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  4. Phospho-FHIT (Y114) Antibody

Phospho-FHIT (Y114) Antibody

  • 货号：
    CSB-PA697203
  • 规格：
    ￥880
  • 其他：

产品详情

  • Uniprot No.：
    P49789
  • 基因名：
    FHIT
  • 别名：
    FHITBis(5'-adenosyl)-triphosphatase antibody; EC 3.6.1.29 antibody; AP3A hydrolase antibody; AP3Aase antibody; Diadenosine 5',5'''-P1,P3-triphosphate hydrolase antibody; Dinucleosidetriphosphatase antibody; Fragile histidine triad protein antibody
  • 宿主：
    Rabbit
  • 反应种属：
    Human
  • 免疫原：
    Synthesized peptide derived from Human Fhit around the phosphorylation site of Y114.
  • 免疫原种属：
    Homo sapiens (Human)
  • 标记方式：
    Non-conjugated
  • 抗体亚型：
    IgG
  • 纯化方式：
    The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
  • 浓度：
    It differs from different batches. Please contact us to confirm it.
  • 保存缓冲液：
    Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
  • 产品提供形式：
    Liquid
  • 应用范围：
    IHC, ELISA
  • 推荐稀释比：
    Application Recommended Dilution
    IHC 1:100-1:300
    ELISA 1:40000
  • Protocols：
  • 储存条件：
    Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
  • 货期：
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

产品评价

靶点详情

  • 功能：
    Possesses dinucleoside triphosphate hydrolase activity. Cleaves P(1)-P(3)-bis(5'-adenosyl) triphosphate (Ap3A) to yield AMP and ADP. Can also hydrolyze P(1)-P(4)-bis(5'-adenosyl) tetraphosphate (Ap4A), but has extremely low activity with ATP. Exhibits adenylylsulfatase activity, hydrolyzing adenosine 5'-phosphosulfate to yield AMP and sulfate. Exhibits adenosine 5'-monophosphoramidase activity, hydrolyzing purine nucleotide phosphoramidates with a single phosphate group such as adenosine 5'monophosphoramidate (AMP-NH2) to yield AMP and NH2. Exhibits adenylylsulfate-ammonia adenylyltransferase, catalyzing the ammonolysis of adenosine 5'-phosphosulfate resulting in the formation of adenosine 5'-phosphoramidate. Also catalyzes the ammonolysis of adenosine 5-phosphorofluoridate and diadenosine triphosphate. Modulates transcriptional activation by CTNNB1 and thereby contributes to regulate the expression of genes essential for cell proliferation and survival, such as CCND1 and BIRC5. Plays a role in the induction of apoptosis via SRC and AKT1 signaling pathways. Inhibits MDM2-mediated proteasomal degradation of p53/TP53 and thereby plays a role in p53/TP53-mediated apoptosis. Induction of apoptosis depends on the ability of FHIT to bind P(1)-P(3)-bis(5'-adenosyl) triphosphate or related compounds, but does not require its catalytic activity, it may in part come from the mitochondrial form, which sensitizes the low-affinity Ca(2+) transporters, enhancing mitochondrial calcium uptake. Functions as tumor suppressor.
  • 基因功能参考文献：
    1. FHIT predicts better clinical relevance for patients with bladder cancer. PMID: 29752880
    2. Fhit expression impacts the translation of a number of cancer associated genes. PMID: 29282095
    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. PMID: 28404875
    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. PMID: 28036263
    5. these results show that squamous cell carcinomas of the vulva presents a characteristic molecular pattern with FHIT being downregulated whereas HMGA2 is upregulated PMID: 27835588
    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) PMID: 27773744
    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. PMID: 29095316
    8. This study demonstrates that Fhit down-regulation is an early event in both multistep carcinogenic processes leading to pancreatic ductal adenocarcinoma PMID: 28289900
    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. PMID: 28093273
    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. PMID: 28639889
    11. The peptide was located within the 'disordered' region, which is invisible in the known crystal structures of Fhit. PMID: 28094435
    12. Both the 3p14.2 locus copy number and FHIT protein expression levels showed significant decreases when CIN transitioned to cervical cancer. PMID: 28414756
    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. PMID: 27572663
    14. High methylation in the FHIT promoter region is associated with lung cancer. PMID: 27716889
    15. the expression profile of miRNAs that may be associated with expression of the FHIT gene in breast cancer, was examined. PMID: 27236032
    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. PMID: 26796853
    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 PMID: 26929601
    18. Low FHIT Gene Expression is associated with Acute Lymphoblastic Leukemia. PMID: 26745060
    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. PMID: 23709347
    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. PMID: 26406001
    21. Review/Meta-analysis: FHIT methylation could be a diagnostic biomarker of breast carcinogenesis. PMID: 26491255
    22. Mutations of the FHIT gene are not major cause of Peutz-Jeghers syndrome. PMID: 27060312
    23. Adenylylsulfate-ammonia adenylyltransferase activity is another inherent property of Fhit proteins. PMID: 26181368
    24. 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. PMID: 25401976
    25. Hypermethylation of FHIT gene is associated with Epstein-Barr virus-associated gastric carcinomas. PMID: 25720522
    26. FHIT promotor hypermethylation is associated with the development of breast cancer. PMID: 25735361
    27. Data indicate that fragile histidine triad protein [FHIT) contributes partially to radioresistance and predicts clinical outcomes in irradiated oral cancer. PMID: 25460508
    28. Fhit nuclear translocation upon mitogenic stimulation may represent a new regulatory mechanism that allows rapid restoration of Fhit cytoplasmic levels and promotes the proliferation cascade activated by mitogenic stimulation PMID: 25711523
    29. Data are consistent with a mechanism in which Fhit protein is required for accumulation of the transcriptional repressor of HMOX1, Bach1 protein. PMID: 25486479
    30. the decrease in the expression of miR-29b by c-Myc may be responsible for FHIT loss-mediated tumor aggressiveness and for poor outcome in non-small cell lung cancer. PMID: 24909176
    31. the induction of Slug expression by AKT/NF-kappaB signaling pathway due to FHIT loss not only promotes tumor invasion, but also confers cisplatin resistance due to Slug-mediated PUMA reduction in lung cancer cells. PMID: 24998847
    32. Patients with FHIT methylation might promote cervical cancer progression. PMID: 25422218
    33. we demonstrate that the expression pattern of FHIT and miR-30c is inversely correlated with that of MTDH and HMGA2 in normal tissue, non-metastatic and metastatic tumors, serving as a potential biomarker for metastasis in lung cancer. PMID: 25340791
    34. The Fhit possesses diadenosine triphosphate hydrolase activity, but although reduction of its enzymatic activity appears to be important for exerting its tumor suppressor function, the regulation of Fhit activity is poorly understood. PMID: 25098403
    35. methylation of FHIT is a useful biomarker of biologically aggressive disease in patients with non-small cell lung carcinomas PMID: 24935385
    36. The total frequency of FHIT, RASSF1A and RARbeta gene methylation was significantly higher in lung cancer. PMID: 25040980
    37. Hypermethylation of FHIT gene promoter region was found more frequent in cancer tissue than controls. PMID: 24667261
    38. FHIT expression can block the PI3K-Akt pathway by suppressing phosphorylation of Akt in cholangiocarcinoma cells. PMID: 24757411
    39. Loss of FHIT function leads to nucleotide imbalance, spontaneous replication stress, and DNA breaks. [review] PMID: 25283145
    40. FHIT loss was observed in 64% of non-small-cell lung carcinoma patients and was significantly associated with squamous cell carcinoma and poor tumor grade. PMID: 24185125
    41. These results showed that Fhit was up-regulated specifically by activating Galpha subunits of the Gq subfamily but not by those of the other G protein subfamilies. PMID: 23993961
    42. The expressions of DAPK1, FHIT, MGMT, and CDKN2A were detected The methylation of the promoter region significantly decreased the expression of only DAPK1 PMID: 23494221
    43. our meta-analysis provides evidences that negative expression of FHIT protein may be correlated with poor prognosis in patients with gastric cancer PMID: 24729090
    44. Fhit delocalizes annexin A4 from plasma membrane to cytosol and sensitizes lung cancer cells to paclitaxel. PMID: 24223161
    45. Results identify a novel member of the miR-548 family in the fourth intron of the human FHIT gene. PMID: 24556720
    46. Data indicate that expression of several predicted chimeric genes and genes with disrupted exon structure including ALK, NBAS, FHIT, PTPRD and ODZ4 in neuroblastoma. PMID: 23991058
    47. Immunohistochemical staining of oral squamous cell carcinoma shows that Fhit negativity is associated with cervical lymph node metastasis and poor disease-specific survival. PMID: 23944951
    48. Our results suggest that loss of Fhit expression in breast cancer is associated with poor prognostic features, and it is also relevant to the results in HER2-negative breast cancer. PMID: 23969757
    49. Reduced expression of FHIT gene is associated with the progression of colon adenocarcinoma. PMID: 24370550
    50. FHIT gene is a "caretaker gene" necessary for maintenance of genome stability. PMID: 23929738

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  • 相关疾病：
    A chromosomal aberration involving FHIT has been found in a lymphoblastoid cell line established from a family with renal cell carcinoma and thyroid carcinoma. Translocation t(3;8)(p14.2;q24.1) with RNF139. Although the 3p14.2 breakpoint has been shown to interrupt FHIT in its 5-prime non-coding region, it is unlikely that FHIT is causally related to renal or other malignancies.
  • 亚细胞定位：
    Cytoplasm. Mitochondrion. Nucleus.
  • 组织特异性：
    Low levels expressed in all tissues tested. Phospho-FHIT observed in liver and kidney, but not in brain and lung. Phospho-FHIT undetected in all tested human tumor cell lines.
  • 数据库链接：

    HGNC: 3701

    OMIM: 601153

    KEGG: hsa:2272

    STRING: 9606.ENSP00000342087

    UniGene: Hs.655995