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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 (30) and FHIT Kits (7) and many more products for this protein.
Showing 10 out of 126 products:
Human Monoclonal FHIT Primary Antibody for WB - ABIN394498
Yin, Wang, Sun, Yin, Yan, Shen, Gao, He: Homozygous deletion but not mutation of exons 5 and 8 of the fragile histidine triad (FHIT) gene is associated with features of differentiated thyroid carcinoma. in Annals of clinical and laboratory science 2010
Show all 5 references for ABIN394498
Human Monoclonal FHIT Primary Antibody for ELISA, WB - ABIN395220
Bailey, Xie, Do, Montpetit, Diaz, Mohan, Keavney, Yusuf, Gerstein, Engert, Anand: Variation at the NFATC2 locus increases the risk of thiazolidinedione-induced edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) study. in Diabetes Care 2010
Show all 5 references for ABIN395220
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 references for ABIN968653
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
Human Polyclonal FHIT Primary Antibody for IHC, ELISA - ABIN1532181
Ohta, Inoue, Cotticelli, Kastury, Baffa, Palazzo, Siprashvili, Mori, McCue, Druck, Croce, Huebner: The FHIT gene, spanning the chromosome 3p14.2 fragile site and renal carcinoma-associated t(3;8) breakpoint, is abnormal in digestive tract cancers. in Cell 1996
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 (show CDKN2A Antibodies) 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.
Adenylylsulfate-ammonia adenylyltransferase activity is another inherent property of Fhit proteins.
APOBEC3B overexpression and Fhit-loss induced DNA damage are independent events that, when occurring together, result in a significantly increased frequency of APOBEC-induced mutations that drive cancer progression.
Hypermethylation of FHIT gene is associated with Epstein-Barr virus-associated gastric carcinomas.
FHIT promotor hypermethylation is associated with the development of breast cancer.
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
UV-induced alterations of the FHIT and WWOX (show WWOX Antibodies) fragile site gene expression are involved at least partially in the checkpoint function of DNA damage
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