Mouse Anti-FLT3 Recombinant Antibody (3H1) (CBMAB-A3041-LY)

Basic Information
Formulations & Storage [For reference only, actual COA shall prevail!]
Target
B cell differentiation Source: UniProtKB
Cellular response to cytokine stimulus Source: UniProtKB
Cellular response to glucocorticoid stimulus Source: Ensembl
Common myeloid progenitor cell proliferation Source: UniProtKB
Cytokine-mediated signaling pathway Source: UniProtKB
Dendritic cell differentiation Source: UniProtKB
Hemopoiesis Source: MGI
Leukocyte homeostasis Source: UniProtKB
Lymphocyte proliferation Source: UniProtKB
Myeloid progenitor cell differentiation Source: UniProtKB
Peptidyl-tyrosine phosphorylation Source: UniProtKB
Positive regulation of cell population proliferation Source: UniProtKB
Positive regulation of kinase activity Source: GO_Central
Positive regulation of MAPK cascade Source: UniProtKB
Positive regulation of MAP kinase activity Source: UniProtKB
Positive regulation of phosphatidylinositol 3-kinase activity Source: UniProtKB
Positive regulation of phosphatidylinositol 3-kinase signaling Source: UniProtKB
Positive regulation of tyrosine phosphorylation of STAT protein Source: UniProtKB
Pro-B cell differentiation Source: UniProtKB
Protein autophosphorylation Source: UniProtKB
Regulation of apoptotic process Source: UniProtKB
Response to organonitrogen compound Source: Ensembl
Transmembrane receptor protein tyrosine kinase signaling pathway Source: GO_Central
The gene represented in this entry may be involved in disease pathogenesis. Somatic mutations that lead to constitutive activation of FLT3 are frequent in AML patients. These mutations fall into two classes, the most common being in-frame internal tandem duplications of variable length in the juxtamembrane region that disrupt the normal regulation of the kinase activity. Likewise, point mutations in the activation loop of the kinase domain can result in a constitutively activated kinase.
A subtype of acute leukemia, a cancer of the white blood cells. AML is a malignant disease of bone marrow characterized by maturational arrest of hematopoietic precursors at an early stage of development. Clonal expansion of myeloid blasts occurs in bone marrow, blood, and other tissue. Myelogenous leukemias develop from changes in cells that normally produce neutrophils, basophils, eosinophils and monocytes.
Helical: 544-563
Cytoplasmic: 564-993
Autophosphorylated on several tyrosine residues in response to FLT3LG binding. FLT3LG binding also increases phosphorylation of mutant kinases that are constitutively activated. Dephosphorylated by PTPRJ/DEP-1, PTPN1, PTPN6/SHP-1, and to a lesser degree by PTPN12. Dephosphorylation is important for export from the endoplasmic reticulum and location at the cell membrane.
Rapidly ubiquitinated by UBE2L6 and the E3 ubiquitin-protein ligase SIAH1 after autophosphorylation, leading to its proteasomal degradation.
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Please try the standard protocols which include: protocols, troubleshooting and guide.
Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols
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Custom Antibody Labeling
We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).
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