Recombinant Human ALK tyrosine kinase receptor(ALK) ,partial

Code CSB-YP890938HU
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Source Yeast
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Code CSB-EP890938HU
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Source E.coli
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Code CSB-EP890938HU-B
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP890938HU
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Source Baculovirus
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Code CSB-MP890938HU
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Source Mammalian cell
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Product Details

Purity >85% (SDS-PAGE)
Target Names ALK
Uniprot No. Q9UM73
Alternative Names Alk; ALK tyrosine kinase receptor; ALK/EML4 fusion gene; included; ALK/NPM1 fusion gene; included; ALK_HUMAN; anaplastic lymphoma kinase (Ki-1); Anaplastic lymphoma kinase; Anaplastic lymphoma kinase Ki1; anaplastic lymphoma receptor tyrosine kinase; CD 246; CD246; CD246 antigen; EC; Ki 1; Ki1; mutant anaplastic lymphoma kinase; NBLST 3; NBLST3; Tcrz; TFG/ALK
Species Homo sapiens (Human)
Protein Length Partial
Tag Info The following tags are available.
N-terminal His-tagged
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Form Lyophilized powder
Buffer before Lyophilization Tris/PBS-based buffer, 6% Trehalose, pH 8.0
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
and FAQs
Protein FAQs
Storage Condition Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet Please contact us to get it.

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Target Background

(From Uniprot)
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. 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. 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.
Gene References into Functions
  1. Baseline Circulating tumor cell count could be a predictive biomarker for EGFR-mutated and ALK-rearranged non-small cell lung cancer , which allows for better guidance and monitoring of patients over the course of molecular targeted therapies. PMID: 29582563
  2. EML4-ALK fusion variant V3 is a high-risk feature for anaplastic lymphoma kinase-driven non-small cell lung cancer PMID: 29363116
  3. In this paper, we reviewed fusion partner genes with ALK, detection methods for ALK-rearrangement (ALK-R), and the ALK-tyrosine kinase inhibitor, crizotinib, used in non-small-cell lung cancer patients. PMID: 29488330
  4. The EML4-ALK fusion gene may be a strong oncogene in younger patients with lung adenocarcinoma. PMID: 29517858
  5. Brigatinib, a next-generation ALK inhibitor, shows promising activity in ALK-rearranged NSCLC that have previously received crizotinib with response rates in ALTA ranging from 42-50%, intracranial response 42-67% and median progression-free survival 9.2-12.9 months. Randomized Phase III trial, ALTA-1 L is investigating brigatinib in ALK inhibitor-naive patients PMID: 29451020
  6. Study based on 47 tissue samples from spitzoid tumors revealed 2 BAP1-inactived cases. The absence of anomalous expression of translocation-related proteins ALK and ROS1 in this series, composed predominantly of low-grade/low-risk tumors, indicates that translocated spitzoid lesions may not be as prevalent as initially suggested, at least in some populations. PMID: 29623743
  7. The results further combined 3D-QSAR can not only profile the binding mechanism between the 2,4-Diarylaminopyrimidines inhibitors and ALK, but also supply the useful information for the rational design of a more potential small molecule inhibitor bound to ALK receptor. PMID: 30001602
  8. Non-Small Cell Lung Cancers positive for ALK mutation by immunohistochemistry but not detected by Fluorescence in situ Hybridization show good response to crizotinib and merit treatment with the same PMID: 30082557
  9. the results from three transcriptome-based platforms (Nanostring Elements, Agena LungFusion panel and ThermoFisher NGS fusion panel) were compared to those obtained from ALK, ROS1 and RET Fluorescence In Situ Hybridization on 51 clinical specimens. PMID: 28181564
  10. ALK Rearrangement is associated with lung Adenocarcinoma. PMID: 29938474
  11. lung adenocarcinoma in Asian patients aged 50 years, especially EML4-ALK and ROS1 fusion. Mutation analysis may be helpful in determining targeted therapy for the majority of these patients PMID: 30107055
  12. Double Mutations of EGFR and ALK Gene in Non-small Cell Lung Cancer PMID: 30201068
  13. characteristics of the expression of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), V-Ki-ras2 Kirsten rat sarcoma viral oncogene homologue (KRAS) in non-small cell lung cancer PMID: 30037374
  14. did identify ALK molecular changes and immunohistochemical staining patterns that have not been previously described in blue/cellular blue nevi or deep penetrating nevi PMID: 29923908
  15. Anaplastic lymphoma kinase (ALK) is a novel regulator of NLRP3 inflammasome activation in macrophages. Mechanically, ALK-mediated NF-kappaB activation was required for the priming step of NLRP3 upregulation, whereas ALK-mediated lipid peroxidation contributed to the sensing step of NLRP3-NEK7 complex formation. PMID: 29723525
  16. ALK expression is therefore a helpful marker to distinguish EFH from cutaneous syncytial myoepithelioma PMID: 27438515
  17. ALK protein expression was found in a significant number of patients and was correlated with advanced stage and high-risk neuroblastoma. PMID: 28546523
  18. The method was successfully applied to a phase I clinical study of ALK-positive advanced NSCLC patients. PMID: 29455091
  19. there are many treatment options for targeting ALK+ non-small-cell lung cancerbut the best treatment sequence remains unanswered PMID: 28589737
  20. The results of this real-life analysis suggest that the prognosis of NSCLC patients with theALK translocation may be better than that of the overall NSCLC population, but the outcomes were poorer than those of ALK+ NSCLC patients included in clinical studies. PMID: 28762087
  21. Our data suggest that targeting Src signaling may be an effective approach to the treatment of ALK-non-small cell lung cancer (NSCLC) with acquired resistance to ALK inhibitors. PMID: 29048652
  22. The frequencies of ALK, ROS1 and RET rearrangements are low in non-adenocarcinoma NSCLC patients. And their clinical characteristics are similar to those in lung adenocarcinoma. Fusions of the above 3 genes are not prognostic factor for non-adnocarcinoma NSCLC patients. PMID: 27635639
  23. Patients whose tumors harbor ALK rearrangements or fusions respond to treatment with crizotinib and alectinib, including tumors not normally associated with ALK mutations, such as non-Langerhans cell histiocytosis or renal cell carcinoma. Comprehensive genomic profiling using next-generation sequencing can detect targetable ALK fusions irrespective of tumor type or fusions partner PMID: 29079636
  24. In xenografts in mice, trametinib inhibited the growth of EML4-ALK-positive non-small cell lung cancer and RAS-mutant neuroblastoma but not ALK-addicted neuroblastoma. PMID: 29184034
  25. In this review, we will discuss the current methods used in ALK rearrangement detection with emphasis on their key advantages and disadvantages. PMID: 29143897
  26. Here, we report our experience with ceritinib in terms of its efficacy and safety among ALK-positive nonsmall cell lung cancer patients who were previously exposed to crizotinib. PMID: 29199678
  27. A negative ALK immunohistochemistry result obviates the need for a FISH test barring those with a strong clinical profile, and a positive ALK immunohistochemistry result is sufficient basis for the initiation of treatment. PMID: 29199679
  28. Mutation testing at diagnosis is feasible in the vast majority of patients with Stage IV adenocarcinoma of the lung. Patients with EGFR or EML4ALK mutation and those who received pemetrexed maintenance had better clinical outcomes. PMID: 29199690
  29. Our analysis indicated that ALK-EML4 positive non-small-cell lung cancers comprised a unique subgroup of adenocarcinomas with distinct clinicopathological characteristics. Incidence of ALK positivity was found to be higher in females and never smokers. PMID: 29199691
  30. Manual Immunohistochemistry is equally effective in the detection of ALK-rearranged cases as automated methods. It can be easily integrated as a screening method into routine practice thus reducing the cost of automated systems. PMID: 29199692
  31. Data from the initial studies revealed, EGFR mutations, and ALK gene rearrangements are mutually exclusive and as mutual causes of resistance to EGFR-TKIs or ALK-TKIs. However, this mutual exclusivity is being challenged with the increasing evidence showing the coexistence of both EGFR and ALK PMID: 29199696
  32. We report higher frequency of ALK positivity (10.9%) in patients with adenocarcinoma of the lung. ALK by immunohistochemistry is more sensitive than FISH for ALK detection with high concordance. These patients had good clinical outcome with TKIs targeting ALK fusion protein. PMID: 29199697
  33. Among 718 patients with newly diagnosed metastasised non-squamous NSCLC, 12% (31/265) showed a positive test result for ALK rearrangements PMID: 28557060
  34. status had a profound influence on the ALK-related prognosis of NSCLC. ALK rearrangement predicted a better prognosis in the general population with NSCLC, but a poor survival in the non-smoking population. PMID: 29191580
  35. ALK and KRAS mutations are associated with acquired resistance to crizotinib in ALK-positive non-small cell lung cancer PMID: 28601386
  36. Case Report: cutaneous anaplastic lymphoma kinase-positive anaplastic large-cell lymphoma with linear distributional lesions and sarcomatoid histologic features. PMID: 29053547
  37. Our data strongly suggest adapting the guidelines and using dichotomous ALK-IHC as standard companion diagnostic test to select patients with NSCLC who benefit from ALK-targeting therapy PMID: 28183714
  38. Results suggest that ALK generated by alternative transcription Initiation induces chromatin structural changes and heterochromatinization through phosphorylation of AKAP8 in the nucleus. PMID: 29093346
  39. TrkA plays an important role in the pathogenesis of NPM-ALK(+) T-cell lymphoma. PMID: 28557340
  40. NLRR1 appears to be an extracellular negative regulator of ALK signalling in neuroblastoma and neuronal development. PMID: 27604320
  41. the present study suggests that HER2 has an important role in the regulation of the cancer stem-like cells phenotype in ALK translocated lung cancers that is mainly orchestrated by HER2/HER3 heterodimers. PMID: 28656214
  42. point out the importance of taking into account both histopathologic and ALK immunohistochemical features to interpret ALK fluorescence in situ hybridization analyses in inflammatory and necrotic tumors PMID: 26945447
  43. despite the marginal occurrence of ALK gene amplification/high polisomy, we did not observed any ALK, MET and ROS deregulation in sarcomatoid carcinoma of head and neck PMID: 27262592
  44. we reviewed the literature related to characteristics of metastatic ovarian malignancies that form from lung tumors, the utility of ALK inhibition for treating ALK-positive NSCLC, the molecular diagnosis of ALK rearrangement and the role of next generation sequencing for ALK rearrangement detection. PMID: 28362192
  45. The study reviews the drug-resistance mechanism of lung neoplasm cells with rearranged ALK. The resultant ALK fusion protein is aberrantly overexpressed and dimerized through the oligomerization domains, such as the coiled-coil domain, in the fusion partner that induces abnormal constitutive activation of ALK tyrosine kinase. Gene amplification or mutation confers tumor resistance to kinase inhibitors. [review] PMID: 29336091
  46. The combination of ribociclib, a dual inhibitor of cyclin-dependent kinase (CDK) 4 and 6, and the ALK inhibitor ceritinib demonstrated higher cytotoxicity and synergy scores (P = 0.006) in cell lines with ALK mutations as compared with cell lines lacking mutations or alterations in ALK . PMID: 27986745
  47. microRNA expression profiles had clinicopathological implications that were related to EGFR and KRAS mutations, as well as ALK-rearrangement in lung adenocarcinoma. PMID: 28035073
  48. Report accurate detect ALK gene rearrangements which could be used for diagnostic screening of lung cancer patients. PMID: 28032602
  49. Combining measurements of sweyjawbu expression and the ratio of the 5' and 3' portions of the ALK transcript provided accurate identification of ALK rearrangement-positive lymphomas. PMID: 27974674
  50. ALK point mutations are associated lung cancer. PMID: 26992209

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Involvement in disease Neuroblastoma 3 (NBLST3)
Subcellular Location Cell membrane, Single-pass type I membrane protein
Protein Families Protein kinase superfamily, Tyr protein kinase family, Insulin receptor subfamily
Tissue Specificity Expressed in brain and CNS. Also expressed in the small intestine and testis, but not in normal lymphoid cells.
Database Links

HGNC: 427

OMIM: 105590

KEGG: hsa:238

STRING: 9606.ENSP00000373700

UniGene: Hs.654469

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