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KHDRBS2 Antibody

Purified Mouse Monoclonal Antibody

     
  • 10 - KHDRBS2 Antibody AO1934a

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

  • 1 - KHDRBS2 Antibody AO1934a
    Figure 1: Western blot analysis using KHDRBS2 mAb against human KHDRBS2 (AA: 160-349) recombinant protein. (Expected MW is 46.3 kDa)
  • 1 - KHDRBS2 Antibody AO1934a
    Figure 2: Western blot analysis using KHDRBS2 mouse mAb against K562 (1), HEK293 (2), NTERA-2 (3), Hela (4), HepG2 (5), Jurkat (6), A431 (7), NIH/3T3 (8) cell lysate.
  • 4 - KHDRBS2 Antibody AO1934a
    Figure 3: Flow cytometric analysis of K562 cells using KHDRBS2 mouse mAb (green) and negative control (red).
  • 2 - KHDRBS2 Antibody AO1934a
    Figure 4: Immunohistochemical analysis of paraffin-embedded cervical cancer tissues using KHDRBS2 mouse mAb with DAB staining.
  • 2 - KHDRBS2 Antibody AO1934a
    Figure 5: Immunohistochemical analysis of paraffin-embedded colon cancer tissues using KHDRBS2 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 Q5VWX1
Reactivity Human, Mouse
Host Mouse
Clonality Monoclonal
Clone Names 7G8C10
Isotype IgG1
Calculated MW 38927 Da
Description RNA-binding protein that plays a role in the regulation of alternative splicing and influences mRNA splice site selection and exon inclusion. Its phosphorylation by FYN inhibits its ability to regulate splice site selection. Induces an increased concentration-dependent incorporation of exon in CD44 pre-mRNA by direct binding to purine-rich exonic enhancer. May function as an adapter protein for Src kinases during mitosis. Binds both poly(A) and poly(U) homopolymers. Phosphorylation by PTK6 inhibits its RNA-binding ability (By similarity)
Immunogen Purified recombinant fragment of human KHDRBS2 (AA: 160-349) expressed in E. Coli.
Formulation Purified antibody in PBS with 0.05% sodium azide.
Additional Information
Gene ID 202559
Other Names KH domain-containing, RNA-binding, signal transduction-associated protein 2, Sam68-like mammalian protein 1, SLM-1, hSLM-1, KHDRBS2, SLM1
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.
PrecautionsKHDRBS2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name KHDRBS2
Synonyms SLM1
Function RNA-binding protein that plays a role in the regulation of alternative splicing and influences mRNA splice site selection and exon inclusion. Binds both poly(A) and poly(U) homopolymers. Phosphorylation by PTK6 inhibits its RNA-binding ability (By similarity). Induces an increased concentration-dependent incorporation of exon in CD44 pre- mRNA by direct binding to purine-rich exonic enhancer. Can regulate alternative splicing of NRXN1 in the laminin G-like domain 6 containing the evolutionary conserved neurexin alternative spliced segment 4 (AS4) involved in neurexin selective targeting to postsynaptic partners. Regulates cell-type specific alternative splicing of NRXN1 at AS4 and acts synergystically with SAM68 in exon skipping. In contrast acts antagonistically with SAM68 in NRXN3 exon skipping at AS4. Its phosphorylation by FYN inhibits its ability to regulate splice site selection. May function as an adapter protein for Src kinases during mitosis.
Cellular Location Nucleus {ECO:0000250|UniProtKB:Q9WU01}.
Tissue Location Highly expressed in brain, lung, kidney and small intestine. Weakly expressed in placenta, liver, spleen, thymus, ovary and colon.
Research Areas

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

REFERENCES

1. Mol Biol Cell. 2003 Jan;14(1):274-87. 2.

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