Fragile Histidine Triad (FHIT) ELISA Kits

FHIT, a member of the histidine triad gene family, encodes a diadenosine 5',5'''-P1,P3-triphosphate hydrolase involved in purine metabolism. Zusätzlich bieten wir Ihnen FHIT Antikörper (150) und FHIT Proteine (25) und viele weitere Produktgruppen zu diesem Protein an.

list all ELISA KIts Gen GeneID UniProt
FHIT 2272 P49789
FHIT 60398 Q9JIX3
FHIT 14198 O89106
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Top FHIT ELISA Kits auf

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Katalog Nr. Reaktivität Sensitivität Bereich Bilder Menge Anbieter Lieferzeit Preis Details
Human 7.8 pg/mL 31.2-2000 pg/mL Typical standard curve 96 Tests Anmelden zum Anzeigen 15 bis 18 Tage
Maus < 0.094 ng/mL 0.156 ng/mL - 10 ng/mL   96 Tests Anmelden zum Anzeigen 11 bis 18 Tage
Ratte < 46.9 pg/mL 78 pg/mL - 5000 pg/mL   96 Tests Anmelden zum Anzeigen 11 bis 18 Tage
Rind (Kuh)
  96 Tests Anmelden zum Anzeigen 15 bis 18 Tage

Weitere ELISA Kits für FHIT Interaktionspartner

Human Fragile Histidine Triad (FHIT) Interaktionspartner

  1. FHIT predicts better clinical relevance for patients with bladder cancer.

  2. Fhit expression impacts the translation of a number of cancer associated genes.

  3. 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.

  4. 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.

  5. these results show that squamous cell carcinomas of the vulva presents a characteristic molecular pattern with FHIT being downregulated whereas HMGA2 is upregulated

  6. It has been proposed that Fhit and Wwox 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 loss could be targeted later in cancer progression, particularly in cancers that develop resistance to genotoxic therapies. (Review)

  7. 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, a critical protein for growth of skeletal muscle, and thus might have influenced the level of maximal voluntary ventilation.

  8. This study demonstrates that Fhit down-regulation is an early event in both multistep carcinogenic processes leading to pancreatic ductal adenocarcinoma

  9. The results have implications for the mechanism by which Fhit regulates TK1 mRNA, and more broadly, for its modulation of multiple functions as tumor suppressor/genome caretaker.

  10. 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.

  11. The peptide was located within the 'disordered' region, which is invisible in the known crystal structures of Fhit.

  12. Both the 3p14.2 locus copy number and FHIT protein expression levels showed significant decreases when CIN transitioned to cervical cancer.

  13. 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.

  14. High methylation in the FHIT promoter region is associated with lung cancer.

  15. the expression profile of miRNAs that may be associated with expression of the FHIT gene in breast cancer, was examined.

  16. 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.

  17. 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

  18. Low FHIT Gene Expression is associated with Acute Lymphoblastic Leukemia.

  19. 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.

  20. 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.

Cow (Bovine) Fragile Histidine Triad (FHIT) Interaktionspartner

  1. 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

Mouse (Murine) Fragile Histidine Triad (FHIT) Interaktionspartner

  1. Fhit loss and subsequent thymidine kinase 1 inactivation, combined with selective pressures, leads to neoplasia-associated alterations in genes and gene expression patterns in vitro and in vivo

  2. 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.

  3. Fhit deficiency-induced global genome instability promotes mutation and clonal expansion

  4. Fhit delocalizes annexin A4 from plasma membrane to cytosol and sensitizes lung cancer cells to paclitaxel.

  5. FHIT gene is a "caretaker gene" necessary for maintenance of genome stability.

  6. Loss of Fhit expression contributes to cell transformation.

  7. Defects in Fhit expression may promote MHC-I down-regulation in cancer cells and allow escape from immunosurveillance.

  8. Human and mouse orthologous genes, FHIT and Fhit, are more highly conserved through evolution than PTPRG/Ptprg and yet contain more sequence elements that are exquisitely sensitive to genomic rearrangements

  9. 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.

  10. Fhit has a role in bladder cancer development

  11. UV-induced alterations of the FHIT and WWOX fragile site gene expression are involved at least partially in the checkpoint function of DNA damage

  12. Data suggest that heterozygosity for FHIT affects susceptibility of mice to spontaneous alopecia areata and benzo[a]pyrene-induced preneoplastic lesions of the uterus and does not alter responsiveness to budesonide and N-acetyl-L-cysteine.

  13. Nit1 and Fhit share tumor suppressor signaling pathways, while localization of the NIT1 gene at a stable chromosome site explains the paucity of gene alterations and in frequent loss of expression of the NIT1 gene in human malignancies.

  14. It is likely that the FHIT transgene is more tightly silenced in female transgenic mice, leading to a lack of protection from tumor induction

  15. tumor-like microdeletions in FHIT/FRA3B are induced by replication stress

  16. reduced oxidative stress, coupled with efficient but not error-free DNA damage repair, allows unscheduled long-term survival of genotoxin-exposed Fhit-deficient hematopoietic stem cells carrying deleterious mutations

  17. the extent of tumor susceptibility due to Nit1 and Fhit deficiency is additive

FHIT Antigen-Profil

Beschreibung des Gens

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.

Genbezeichner und Symbole assoziert mit FHIT

  • fragile histidine triad (FHIT) Antikörper
  • fragile histidine triad (Fhit) Antikörper
  • fragile histidine triad gene (fhit) Antikörper
  • fragile histidine triad gene (Fhit) Antikörper
  • fragile histidine triad (fhit) Antikörper
  • fragile histidine triad protein (PY07476) Antikörper
  • fragile histidine triad L homeolog (fhit.L) Antikörper
  • AP3Aase Antikörper
  • AW045638 Antikörper
  • FHIT Antikörper
  • FRA3B Antikörper
  • Fra14A2 Antikörper
  • LOC100223655 Antikörper
  • zgc:73176 Antikörper

Bezeichner auf Proteinebene für FHIT

AP3A hydrolase , bis(5'-adenosyl)-triphosphatase , diadenosine 5',5'''-P1,P3-triphosphate hydrolase , dinucleosidetriphosphatase , tumor suppressor protein , AP3Aase , fragile histidine triad protein , fragile histidine triad gene , diadenosine triphosphate hydrolase , fragile histidine triad

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