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Mouse ALK Protein 3269

$255.00$850.00

Summary

  • Expression: HEK293
  • Pure: Yes (HPLC)
  • Amino Acid Range: Ser19-Cys692
SKU: 3269parent Categories: , Tag:
Weight1 lbs
Dimensions9 × 5 × 2 in
accession

P97793

express system

HEK293

product tag

C-hFc

purity

> 95% as determined by Tris-Bis PAGE;> 95% as determined by HPLC

background

Anaplastic lymphoma kinase (ALK) is mostly known for its oncogenic role in several human cancers. Recent evidences clearly indicate new roles of ALK and its genetic aberrations (e.g. gene rearrangements and mutations) in immune evasion, innate and cell-mediated immunity. New ALK-related immunotherapy approaches are demonstrating both preclinical and clinical promises.

molecular weight

The protein has a predicted MW of 101.11 kDa. Due to glycosylation, the protein migrates to 115-125 kDa based on Tris-Bis PAGE result.

available size

100 µg, 500 µg

endotoxin

Less than 1EU per μg by the LAL method.

Mouse ALK Protein 3269

protein
Size and concentration
100, 500µg and liquid
Form
Liquid
Storage Instructions
Valid for 12 months from date of receipt when stored at -80°C. Recommend to aliquot the protein into smaller quantities for optimal storage. Please minimize freeze-thaw cycles.
Storage buffer
Shipped with dry ice.
Purity
> 95% as determined by Tris-Bis PAGE
target relevance
Anaplastic lymphoma kinase (ALK) is mostly known for its oncogenic role in several human cancers. Recent evidences clearly indicate new roles of ALK and its genetic aberrations (e.g. gene rearrangements and mutations) in immune evasion, innate and cell-mediated immunity. New ALK-related immunotherapy approaches are demonstrating both preclinical and clinical promises.
Protein names
ALK tyrosine kinase receptor (EC 2.7.10.1) (Anaplastic lymphoma kinase) (CD antigen CD246)
Gene names
Alk,Alk
Protein family
Protein kinase superfamily, Tyr protein kinase family, Insulin receptor subfamily
Mass
10090Da
Function
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:15226403, PubMed:16458083, PubMed:16878150, PubMed:19200234, PubMed:30497772). 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 (PubMed:32442405). Following activation by ALKAL2 ligand at the cell surface, transduces an extracellular signal into an intracellular response. In contrast, ALKAL1 is not a potent physiological ligand for ALK. Ligand-binding to the extracellular domain induces tyrosine kinase activation, leading to 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. Induces tyrosine phosphorylation of CBL, FRS2, IRS1 and SHC1, as well as of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1. ALK activation may also be regulated by pleiotrophin (PTN) and midkine (MDK). PTN-binding induces MAPK pathway activation, which is important for the anti-apoptotic signaling of PTN and regulation of cell proliferation. 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. Drives NF-kappa-B activation, probably through IRS1 and the activation of the AKT serine/threonine kinase. Recruitment of IRS1 to activated ALK and the activation of NF-kappa-B are essential for the autocrine growth and survival signaling of MDK (By similarity).
Catalytic activity
BINDING 1126..1134; /ligand="ATP"; /ligand_id="ChEBI:CHEBI:30616"; /evidence="ECO:0000255|PROSITE-ProRule:PRU00159"; BINDING 1128; /ligand="ATP"; /ligand_id="ChEBI:CHEBI:30616"; /evidence="ECO:0000255|PROSITE-ProRule:PRU00159"; BINDING 1154; /ligand="ATP"; /ligand_id="ChEBI:CHEBI:30616"; /evidence="ECO:0000255|PROSITE-ProRule:PRU00159"; BINDING 1201..1203; /ligand="ATP"; /ligand_id="ChEBI:CHEBI:30616"; /evidence="ECO:0000255|PROSITE-ProRule:PRU00159"; BINDING 1274; /ligand="ATP"; /ligand_id="ChEBI:CHEBI:30616"; /evidence="ECO:0000255|PROSITE-ProRule:PRU00159"
Subellular location
Cell membrane ; Single-pass type I membrane protein. Note=Membrane attachment is essential for promotion of neuron-like differentiation and cell proliferation arrest through specific activation of the MAP kinase pathway.
Tissues
Mainly expressed in central nervous system (CNS) and other parts of the brain such as the paraventricular nucleus (PVN) of the hypothalamus. Expression is also found in peripheral nervous systems, eye, nasal epithelium, olfactory nerve, tongue, skin, tissue surrounding the esophagus, stomach, midgut, as well as testis and ovary.
Structure
Homodimer; homodimerizes following heparin- and ligand-binding (By similarity). Interacts with CBL, IRS1, PIK3R1 and PLCG1 (PubMed:15226403, PubMed:16878150). Interacts with FRS2 and SHC1 (PubMed:15226403, PubMed:16878150). Interacts with PTN and MDK (By similarity).
Post-translational modification
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.
Domain
Th
Target Relevance information above includes information from UniProt accession: P97793
The UniProt Consortium

Data

HPLC of Mouse ALK Protein
The purity of Mouse ALK is greater than 95% as determined by SEC-HPLC.
SDS-PAGE gel of Mouse ALK Protein
Mouse ALK on Tris-Bis PAGE under reduced condition. The purity is greater than 95%.

Publications

Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from PubMed database provided by The United States National Library of Medicine at the National Institutes of Health.




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