FLT3 Antibody [H6L24] | Primary Antibodies

Application: Reactivity: Human, Mouse

Lane 1: 293T, Lane 2: 293T (FLT3 transfected)

Usage Information

Dilution
WB1:1000 IP1:100

Application
WB, IP

Reactivity
Human, Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
113 kDa 130 kDa (nonglycosylated);160 kDa (glycosylated)
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
FLT3 Antibody [H6L24] detects endogenous levels of total FLT3 protein.

Clone
H6L24

Synonym(s)
CD135; CD135 antigen; fetal liver kinase 2; Fetal liver kinase-2; FL cytokine receptor; FLK-2; FLK2; FLT-3; FLT3; Stem cell tyrosine kinase 1; STK-1; STK1; Tyrosine-protein kinase receptor FLT3

Background
FLT3 (FMS‑like tyrosine kinase 3, also called FLK2 or CD135) is a class III receptor tyrosine kinase in the c‑Kit/PDGFR family that is expressed on early hematopoietic stem and progenitor cells and functions as a key regulator of their survival, proliferation, and differentiation in response to its cognate cytokine FLT3 ligand. The receptor is a type I transmembrane glycoprotein with an extracellular region containing five immunoglobulin‑like domains that mediate FLT3 ligand binding and receptor dimerization, a single transmembrane helix, a juxtamembrane regulatory segment that restrains kinase activity in the absence of ligand, and a split cytoplasmic tyrosine kinase domain with multiple autophosphorylation sites that serve as docking sites for signaling effectors when the receptor is activated. FLT3 ligand, produced by bone marrow stromal cells and other stromal elements, binds monomeric FLT3 and promotes formation of a ternary complex in which a homodimeric FLT3L bridges two FLT3 molecules, bringing the intracellular kinase domains into proximity, triggering trans‑autophosphorylation within the activation loop and juxtamembrane tyrosines, and creating binding platforms for SH2‑containing adaptor and effector proteins. Activated FLT3 recruits and phosphorylates complexes containing Shc, Grb2, Gab1/2, SHP‑2, SHIP, and CrkL, which link the receptor to RAS–RAF–MEK–ERK signaling for mitogenic responses, to PI3K–AKT–mTOR pathways that promote cell survival and metabolic support, and to JNK and p38 MAPK modules that modulate stress responses, cytokine production, and differentiation outcomes in hematopoietic progenitors. These signaling networks act in synergy with other cytokine receptors such as c‑Kit, GM‑CSF receptor, and interleukin receptors to expand multipotent progenitors, support dendritic cell and NK cell development, and maintain stem and progenitor pools in bone marrow, thymus, and lymphoid organs, with FLT3 ligand alone showing modest proliferative activity but strong cooperative effects in combination with other growth factors. FLT3 expression is normally confined to early progenitors and is downregulated upon maturation, but high‑level expression persists in most acute myeloid leukemia blasts and in a substantial subset of acute lymphoblastic leukemias, providing a platform for oncogenic activation. Somatic FLT3 mutations, particularly internal tandem duplications in the juxtamembrane region and activating point mutations in the kinase domain, are among the most frequent lesions in AML, occurring in roughly one‑third of cases, and lead to ligand‑independent receptor dimerization or relief of juxtamembrane autoinhibition, chronic autophosphorylation, and constitutive activation of STAT5, PI3K–AKT, and RAS–ERK pathways that drive uncontrolled proliferation, survival, and impaired differentiation of myeloid progenitors.

Background

FLT3 (FMS‑like tyrosine kinase 3, also called FLK2 or CD135) is a class III receptor tyrosine kinase in the c‑Kit/PDGFR family that is expressed on early hematopoietic stem and progenitor cells and functions as a key regulator of their survival, proliferation, and differentiation in response to its cognate cytokine FLT3 ligand. The receptor is a type I transmembrane glycoprotein with an extracellular region containing five immunoglobulin‑like domains that mediate FLT3 ligand binding and receptor dimerization, a single transmembrane helix, a juxtamembrane regulatory segment that restrains kinase activity in the absence of ligand, and a split cytoplasmic tyrosine kinase domain with multiple autophosphorylation sites that serve as docking sites for signaling effectors when the receptor is activated. FLT3 ligand, produced by bone marrow stromal cells and other stromal elements, binds monomeric FLT3 and promotes formation of a ternary complex in which a homodimeric FLT3L bridges two FLT3 molecules, bringing the intracellular kinase domains into proximity, triggering trans‑autophosphorylation within the activation loop and juxtamembrane tyrosines, and creating binding platforms for SH2‑containing adaptor and effector proteins. Activated FLT3 recruits and phosphorylates complexes containing Shc, Grb2, Gab1/2, SHP‑2, SHIP, and CrkL, which link the receptor to RAS–RAF–MEK–ERK signaling for mitogenic responses, to PI3K–AKT–mTOR pathways that promote cell survival and metabolic support, and to JNK and p38 MAPK modules that modulate stress responses, cytokine production, and differentiation outcomes in hematopoietic progenitors. These signaling networks act in synergy with other cytokine receptors such as c‑Kit, GM‑CSF receptor, and interleukin receptors to expand multipotent progenitors, support dendritic cell and NK cell development, and maintain stem and progenitor pools in bone marrow, thymus, and lymphoid organs, with FLT3 ligand alone showing modest proliferative activity but strong cooperative effects in combination with other growth factors. FLT3 expression is normally confined to early progenitors and is downregulated upon maturation, but high‑level expression persists in most acute myeloid leukemia blasts and in a substantial subset of acute lymphoblastic leukemias, providing a platform for oncogenic activation. Somatic FLT3 mutations, particularly internal tandem duplications in the juxtamembrane region and activating point mutations in the kinase domain, are among the most frequent lesions in AML, occurring in roughly one‑third of cases, and lead to ligand‑independent receptor dimerization or relief of juxtamembrane autoinhibition, chronic autophosphorylation, and constitutive activation of STAT5, PI3K–AKT, and RAS–ERK pathways that drive uncontrolled proliferation, survival, and impaired differentiation of myeloid progenitors.

References
https://pubmed.ncbi.nlm.nih.gov/12951584/ https://pubmed.ncbi.nlm.nih.gov/12176867/

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%