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AB190998

重组人ALK + EML4蛋白

Recombinant human ALK + EML4 protein

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Recombinant human ALK + EML4 protein is a Human Fragment protein, in the 1 to 496 aa range, expressed in Baculovirus infected Sf9 cells, with >70%, suitable for SDS-PAGE, FuncS.

查看别名

CD246, ALK tyrosine kinase receptor, Anaplastic lymphoma kinase, ALK

4 Images
Functional Studies - Recombinant human ALK + EML4 protein (AB190998)
  • FuncS

Unknown

Functional Studies - Recombinant human ALK + EML4 protein (AB190998)

The specific activity of ALK+EML4 (ab190998) was determined to be 1.9 nmol/min/mg as per activity assay protocol and was equivalent to 5 nmol/min/mg as per radiometric assay

Functional Studies - Recombinant human ALK + EML4 protein (AB190998)
  • FuncS

Supplier Data

Functional Studies - Recombinant human ALK + EML4 protein (AB190998)

Kinase Assay : The specific activity of ab190998 was determined to be 4.8 nmol /min/mg.

SDS-PAGE - Recombinant human ALK + EML4 protein (AB190998)
  • SDS-PAGE

Unknown

SDS-PAGE - Recombinant human ALK + EML4 protein (AB190998)

SDS PAGE analysis of ab190998

SDS-PAGE - Recombinant human ALK + EML4 protein (AB190998)
  • SDS-PAGE

Supplier Data

SDS-PAGE - Recombinant human ALK + EML4 protein (AB190998)

SDS-PAGE analysis of ab190998.

关键信息

纯度

>70% Densitometry

表达系统

Baculovirus infected Sf9 cells

标签

Tag free

应用

SDS-PAGE, FuncS

applications

生物活性

Yes

生物学活性

Specific activity is lot specific. Please contact our Scientific Support team for more information.

访问

Q9UM73

不含动物源

No

不含载体蛋白

No

种属

Human

存储溶液

pH: 7.5 Preservative: 1.02% Imidazole Constituents: 25% Glycerol (glycerin, glycerine), 1.74% Sodium chloride, 0.82% Sodium phosphate, 0.00385% (R*,R*)-1,4-Dimercaptobutan-2,3-diol, 0.002% PMSF

storage-buffer

反应性数据

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" }, "FuncS": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }

序列信息

[{"linker":null,"sequence":"","proteinLength":"Fragment","predictedMolecularWeight":"150 kDa","actualMolecularWeight":null,"aminoAcidEnd":496,"aminoAcidStart":1,"nature":"Recombinant","expressionSystem":null,"accessionNumber":"Q9HC35","tags":[{"tag":"GST","terminus":"N-Terminus"}]},{"linker":null,"sequence":"","proteinLength":"Fragment","predictedMolecularWeight":null,"actualMolecularWeight":null,"aminoAcidEnd":1620,"aminoAcidStart":1058,"nature":"Recombinant","expressionSystem":null,"accessionNumber":"Q9UM73","tags":[]}]

性能和储存信息

运输条件
Dry Ice
推荐的短期储存条件
-80°C
推荐的长期储存条件
-80°C
分装信息
Upon delivery aliquot
储存信息
Avoid freeze / thaw cycle
True

补充信息

This supplementary information is collated from multiple sources and compiled automatically.

The ALK EML4 fusion also referred to as EML4-ALK or ALK EML4 is a fusion protein resulting from a chromosomal rearrangement between the genes encoding ALK (anaplastic lymphoma kinase) and EML4 (echinoderm microtubule-associated protein-like 4). This rearrangement generates a fusion gene that translates into a fusion protein commonly found in certain cancers. This protein retains the enzymatic activity of ALK allowing it to act as an aberrant tyrosine kinase. The mass of the EML4-ALK fusion protein typically varies depending on the exact breakpoints involved but it is widely expressed in the cells of lung adenocarcinoma.
Biological function summary

The EML4-ALK fusion protein functions as an oncoprotein promoting uncontrolled cell proliferation and survival. It is not necessarily part of a complex but acts within signaling networks due to its kinase activity. By phosphorylating downstream substrates the EML4-ALK fusion disrupts normal cellular signaling enabling cancerous characteristics in affected cells. Its aberrant activation of signaling pathways can lead to sustained oncogenic signaling bypassing normal growth factor receptor regulation.

Pathways

ALK EML4 fusion interacts within key pathways like the PI3K/AKT and MAPK signaling cascades. These pathways are critical for cell growth survival and metabolism and the presence of EML4-ALK fusion causes constitutive activation promoting oncogenesis. The protein often impacts other signaling proteins such as mTOR and ERK which are downstream effectors within these pathways leading to enhanced cell proliferation and resistance to apoptosis.

The EML4-ALK fusion has a strong connection with non-small cell lung cancer (NSCLC) particularly in patients who are non-smokers or young. It also appears in anaplastic large cell lymphoma (ALCL). Within these conditions the abnormal activity of the fusion protein drives oncogenic processes making it a target for specific therapies like ALK inhibitors. The EML4-ALK fusion-associated cancers sometimes show resistance or less efficacy to standard chemotherapy highlighting the need for targeted approaches in its management.

特殊说明

形式

Liquid

附加说明

Affinity purified.

常规信息

功能

Neuronal 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 (PubMed : 11121404, PubMed : 11387242, PubMed : 16317043, PubMed : 17274988, PubMed : 30061385, PubMed : 34646012, PubMed : 34819673). Also acts as a key thinness protein involved in the resistance to weight gain : in hypothalamic neurons, controls energy expenditure acting as a negative regulator of white adipose tissue lipolysis and sympathetic tone to fine-tune energy homeostasis (By similarity). Following activation by ALKAL2 ligand at the cell surface, transduces an extracellular signal into an intracellular response (PubMed : 30061385, PubMed : 33411331, PubMed : 34646012, PubMed : 34819673). In contrast, ALKAL1 is not a potent physiological ligand for ALK (PubMed : 34646012). Ligand-binding to the extracellular domain induces tyrosine kinase activation, leading to activation of the mitogen-activated protein kinase (MAPK) pathway (PubMed : 34819673). Phosphorylates almost exclusively at the first tyrosine of the Y-x-x-x-Y-Y motif (PubMed : 15226403, PubMed : 16878150). Induces tyrosine phosphorylation of CBL, FRS2, IRS1 and SHC1, as well as of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1 (PubMed : 15226403, PubMed : 16878150). ALK activation may also be regulated by pleiotrophin (PTN) and midkine (MDK) (PubMed : 11278720, PubMed : 11809760, PubMed : 12107166, PubMed : 12122009). PTN-binding induces MAPK pathway activation, which is important for the anti-apoptotic signaling of PTN and regulation of cell proliferation (PubMed : 11278720, PubMed : 11809760, PubMed : 12107166). MDK-binding induces phosphorylation of the ALK target insulin receptor substrate (IRS1), activates mitogen-activated protein kinases (MAPKs) and PI3-kinase, resulting also in cell proliferation induction (PubMed : 12122009). Drives NF-kappa-B activation, probably through IRS1 and the activation of the AKT serine/threonine kinase (PubMed : 15226403, PubMed : 16878150). Recruitment of IRS1 to activated ALK and the activation of NF-kappa-B are essential for the autocrine growth and survival signaling of MDK (PubMed : 15226403, PubMed : 16878150). May function as regulator of gastric epithelial differentiation (By similarity).

序列相似性

Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily.

翻译后修饰

Phosphorylated at tyrosine residues by autocatalysis, which activates kinase activity (PubMed:11121404, PubMed:15938644, PubMed:16878150, PubMed:34819673). 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 (PubMed:17681947). Phosphorylation at Tyr-1507 is critical for SHC1 association (PubMed:17274988).. N-glycosylated.

产品实验方案

靶点信息

Neuronal 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 (PubMed : 11121404, PubMed : 11387242, PubMed : 16317043, PubMed : 17274988, PubMed : 30061385, PubMed : 34646012, PubMed : 34819673). Also acts as a key thinness protein involved in the resistance to weight gain : in hypothalamic neurons, controls energy expenditure acting as a negative regulator of white adipose tissue lipolysis and sympathetic tone to fine-tune energy homeostasis (By similarity). Following activation by ALKAL2 ligand at the cell surface, transduces an extracellular signal into an intracellular response (PubMed : 30061385, PubMed : 33411331, PubMed : 34646012, PubMed : 34819673). In contrast, ALKAL1 is not a potent physiological ligand for ALK (PubMed : 34646012). Ligand-binding to the extracellular domain induces tyrosine kinase activation, leading to activation of the mitogen-activated protein kinase (MAPK) pathway (PubMed : 34819673). Phosphorylates almost exclusively at the first tyrosine of the Y-x-x-x-Y-Y motif (PubMed : 15226403, PubMed : 16878150). Induces tyrosine phosphorylation of CBL, FRS2, IRS1 and SHC1, as well as of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1 (PubMed : 15226403, PubMed : 16878150). ALK activation may also be regulated by pleiotrophin (PTN) and midkine (MDK) (PubMed : 11278720, PubMed : 11809760, PubMed : 12107166, PubMed : 12122009). PTN-binding induces MAPK pathway activation, which is important for the anti-apoptotic signaling of PTN and regulation of cell proliferation (PubMed : 11278720, PubMed : 11809760, PubMed : 12107166). MDK-binding induces phosphorylation of the ALK target insulin receptor substrate (IRS1), activates mitogen-activated protein kinases (MAPKs) and PI3-kinase, resulting also in cell proliferation induction (PubMed : 12122009). Drives NF-kappa-B activation, probably through IRS1 and the activation of the AKT serine/threonine kinase (PubMed : 15226403, PubMed : 16878150). Recruitment of IRS1 to activated ALK and the activation of NF-kappa-B are essential for the autocrine growth and survival signaling of MDK (PubMed : 15226403, PubMed : 16878150). May function as regulator of gastric epithelial differentiation (By similarity).
See full target information ALK

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