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人 FLT3 抗体对
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人 FLT3 抗体对

01AB00816

Fms related receptor tyrosine kinase 3 (FLT3) is a class III receptor tyrosine kinase that plays a crucial role in hematopoiesis. The 993-amino acid human FLT3 protein consists of an extracellular domain with five immunoglobulin-like domains, a transmembrane domain, a juxtamembrane domain, and a tyrosine kinase domain. FLT3 is activated by binding its ligand, FLT3L, leading to receptor dimerization and autophosphorylation, which triggers downstream signaling pathways controlling cell proliferation, differentiation, and survival of hematopoietic progenitor cells. Mutations in the FLT3 gene, particularly internal tandem duplications (ITD) in the juxtamembrane domain and point mutations in the tyrosine kinase domain, are frequently found in acute myeloid leukemia (AML). These mutations result in constitutive activation of FLT3, promoting uncontrolled proliferation of leukemic cells and conferring a poor prognosis in AML patients.

Human
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技术参数

靶点基因名
FLT3
基因别名
CD135; FLK2; STK1
蛋白别名
fms related receptor tyrosine kinase 3; FLT3
UniProt
P36888
物种
Human

产品详情

靶点名称
FLT3
蛋白名称
fms related receptor tyrosine kinase 3
蛋白别名
Receptor-type tyrosine-protein kinase FLT3; FL cytokine receptor; Fetal liver kinase-2; FLK-2; Fms-like tyrosine kinase 3; FLT-3; Stem cell tyrosine kinase 1; STK-1; CD antigen CD135
靶点基因名
FLT3
基因别名
CD135; FLK2; STK1
UniProt
P36888
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Fms related receptor tyrosine kinase 3 (FLT3) is a class III receptor tyrosine kinase that plays a crucial role in hematopoiesis. The 993-amino acid human FLT3 protein consists of an extracellular domain with five immunoglobulin-like domains, a transmembrane domain, a juxtamembrane domain, and a tyrosine kinase domain. FLT3 is activated by binding its ligand, FLT3L, leading to receptor dimerization and autophosphorylation, which triggers downstream signaling pathways controlling cell proliferation, differentiation, and survival of hematopoietic progenitor cells. Mutations in the FLT3 gene, particularly internal tandem duplications (ITD) in the juxtamembrane domain and point mutations in the tyrosine kinase domain, are frequently found in acute myeloid leukemia (AML). These mutations result in constitutive activation of FLT3, promoting uncontrolled proliferation of leukemic cells and conferring a poor prognosis in AML patients.