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CD135 / FLT3 Antibody (Internal)

Rabbit Polyclonal Antibody

     
  • IF - CD135 / FLT3 Antibody (Internal) ALS15658
    Immunofluorescence of FLT3 in human kidney tissue with FLT3 antibody at 20 ug/ml.
  • SPECIFICATION
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Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
WB, IHC-P, IF
Primary Accession P36888
Reactivity Human
Host Rabbit
Clonality Polyclonal
Calculated MW 113kDa
Dilution IHC-P (5 µg/ml), WB (1-2 µg/ml),
Additional Information
Gene ID 2322
Other Names Receptor-type tyrosine-protein kinase FLT3, 2.7.10.1, FL cytokine receptor, Fetal liver kinase-2, FLK-2, Fms-like tyrosine kinase 3, FLT-3, Stem cell tyrosine kinase 1, STK-1, CD135, FLT3, CD135, FLK2, STK1
Target/Specificity Human FLT3 / CD135. At least three isoforms of FLT3 are known to exist; this antibody will detect all isoforms.
Reconstitution & Storage Long term: -20°C; Short term: +4°C. Avoid repeat freeze-thaw cycles.
PrecautionsCD135 / FLT3 Antibody (Internal) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name FLT3
Synonyms CD135, FLK2, STK1
Function Tyrosine-protein kinase that acts as cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways.
Cellular Location Membrane; Single-pass type I membrane protein. Endoplasmic reticulum lumen. Note=Constitutively activated mutant forms with internal tandem duplications are less efficiently transported to the cell surface and a significant proportion is retained in an immature form in the endoplasmic reticulum lumen. The activated kinase is rapidly targeted for degradation
Tissue Location Detected in bone marrow, in hematopoietic stem cells, in myeloid progenitor cells and in granulocyte/macrophage progenitor cells (at protein level). Detected in bone marrow, liver, thymus, spleen and lymph node, and at low levels in kidney and pancreas. Highly expressed in T-cell leukemia
Research Areas
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Background

Tyrosine-protein kinase that acts as cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways.

References

Small D.,et al.Proc. Natl. Acad. Sci. U.S.A. 91:459-463(1994).
Rosnet O.,et al.Blood 82:1110-1119(1993).
Dunham A.,et al.Nature 428:522-528(2004).
Mural R.J.,et al.Submitted (JUL-2005) to the EMBL/GenBank/DDBJ databases.
Rosnet O.,et al.Genomics 9:380-385(1991).

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$ 395.00
Cat# ALS15658
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