The tumor-suppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control - Wikidata - wikimedia - TriplyDB

The tumor-suppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control

The tumor-suppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control

http://www.wikidata.org/entity/Q35552007

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The histidine triad protein Hint1 triggers apoptosis independent of its enzymatic activity Designed FHIT alleles establish that Fhit-induced apoptosis in cancer cells is limited by substrate binding The nitrilase superfamily: classification, structure and function Adenosine monophosphoramidase activity of Hint and Hnt1 supports function of Kin28, Ccl1, and Tfb3 Fhit-nucleotide specificity probed with novel fluorescent and fluorogenic substrates Hint, Fhit, and GalT: function, structure, evolution, and mechanism of three branches of the histidine triad superfamily of nucleotide hydrolases and transferases Di-, tri- and tetra-5'-O-phosphorothioadenosyl substituted polyols as inhibitors of Fhit: Importance of the alpha-beta bridging oxygen and beta phosphorus replacement The common fragile site FRA16D and its associated gene WWOX are highly conserved in the mouse at Fra8E1 High-resolution chromosome 3p allelotyping of breast carcinomas and precursor lesions demonstrates frequent loss of heterozygosity and a discontinuous pattern of allele loss Impaired FHIT expression characterizes serous ovarian carcinoma Tumor suppressor and hepatocellular carcinoma A hybrid machine learning-based method for classifying the Cushing's Syndrome with comorbid adrenocortical lesions.Association of allelic loss at the FHIT locus and p53 alterations with tumour kinetics and chromosomal instability in non-small cell lung carcinomas (NSCLCs).A novel approach to simultaneously scan genes at fragile sites The DNA unwinding element binding protein DUE-B interacts with Cdc45 in preinitiation complex formation.The histidine triad superfamily of nucleotide-binding proteins.Fhit, a tumor suppressor protein, induces autophagy via 14-3-3τ in non-small cell lung cancer cells.Chromosomal and genomic changes in lung cancer.Restoration of fragile histidine triad (FHIT) expression induces apoptosis and suppresses tumorigenicity in lung and cervical cancer cell lines.P53 nuclear stabilization is associated with FHIT loss and younger age of onset in squamous cell carcinoma of oral tongue.The tumour suppressor Fhit positively regulates MHC class I expression on cancer cells.Expression of fragile histidine triad in primary hepatocellular carcinoma and its relation with cell proliferation and apoptosis.Fragile site orthologs FHIT/FRA3B and Fhit/Fra14A2: evolutionarily conserved but highly recombinogenic Predictive and prognostic markers for invasive breast cancer.FHIT gene therapy prevents tumor development in Fhit-deficient mice.Genetic alterations of multiple tumor suppressors and oncogenes in the carcinogenesis and progression of lung cancer.Cytogenetics and molecular genetics of lung cancer.Review article: molecular basis of gastric carcinogenesis.Effect of eradication of Helicobacter pylori on expression levels of FHIT, IL-8 and P73 in gastric mucosa of first-degree relatives of gastric cancer patients.Mechanisms of genomic instability in human cancer: insights from studies with human papillomavirus oncoproteins.The roles of sphingosine kinases 1 and 2 in regulating the Warburg effect in prostate cancer cells.Molecular profiling of lung carcinoma: identifying clinically useful tumor markers for diagnosis and prognosis.Frequent allelic deletion at the FHIT locus associated with p53 overexpression in squamous cell carcinoma subtype of Taiwanese non-small-cell lung cancers.The role of human papillomavirus type 16 and the fragile histidine triad gene in the outcome of cervical neoplastic lesions Fhit-deficient normal and cancer cells are mitomycin C and UVC resistant.Regions of variable DNA methylation in human placenta associated with newborn neurobehavior Fhit deficiency-induced global genome instability promotes mutation and clonal expansion.Specifically targeted gene therapy for small-cell lung cancer.Fhit loss-associated initiation and progression of neoplasia in vitro.Increased sensitivity to cisplatin in non-small cell lung cancer cell lines after FHIT gene transfer.

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The tumor-suppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control

http://www.wikidata.org/entity/Q35552007

description

1999 nî lūn-bûn

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1999 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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1999 թվականի հուլիսին հրատարակված գիտական հոդված

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1999年の論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年论文

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The tumor-suppressor gene FHIT ...... osis and in cell cycle control

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The tumor-suppressor gene FHIT ...... osis and in cell cycle control

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The tumor-suppressor gene FHIT ...... osis and in cell cycle control

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The tumor-suppressor gene FHIT ...... osis and in cell cycle control

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The tumor-suppressor gene FHIT ...... osis and in cell cycle control

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The tumor-suppressor gene FHIT ...... osis and in cell cycle control

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Proceedings of the National Academy of Sciences of the United States of America

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The tumor-suppressor gene FHIT ...... osis and in cell cycle control

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P2860

Genetic, biochemical, and crystallographic characterization of Fhit-substrate complexes as the active signaling form of Fhit

The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases

Fhit, a putative tumor suppressor in humans, is a dinucleoside 5',5"'-P1,P3-triphosphate hydrolase

The FHIT gene, spanning the chromosome 3p14.2 fragile site and renal carcinoma-associated t(3;8) breakpoint, is abnormal in digestive tract cancers

WAF1, a potential mediator of p53 tumor suppression

p21 is a universal inhibitor of cyclin kinases

Induction of apoptosis by the Bcl-2 homologue Bak

A rapid and simple method for measuring thymocyte apoptosis by propidium iodide staining and flow cytometry

Simultaneous visualization of seven different DNA probes by in situ hybridization using combinatorial fluorescence and digital imaging microscopy.

Replacement of Fhit in cancer cells suppresses tumorigenicity

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Marco A. Pierotti

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Carlo Maria Croce

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