Fragile Histidine Triad (FHIT) Kits ELISA

FHIT, a member of the histidine triad gene family, encodes a diadenosine 5',5'''-P1,P3-triphosphate hydrolase involved in purine metabolism. De plus, nous expédions FHIT Anticorps (166) et FHIT Protéines (25) et beaucoup plus de produits pour cette protéine.

list all ELISA KIts Gène GeneID UniProt
FHIT 2272 P49789
FHIT 60398 Q9JIX3
FHIT 14198 O89106
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Top FHIT Kits ELISA sur anticorps-enligne.fr

Showing 4 out of 10 products:

Catalogue No. Reactivité Sensibilité Gamme Images Quantité Livraison Prix Détails
Humain 7.8 pg/mL 31.2-2000 pg/mL Typical standard curve 96 Tests 15 to 18 Days
$1,026.67
Détails
Rat < 46.9 pg/mL 78 pg/mL - 5000 pg/mL   96 Tests 11 to 18 Days
$838.60
Détails
Souris < 0.094 ng/mL 0.156 ng/mL - 10 ng/mL   96 Tests 11 to 18 Days
$838.60
Détails
Boeuf (Vache)
  96 Tests 15 to 18 Days
$1,029.60
Détails

Plus Kits ELISA pour FHIT partenaires d'interaction

Human Fragile Histidine Triad (FHIT) interaction partners

  1. a novel modifier gene in pulmonary arterial hypertension

  2. The authors identified that FHIT is significantly associated with hypertensive Intracranial Aneurysm in the French-Canadian population.

  3. Decreased expressions of FHIT is associated with breast cancer.

  4. The varied expression or negative expression of FHIT could be considered as an indicator for aggressive behavior and transformation of preneoplastic/cystic epithelium.

  5. This literature review aims to clarify the involvement of the FHIT gene in carcinogenesis, tumor progression and clinical outcome in prevalent solid malignancies, such as breast, lung, cervical, esophageal, gastric and colorectal cancers

  6. The incidence of FHIT and p16 methylation in serum from the liver cancer group was 51.8% and 67.9%, respectively. The incidence of FHIT and p16 methylation in the non-hepatoma group was 16.7% and 25.0%.

  7. Under the high exposure of 1-hydroxy pyrene and the CpG island methylation of p16, FHIT appeared to have increased the risk of cervical intraepithelial neoplasia and causing synergistic effect in cervical intraepithelial neoplasia.

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

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

  10. 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.

  11. 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.

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

  13. 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)

  14. 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.

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

  16. 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.

  17. 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.

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

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

  20. 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.

Cow (Bovine) Fragile Histidine Triad (FHIT) interaction partners

  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) interaction partners

  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 profil antigène

Antigen Summary

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.

Gene names and symbols associated with FHIT

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

Protein level used designations for 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

GENE ID SPECIES
2272 Homo sapiens
100215999 Canis lupus familiaris
692183 Bos taurus
60398 Rattus norvegicus
100307043 Ovis aries
393713 Danio rerio
14198 Mus musculus
448702 Xenopus (Silurana) tropicalis
100223655 Taeniopygia guttata
3800584 Plasmodium yoelii yoelii 17XNL
416071 Gallus gallus
495983 Xenopus laevis
700974 Macaca mulatta
747260 Pan troglodytes
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