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Rabbit Anti-ALK  antibody (bs-0097R)
~~~促銷代碼KT202410~~~
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產(chǎn)品編號 bs-0097R
英文名稱 Rabbit Anti-ALK  antibody
中文名稱 間變型淋巴瘤激酶抗體
別    名 ALK tyrosine kinase receptor; ALK tyrosine kinase receptor precursor; ALK/EML4 fusion gene, included; ALK/NPM1 fusion gene, included; anaplastic lymphoma kinase (Ki-1); Anaplastic lymphoma kinase; Anaplastic lymphoma kinase Ki 1; Anaplastic lymphoma kinase Ki1; Anaplastic lymphoma kinase p80; CD 246; CD246; CD-246; CD246 antigen; EC 2.7.10.1; Ki 1; Ki1; NBLST3; Tcrz; TFG/ALK.   
研究領(lǐng)域 免疫學  神經(jīng)生物學  信號轉(zhuǎn)導  生長因子和激素  轉(zhuǎn)錄調(diào)節(jié)因子  激酶和磷酸酶  b-淋巴細胞  腫瘤細胞生物標志物  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) Human (predicted: Mouse,Rat,Cow,Dog,Horse)
產(chǎn)品應(yīng)用 IHC-P=1:100-500,IHC-F=1:100-500,Flow-Cyt=1μg /test,IF=1:100-500,ELISA=1:5000-10000
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
理論分子量 174kDa
細胞定位 細胞膜 
性    狀 Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human CD246: 329-342/1620 <Extracellular>
亞    型 IgG
純化方法 affinity purified by Protein A
緩 沖 液 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
保存條件 Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.
注意事項 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed PubMed
產(chǎn)品介紹 This gene encodes a receptor tyrosine kinase, which belongs to the insulin receptor superfamily. This protein comprises an extracellular domain, an hydrophobic stretch corresponding to a single pass transmembrane region, and an intracellular kinase domain. It plays an important role in the development of the brain and exerts its effects on specific neurons in the nervous system. This gene has been found to be rearranged, mutated, or amplified in a series of tumours including anaplastic large cell lymphomas, neuroblastoma, and non-small cell lung cancer. The chromosomal rearrangements are the most common genetic alterations in this gene, which result in creation of multiple fusion genes in tumourigenesis, including ALK (chromosome 2)/EML4 (chromosome 2), ALK/RANBP2 (chromosome 2), ALK/ATIC (chromosome 2), ALK/TFG (chromosome 3), ALK/NPM1 (chromosome 5), ALK/SQSTM1 (chromosome 5), LK/KIF5B (chromosome 10), ALK/CLTC (chromosome 17), ALK/TPM4 (chromosome 19), and ALK/MSN (chromosome X).[provided by RefSeq, Jan 2011].

Function:
Neuronal orphan receptor tyrosine kinase that is essentially and transiently expressed in specific regions of the central and peripheral nervous systems and plays an important role in the genesis and differentiation of the nervous system. Transduces signals from ligands at the cell surface, through specific activation of the mitogen-activated protein kinase (MAPK) pathway. Phosphorylates almost exclusively at the first tyrosine of the Y-x-x-x-Y-Y motif. Following activation by ligand, ALK induces tyrosine phosphorylation of CBL, FRS2, IRS1 and SHC1, as well as of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1. Acts as a receptor for ligands pleiotrophin (PTN), a secreted growth factor, and midkine (MDK), a PTN-related factor, thus participating in PTN and MDK signal transduction.

Subunit:
Homodimer. Homodimerizes when bound to ligand. Interacts with FRS2, IRS1, MDK, PTN and SHC1. Interacts with CBL, PIK3R1 and PLCG1.

Subcellular Location:
Cell membrane; Single-pass type I membrane protein. Note=Membrane attachment was crucial for promotion of neuron-like differentiation and cell proliferation arrest through specific activation of the MAP kinase pathway.

Tissue Specificity:
Expressed in brain and CNS. Also expressed in the small intestine and testis, but not in normal lymphoid cells.

Post-translational modifications:
Phosphorylated at tyrosine residues by autocatalysis, which activates kinase activity. In cells not stimulated by a ligand, receptor protein tyrosine phosphatase beta and zeta complex (PTPRB/PTPRZ1) dephosphorylates ALK at the sites in ALK that are undergoing autophosphorylation through autoactivation.
N-glycosylated.

DISEASE:
Note=A chromosomal aberration involving ALK is found in a form of non-Hodgkin lymphoma. Translocation t(2;5)(p23;q35) with NPM1. The resulting chimeric NPM1-ALK protein homodimerize and the kinase becomes constitutively activated. The constitutively active fusion proteins are responsible for 5-10% of non-Hodgkin
Note=A chromosomal aberration involving ALK is associated with inflammatory myofibroblastic tumors (IMTs). Translocation t(2;11)(p23;p15) with CARS; translocation t(2;4)(p23;q21) with SEC31A.

Similarity:
Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily.
Contains 1 LDL-receptor class A domain.
Contains 2 MAM domains.
Contains 1 protein kinase domain.

SWISS:
Q9UM73

Gene ID:
238

Database links:

Entrez Gene: 238 Human

Entrez Gene: 11682 Mouse

Entrez Gene: 266802 Rat

Omim: 105590 Human

SwissProt: Q9UM73 Human

SwissProt: P97793 Mouse

Unigene: 654469 Human

Unigene: 311854 Mouse

Unigene: 201918 Rat




ALK蛋白在細胞生長調(diào)控中起重要作用,主要表達在神經(jīng)細胞,白細胞癌基因蛋白。
ALK p80是多向性生長因子酪氨酸激酶受體蛋白, 間變性大細胞淋巴瘤伴有t(2;5) (p23;q35)染色體的易位,易位后的細胞基因表達分子量為80kD,常伴有CD30陽性,ALK p80陽性的間變性大細胞淋巴瘤預后好于陰性病例。
主要用于間變性大細胞淋巴瘤與何杰金氏淋巴瘤的鑒別診斷,間變性大細胞淋巴瘤中陽性率大約為70%左右,還可以用于骨髓中間變性大細胞淋巴瘤的診斷.
產(chǎn)品圖片
Blank control: Jurkat cells(blue). Primary Antibody:Rabbit Anti-ALK antibody(bs-0097R), Dilution: 1μg in 100 μL 1X PBS containing 0.5% BSA; Isotype Control Antibody: Rabbit IgG(orange) ,used under the same conditions ); Secondary Antibody: Goat anti-rabbit IgG-PE(white blue), Dilution: 1:200 in 1 X PBS containing 0.5% BSA. Protocol The cells were fixed with 2% paraformaldehyde (10 min) . Primary antibody (bs-0097R, 1μg /1x10^6 cells) were incubated for 30 min on the ice, followed by 1 X PBS containing 0.5% BSA + 1 0% goat serum (15 min) to block non-specific protein-protein interactions. Then the Goat Anti-rabbit IgG/PE antibody was added into the blocking buffer mentioned above to react with the primary antibody at 1/200 dilution for 30 min on ice. Acquisition of 20,000 events was performed.
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