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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 (149) and FHIT Proteins (23) and many more products for this protein.
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overexpression of Fhit, a tumor suppressor protein, induces autophagy in NSCLC cells. Further, we found that this autophagy is mediated by 14-3-3tau and plays a cytoprotective role against the antitumor effect of Fhit both in vitro and in vivo.
Review/Meta-analysis: significant difference in FHIT gene promoter methylation status in non-small cell lung carcinoma patients was found in Asians but not in Caucasian population.
these results show that squamous cell carcinomas of the vulva presents a characteristic molecular pattern with FHIT being downregulated whereas HMGA2 is upregulated
It has been proposed that Fhit and Wwox (show WWOX ELISA Kits) loss work synergistically in cancer progression and that DNA damage caused by Fhit could be targeted early in cancer initiation for prevention, while DNA damage caused by Wwox (show WWOX ELISA Kits) loss could be targeted later in cancer progression, particularly in cancers that develop resistance to genotoxic therapies. (Review)
Two variants were identified for maximal voluntary ventilation and located in the genes of LOC102724340 (rs41434646) and FHIT (rs9833533). FHIT represses transcriptional activity of beta-catenin (show CTNNB1 ELISA Kits), a critical protein for growth of skeletal muscle, and thus might have influenced the level of maximal voluntary ventilation.
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 ELISA Kits) 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 ELISA Kits) transitioned to cervical cancer.
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 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) 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