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FHIT, a member of the histidine triad gene family, encodes a diadenosine 5',5'''-P1,P3-triphosphate hydrolase involved in purine metabolism. Additionally we are shipping FHIT Proteins (37) and FHIT Kits (8) and many more products for this protein.
Showing 10 out of 136 products:
Mouse (Murine) Monoclonal FHIT Primary Antibody for IF, WB - ABIN968653
Fong, Fidanza, Zanesi, Lock, Siracusa, Mancini, Siprashvili, Ottey, Martin, Druck, McCue, Croce, Huebner: Muir-Torre-like syndrome in Fhit-deficient mice. in Proceedings of the National Academy of Sciences of the United States of America 2000
Show all 3 Pubmed References
Human Polyclonal FHIT Primary Antibody for IHC, IHC (p) - ABIN4311628
Diaz, Guduk, Romagnuolo, Smith, Northcott, Shih, Berisha, Flanagan, Munoz, Cusimano, Pamir, Rutka: High-resolution whole-genome analysis of skull base chordomas implicates FHIT loss in chordoma pathogenesis. in Neoplasia (New York, N.Y.) 2012
Show all 2 Pubmed References
Human Polyclonal FHIT Primary Antibody for IF (p), IHC (p) - ABIN734198
Liu, Ao, Zhou, Cui, Zhou, Yuan, Xiang, Cao, Liu: CpG island hypermethylation of multiple tumor suppressor genes associated with loss of their protein expression during rat lung carcinogenesis induced by 3-methylcholanthrene and diethylnitrosamine. in Biochemical and biophysical research communications 2010
This study demonstrates that Fhit down-regulation is an early event in both multistep carcinogenic processes leading to pancreatic ductal adenocarcinoma
The results have implications for the mechanism by which Fhit regulates TK1 (show TK1 Antibodies) mRNA, and more broadly, for its modulation of multiple functions as tumor suppressor/genome caretaker.
RARb and FHIT promoter methylation may be associated with the carcinogenesis of cervical cancer. FHIT promoter methylation may play a crucial role in cervical cancer progression. Additional studies with large sample sizes are essential to confirm our findings.
The peptide was located within the 'disordered' region, which is invisible in the known crystal structures of Fhit.
Both the 3p14.2 locus copy number and FHIT protein expression levels showed significant decreases when CIN (show PDXP Antibodies) transitioned to cervical cancer.
Study indicate that the observed level of FHIT promoter methylation was not enough to suppress gene expression in non-small cell lung cancer (NSCLC). Lack of negative correlation between FHIT expression and methylation, or positive correlation between gene expression and immunoexpression suggest the role of another molecular mechanisms regulating FHIT expression on mRNA and protein levels in NSCLC patients.
High methylation in the FHIT promoter region is associated with lung cancer.
the expression profile of miRNAs that may be associated with expression of the FHIT gene in breast cancer, was examined.
FHIT hypermethylation, which induces the inactivation of FHIT gene, plays an important role in the carcinogenesis and clinical outcome and may serve as a potential drug target of non-small cell lung cancer.
FHIT hypermethylation, which induces the inactivation of FHIT gene, plays an important role in the carcinogenesis and clinical outcome and may serve as a potential diagnostic marker and drug target of non-small-cell lung carcinoma
the same mRNA isoforms of FHIT were detected in bladder tumors and in healthy tissues, including a novel isoform that was found in this study, suggesting that epigenetic modifications and altered expression profiles are not a hallmark of vesical tumors
Fhit loss and subsequent thymidine kinase 1 (show TK1 Antibodies) inactivation, combined with selective pressures, leads to neoplasia-associated alterations in genes and gene expression patterns in vitro and in vivo
Fhit-deficiency mutation signature also resembles a C>T and T>C mutation signature reported for human papillary kidney cancers and a similar signature recently reported for esophageal and bladder cancers, cancers that are frequently Fhit deficient.
Fhit deficiency-induced global genome instability promotes mutation and clonal expansion
Fhit delocalizes annexin A4 (show ANXA4 Antibodies) from plasma membrane to cytosol and sensitizes lung cancer cells to paclitaxel.
FHIT gene is a "caretaker gene" necessary for maintenance of genome stability.
Loss of Fhit expression contributes to cell transformation.
Defects in Fhit expression may promote MHC-I down-regulation in cancer cells and allow escape from immunosurveillance.
Human and mouse orthologous genes, FHIT and Fhit, are more highly conserved through evolution than PTPRG/Ptprg (show PTPRG Antibodies) and yet contain more sequence elements that are exquisitely sensitive to genomic rearrangements
Association of Fhit gene inactivation with increased survival after DNA damage, related to over-active checkpoints regulated by ATR/CHK1 pathway. Potential effects of Fhit-dependent DNA damage response on tumor progression.
Fhit has a role in bladder cancer development
This gene, a member of the histidine triad gene family, encodes a diadenosine 5',5'''-P1,P3-triphosphate hydrolase involved in purine metabolism. The gene encompasses the common fragile site FRA3B on chromosome 3, where carcinogen-induced damage can lead to translocations and aberrant transcripts of this gene. In fact, aberrant transcripts from this gene have been found in about half of all esophageal, stomach, and colon carcinomas. Alternatively spliced transcript variants have been found for this gene.
, diadenosine 5',5'''-P1,P3-triphosphate hydrolase
, tumor suppressor protein
, fragile histidine triad protein
, fragile histidine triad gene
, diadenosine triphosphate hydrolase
, fragile histidine triad