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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 Antibodies (133) and FHIT Kits (7) and many more products for this protein.
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Human FHIT Protein expressed in Escherichia coli (E. coli) - ABIN667000
Hassan, Naiyer, Ahmad: Fragile histidine triad protein: structure, function, and its association with tumorogenesis. in Journal of cancer research and clinical oncology 2010
Show all 2 references for ABIN667000
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
Low FHIT Gene Expression is associated with Acute Lymphoblastic Leukemia.
In 22 lung cancer patients with negative histology and cytology at initial bronchoscopy, FHIT and p16 mRNA loss was detected in 40.9% (9/22) and 36.4% (8/22) cases, respectively.
The results showed that the methylation levels of both BRCA1 and FHIT promoters were higher in the serum of the breast ductal carcinoma group than those of the breast fibroadenoma group.
Review/Meta-analysis: FHIT methylation could be a diagnostic biomarker of breast carcinogenesis.
Mutations of the FHIT gene are not major cause of Peutz-Jeghers syndrome.
Fhit loss and subsequent thymidine kinase 1 (show TK1 Proteins) 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 Proteins) 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 Proteins) 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
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
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
, diadenosine triphosphate hydrolase