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HPRT1 Antibody

Purified Mouse Monoclonal Antibody

     
  • 10 - HPRT1 Antibody AO1947a

    Black line: Control Antigen (100 ng);
    Purple line: Antigen(10ng);
    Blue line: Antigen (50 ng);
    Red line: Antigen (100 ng);

  • 1 - HPRT1 Antibody AO1947a
    Figure 1: Western blot analysis using HPRT1 mAb against human HPRT1 (AA: FULL(1-218)) recombinant protein. (Expected MW is 50.5 kDa)
  • 1 - HPRT1 Antibody AO1947a
    Figure 2: Western blot analysis using HPRT1 mAb against HEK293 (1) and HPRT1 (AA: FULL(1-218))-hIgGFc transfected HEK293 (2) cell lysate.
  • 1 - HPRT1 Antibody AO1947a
    Figure 3: Western blot analysis using HPRT1 mouse mAb against Hela (1), A431 (2), A549 (3) cell lysate.
  • 4 - HPRT1 Antibody AO1947a
    Figure 4: Flow cytometric analysis of Hela cells using HPRT1 mouse mAb (green) and negative control (red).
  • 2 - HPRT1 Antibody AO1947a
    Figure 5: Immunohistochemical analysis of paraffin-embedded kidney tissues using HPRT1 mouse mAb with DAB staining.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, IHC, FC, E
Primary Accession P00492
Reactivity Human
Host Mouse
Clonality Monoclonal
Clone Names 5F11A7
Isotype IgG1
Calculated MW 24579 Da
Description The protein encoded by this gene is a transferase, which catalyzes conversion of hypoxanthine to inosine monophosphate and guanine to guanosine monophosphate via transfer of the 5-phosphoribosyl group from 5-phosphoribosyl 1-pyrophosphate. This enzyme plays a central role in the generation of purine nucleotides through the purine salvage pathway. Mutations in this gene result in Lesch-Nyhan syndrome or gout.
Immunogen Purified recombinant fragment of human HPRT1 (AA: FULL(1-218)) expressed in E. Coli.
Formulation Purified antibody in PBS with 0.05% sodium azide.
Additional Information
Gene ID 3251
Other Names Hypoxanthine-guanine phosphoribosyltransferase, HGPRT, HGPRTase, 2.4.2.8, HPRT1, HPRT
Dilution WB~~1/500 - 1/2000
IHC~~1/200 - 1/1000
FC~~1/200 - 1/400
E~~1/10000
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsHPRT1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name HPRT1
Synonyms HPRT
Function Converts guanine to guanosine monophosphate, and hypoxanthine to inosine monophosphate. Transfers the 5-phosphoribosyl group from 5- phosphoribosylpyrophosphate onto the purine. Plays a central role in the generation of purine nucleotides through the purine salvage pathway.
Cellular Location Cytoplasm.
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

C17orf53 (chromosome 17 open reading frame 53) is a 647 amino acid protein that is encoded by a gene mapping to human chromosome 17. Chromosome 17 makes up over 2.5% of the human genome with about 81 million bases encoding over 1,200 genes. Two key tumor suppressor genes are associated with chromosome 17, namely, p53 and BRCA1. Tumor suppressor p53 is necessary for maintenance of cellular genetic integrity by moderating cell fate through DNA repair versus cell death. Malfunction or loss of p53 expression is associated with malignant cell growth and Li-Fraumeni syndrome. Like p53, BRCA1 is directly involved in DNA repair, specifically it is recognized as a genetic determinant of early onset breast cancer and predisposition to cancers of the ovary, colon, prostate gland and fallopian tubes. Chromosome 17 is also linked to neurofibromatosis, a condition characterized by neural and epidermal lesions, and dysregulated Schwann cell growth. Alexander disease, Birt-Hogg-Dube syndrome and Canavan disease are also associated with chromosome 17. ; ;

REFERENCES

1. Nucleosides Nucleotides Nucleic Acids. 2011 Dec;30(12):1248-55.2. Mol Ther. 2010 Jan;18(1):54-62.

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