FITC标记的FMS样酪氨酸激酶3
产品名称： FITC标记的FMS样酪氨酸激酶3
英文名称： Anti-FLT-3/FITC
产品编号： HZ-2767R-FITC
产品价格： null
产品产地： 中国/上海
品牌商标： HZbscience
更新时间： 2023-08-17T10:24:20
使用范围： IF=1:50-200
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Rabbit Anti-FLT-3/FITC Conjugated antibody
| FITC标记的FMS样酪氨酸激酶3 |
| 英文名称 | Anti-FLT-3/FITC |
| 中文名称 | FITC标记的FMS样酪氨酸激酶3 |
| 别 名 | CD135 antigen; Fetal liver kinase 2; FL cytokine receptor; Flk 2; Flk2; Flt 3; Flt3; FMS like tyrosine kinase 3; Fms related tyrosine kinase 3; Growth factor receptor tyrosine kinase type III; Stem cell tyrosine kinase 1; Stk 1; Stk1; Tyrosine protein kinase receptor FLT3; FLT3_HUMAN. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 研究领域 | 激酶和磷酸酶 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Mouse, Rat, Dog, Cow, Horse, Rabbit, |
| 产品应用 | IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 109kDa |
| 细胞定位 | 细胞膜 |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human FLT-3 |
| 亚 型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 储 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存条件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| 产品介绍 | 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. 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. Subunit: Monomer in the absence of bound FLT3LG. Homodimer in the presence of bound FLT3LG. One homodimer interacts with one FLT3LG molecule. Interacts with FIZ1 following ligand activation (By similarity). Interacts with FES, FER and GRB2. Interacts with PTPRJ/DEP-1 and PTPN11/SHP2. Subcellular Location: Membrane; Single-pass type I membrane protein. Endoplasmic reticulum lumen. 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. Post-translational modifications: N-glycosylated, contains complex N-glycans with sialic acid. 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. DISEASE: Defects in FLT3 are a cause of acute myelogenous leukemia (AML) [MIM:601626]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development. Note=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. Similarity: 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. Database links: Entrez Gene: 2322 Human Entrez Gene: 14255 Mouse Entrez Gene: 140635 Rat Omim: 136351 Human SwissProt: P36888 Human SwissProt: Q00342 Mouse Unigene: 507590 Human Unigene: 194 Mouse Unigene: 6774 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications |
酪氨酸蛋白激酶作为细胞因子FLT3LG的细胞表面受体，调节造血祖细胞和树突状细胞的分化、增殖和存活。促进SHC1和Akt1的磷酸化，并激活下游效应分子mTOR。促进RAS信号转导和下游激酶磷酸化，包括MAPK1/ERK2和/或MAPK3/ERK1。促进FES、FER、PTPN6/SHP、PTPN11/SMP-2、PLCG1和STAT5A和/或STAT5B的磷酸化。野生型FLT3的激活仅导致STAT5A或STAT5B的边缘激活。多种信号通路的研究。