antibody

Mouse Anti-Human Flt-3 Ligand

MBS690558

0.1 mg

475 USD

monoclonal

mouse

nonconjugated

(9G23)

western blot, neutralization

Antibody

Mouse Anti-Human Flt-3 Ligand

Flt-3 Ligand

FLT3LG; FL; FLT3L

receptor-type tyrosine-protein kinase FLT3; Receptor-type tyrosine-protein kinase FLT3; receptor-type tyrosine-protein kinase FLT3; STK-1; CD135 antigen; FL cytokine receptor; fetal liver kinase 2; fms-like tyrosine kinase 3; stem cell tyrosine kinase 1; growth factor receptor tyrosine kinase type III; fms-related tyrosine kinase 3; FL cytokine receptor; Fetal liver kinase-2; FLK-2; Fms-like tyrosine kinase 3; FLT-3; Stem cell tyrosine kinase 1

Flt-3 Ligand

FLT3; FLT3; FLK2; STK1; CD135; FLK-2; CD135; FLK2; STK1; FLK-2; FLT-3; STK-1

FLT3_HUMAN

Monoclonal

IgG1

(9G23)

Mouse

Human

993

Protein G chromatography

Lyophilized

Lyophilized samples are stable for 2 years from date of receipt when stored at -70 degree C. Reconstituted antibody can be aliquoted and stored frozen at < -20 degree C for at least for six months without detectable loss of activity.

Western Blot (WB), Neutralization

Western Blot: 1:500-1:1000. Neutralization of Flt3-L bioactivity: Yes

Antibody Generation: This antibody was produced from a hybridoma (mouse myeloma fused with spleen cells from a mouse) immunized with human recombinant protein of Flt-3 ligand. Antigen: Recombinant human Flt-3 ligand. Reconstitution buffer: PBS (Sterile). mRNA RefSeq: NM_004119

Reconstitution: Reconstitute the antibody with 200 ul sterile PBS and the final concentration is 500 ug/ml. Remarks: This antibody was selected for its ability to detect human Flt-3 Ligand.

Flt-3 Ligand, also known as FL, is an alpha-helical cytokine that promotes the differentiation of multiple hematopoietic cell lineages. Mature human Flt-3 Ligand consists of a 158 amino acid (aa) extracellular domain (ECD) with a cytokine-like domain and a juxtamembrane region, a 21 aa transmembrane segment, and a 30 aa cytoplasmic tail. Within the ECD, human Flt-3 Ligand shares 71% and 65% aa sequence identity with mouse and rat Flt-3 Ligand, respectively. Human and mouse Flt-3 Ligand show cross-species activity. Flt-3 Ligand is expressed as a non-covalentlylinked dimer by T cells and bone marrow and thymic fibroblasts. Each 36 kDa chain carries approximately 12 kDa of N- and O-linked carbohydrates. Alternate splicing and proteolytic cleavage of the transmembrane form can generate a soluble 30 kDa fragment that includes the cytokine domain. Alternate splicing of human Flt -3 Ligand also generates membraneassociated isoforms that contain either a truncated cytoplasmic tail or an 85 aa substitution following the cytokine domain. Both transmembrane and soluble Flt-3 Ligand signal through the tyrosine kinase receptor Flt3/ FlK-1. Flt-3 Ligand induces the expansion of monocytes and immature dendritic cells as well as early B cell lineage differentiation.

121114304

NP_004110.2

NM_004119.2

P36888

112,903 Da

Acute Myeloid Leukemia Pathway (83117); Acute Myeloid Leukemia Pathway (529); Cytokine-cytokine Receptor Interaction Pathway (83051); Cytokine-cytokine Receptor Interaction Pathway (460); Hematopoietic Cell Lineage Pathway (83078); Hematopoietic Cell Lineage Pathway (489); Pathways In Cancer (83105); Transcriptional Misregulation In Cancer Pathway (523016); Transcriptional Misregulation In Cancer Pathway (522987)

This gene encodes a class III receptor tyrosine kinase that regulates hematopoiesis. The receptor consists of an extracellular domain composed of five immunoglobulin-like domains, one transmembrane region, and a cytoplasmic kinase domain split into two parts by a kinase-insert domain. The receptor is activated by binding of the fms-related tyrosine kinase 3 ligand to the extracellular domain, which induces homodimer formation in the plasma membrane leading to autophosphorylation of the receptor. The activated receptor kinase subsequently phosphorylates and activates multiple cytoplasmic effector molecules in pathways involved in apoptosis, proliferation, and differentiation of hematopoietic cells in bone marrow. Mutations that result in the constitutive activation of this receptor result in acute myeloid leukemia and acute lymphoblastic leukemia. [provided by RefSeq, Jul 2008]

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. Ref.1 Ref.10 Ref.11 Ref.12 Ref.14 Ref.17 Ref.20 Ref.22 Ref.23 Ref.24 Ref.31. Catalytic activity: ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate. Ref.13. Enzyme regulation: Present in an inactive conformation in the absence of bound ligand. FLT3LG binding leads to dimerization and activation by autophosphorylation. Ref.24 Ref.27. Subunit structure: Monomer in the absence of bound FLT3LG. Homodimer in the presence of bound FLT3LG. Interacts with FIZ1 following ligand activation . By similarity. Interacts with FES, FER, LYN, FGR, HCK, SRC and GRB2. Interacts with PTPRJ/DEP-1 and PTPN11/SHP2. Ref.9 Ref.10 Ref.15 Ref.20 Ref.23 Ref.28. Subcellular 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. Ref.7 Ref.13 Ref.17. Tissue specificity: 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. Ref.1 Ref.2 Ref.7 Ref.17. Domain: The juxtamembrane autoregulatory region is important for normal regulation of the kinase activity and for maintaining the kinase in an inactive state in the absence of bound ligand. Upon tyrosine phosphorylation, it mediates interaction with the SH2 domains of numerous signaling partners. In-frame internal tandem duplications (ITDs) result in constitutive activation of the kinase. The activity of the mutant kinase can be stimulated further by FLT3LG binding. Ref.16. Post-translational modification: N-glycosylated, contains complex N-glycans with sialic acid. Ref.13 Ref.23 Ref.28Autophosphorylated 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. Ref.9 Ref.10 Ref.11 Ref.13 Ref.14 Ref.15 Ref.18 Ref.23 Ref.30 Ref.31Rapidly ubiquitinated by UBE2L6 and the E3 ubiquitin-protein ligase SIAH1 after autophosphorylation, leading to its proteasomal degradation. Involvement in disease: Leukemia, acute myelogenous (AML) [MIM:601626]: 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.Note: 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. Ref.8 Ref.9 Ref.11 Ref.12 Ref.16 Ref.29 Ref.30 Ref.31. Miscellaneous: Can be used as diagnostic tool to establish the exact cause of acute myeloid leukemia, and to determine the optimal therapy. Sequence similarities: Belongs to the protein kinase superfamily. Tyr protein kinase family. CSF-1/PDGF receptor subfamily.Contains 1 Ig-like C2-type (immunoglobulin-like) domain.Contains 1 protein kinase domain.

0.1 mg

475 USD