McCorkell | P N Garrison | Carlo M. Croce | Shuho Semba | Dimitrios Iliopoulos | Hideshi Ishii | Preston N. Garrison | Larry D. Barnes | Kay Huebner
[1] L. D. Barnes,et al. Phosphorylation of the human Fhit tumor suppressor on tyrosine 114 in Escherichia coli and unexpected steady state kinetics of the phosphorylated forms. , 2005, Biochemistry.
[2] Dimitrios Iliopoulos,et al. Fragile genes as biomarkers: epigenetic control of WWOX and FHIT in lung, breast and bladder cancer , 2005, Oncogene.
[3] K. Huebner,et al. Involvement of the Fhit gene in the ionizing radiation‐activated ATR/CHK1 pathway , 2005, Journal of cellular physiology.
[4] M. Kasuga,et al. High Expression of PRL-3 Promotes Cancer Cell Motility and Liver Metastasis in Human Colorectal Cancer , 2004, Clinical Cancer Research.
[5] C. Croce,et al. Fhit-deficient normal and cancer cells are mitomycin C and UVC resistant , 2004, British Journal of Cancer.
[6] C. Croce,et al. Development of spontaneous tumours and intestinal lesions in Fhit gene knockout mice , 2004, British Journal of Cancer.
[7] J. Minna,et al. Synergistic Tumor Suppression by Coexpression of FHIT and p53 Coincides with FHIT-Mediated MDM2 Inactivation and p53 Stabilization in Human Non-Small Cell Lung Cancer Cells , 2004, Cancer Research.
[8] L. D. Barnes,et al. Fhit is a physiological target of the protein kinase Src. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[9] D. Coppola,et al. Phosphatidylinositol-3-OH kinase/AKT and survivin pathways as critical targets for geranylgeranyltransferase I inhibitor-induced apoptosis , 2004, Oncogene.
[10] M. Fornaro,et al. Fibronectin Protects Prostate Cancer Cells from Tumor Necrosis Factor-α-induced Apoptosis via the AKT/Survivin Pathway* , 2003, Journal of Biological Chemistry.
[11] Yiling Lu,et al. Src Family Protein-tyrosine Kinases Alter the Function of PTEN to Regulate Phosphatidylinositol 3-Kinase/AKT Cascades* , 2003, Journal of Biological Chemistry.
[12] C. Croce,et al. Cancer and the FRA3B/FHIT fragile locus: it's a HIT , 2003, British Journal of Cancer.
[13] C. Croce,et al. Designed FHIT alleles establish that Fhit-induced apoptosis in cancer cells is limited by substrate binding , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[14] Masaharu Akiyama,et al. Activation of NF-κB and upregulation of intracellular anti-apoptotic proteins via the IGF-1/Akt signaling in human multiple myeloma cells: therapeutic implications , 2002, Oncogene.
[15] C. Sawyers,et al. The phosphatidylinositol 3-Kinase–AKT pathway in human cancer , 2002, Nature Reviews Cancer.
[16] C. Croce,et al. Restoration of fragile histidine triad (FHIT) expression induces apoptosis and suppresses tumorigenicity in lung and cervical cancer cell lines , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[17] C. Croce,et al. The tumor spectrum in FHIT-deficient mice , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[18] Christine Brun,et al. In silico prediction of protein-protein interactions in human macrophages , 2001, BMC Research Notes.
[19] M. Paterson,et al. Association of FHIT (fragile histidine triad), a candidate tumour suppressor gene, with the ubiquitin-conjugating enzyme hUBC9. , 2000, The Biochemical journal.
[20] R. Kalb,et al. Angiopoietin-1 Inhibits Endothelial Cell Apoptosis via the Akt/Survivin Pathway* , 2000, The Journal of Biological Chemistry.
[21] C. Croce,et al. Role of FHIT in Human Cancer , 1999 .
[22] Fengzhi Li,et al. Control of apoptosis and mitotic spindle checkpoint by survivin , 1998, Nature.
[23] L. D. Barnes,et al. Genetic, biochemical, and crystallographic characterization of Fhit-substrate complexes as the active signaling form of Fhit. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[24] L. D. Barnes,et al. Replacement of Fhit in cancer cells suppresses tumorigenicity. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[25] L. D. Barnes,et al. Purification and crystallization of complexes modeling the active state of the fragile histidine triad protein. , 1997, Protein engineering.
[26] D. Altieri,et al. A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma , 1997, Nature Medicine.
[27] J S Lee,et al. Clonal genetic alterations in the lungs of current and former smokers. , 1997, Journal of the National Cancer Institute.
[28] L. D. Barnes,et al. Fhit, a putative tumor suppressor in humans, is a dinucleoside 5',5"'-P1,P3-triphosphate hydrolase. , 1996, Biochemistry.
[29] C. Croce,et al. The FHIT Gene at 3p14.2 Is Abnormal in Lung Cancer , 1996, Cell.
[30] C. Croce,et al. The FHIT Gene, Spanning the Chromosome 3p14.2 Fragile Site and Renal Carcinoma–Associated t(3;8) Breakpoint, Is Abnormal in Digestive Tract Cancers , 1996, Cell.
[31] D. Altieri. Validating survivin as a cancer therapeutic target , 2003, Nature Reviews Cancer.
[32] L. D. Barnes,et al. The role of the FHIT/FRA3B locus in cancer. , 1998, Annual review of genetics.