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Validated All-in-One™ qPCR Primer for ALK(NM_004304.4) Search again
Product ID:
HQP006353
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ALK1, CD246, NBLST3
Gene Description:
ALK receptor tyrosine kinase
Target Gene Accession:
NM_004304.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The 2;5 chromosomal translocation is frequently associated with anaplastic large cell lymphomas (ALCLs). The translocation creates a fusion gene consisting of the ALK (anaplastic lymphoma kinase) gene and the nucleophosmin (NPM) gene: the 3' half of ALK, derived from chromosome 2, is fused to the 5' portion of NPM from chromosome 5. A recent study shows that the product of the NPM-ALK fusion gene is oncogenic. The deduced amino acid sequences reveal that ALK is a novel receptor protein-tyrosine kinase having a putative transmembrane domain and an extracellular domain. These sequences are absent in the product of the transforming NPM-ALK gene. ALK shows the greatest sequence similarity to LTK (leukocyte tyrosine kinase). ALK plays an important role in the development of the brain and exerts its effects on specific neurons in the nervous system. [provided by RefSeq].
Gene References into function
- Pleiotrophin signaling through anaplastic lymphoma kinase is rate-limiting for glioblastoma growth
- ALK as a novel lymphoma-associated tumor antigen: identification of 2 HLA-A2.1-restricted CD8+ T-cell epitopes.
- ALK-positive anaplastic large cell lymphoma had significantly higher levels of caspase 3, while high expression of the antiapoptotic proteins Bcl-2 and PI9 was almost completely restricted to ALK-negative cases.
- Novel fusion partners CARS and KIAA1618 (ALO17) have been detected with variant rearrangements of ALK in anaplastic large-cell lymphoma and inflammatory myofibroblastic tumor cases.
- results do not support any involvement of ALK in the stimulation of tumorigenic cell growth or differentiation
- midkine binds to ALK and has a role in signal transduction for cell growth and survival
- ALK-ShcC signal activation, possibly caused by co-amplification with the N-myc gene, might give additional effects on malignant tumor progression of neuroblastoma.ShcC is a potent substrate of the activated ALK kinase.
- co-expression of c-Myc and ALK was seen in tumor cells of ALK-positive anaplastic large cell lymphomas; C-Myc may be a downstream target of ALK signaling
- novel fusion created by the ALK gene on chromosome 2p23 and NPM on 5q35 or other variant translocation partners in a rare variant of diffuse large B-cell lymphoma
- In a case of anaplastic large cell lymphoma, ALK is fused to a portion of non-muscle myosin heavy chain gene, MYH9, localized 6 bp downstream of MSN-ALK in the same exonic sequence, resulting in an in-frame fusion of the two partner proteins.
- Src-kinases, particularly pp60(c-src), associate with and are activated by NPM-ALK expression in various cells, and in cell lines established from patients with large cell lymphoma
- results show a pivotal role for Bcl-XL in ALK-mediated oncogenicity
- FOXO3a is a barrier to hematopoietic transformation that is overcome by phosphorylation and cytoplasmic relocalization induced by the expression of NPM-ALK
- High dose therapy and stem cell transplantation does not produce long-term disease free survival in patients with recurrent chemotherapy-sensitive ALK-negative large cell lymphoma.
- STAT3 directly contributes to the high level of TIMP1 expression in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.
- ALK receptor tyrosine kinase has roles promoting cell growth and neurite outgrowth
- ALK has roles in oncogenesis of haematopoietic and non-haematopoietic tumors [review]
- Although 9 of 36 patients with cutaneous CD30(+) lymphoproliferative diseases had progression of their disease, neither mutations of the p53 gene nor ALK immunoreactivity were found in any of these biopsies.
- analysis of differentiation of PC12 cells and human embryonic kidney 293 cells transfected with ALK shows absence of agonist activity of pleiotrophin
- ALK-mediated alphaDGK activation is dependent on p60src tyrosine kinase, with which alphaDGK forms a complex; alphaDGK activation is involved in the control of ALK-mediated mitogenic properties.
- CONCLUSIONS: ALK-ALCL arising in the skin represents a single disease with a broad spectrum of morphology; clinicians and pathologists should be aware of this neutrophil-rich (NR) variant with aggressive clinical presentation.
- We conclude that Jak3 activation is predominantly restricted to ALK-positive ALCL tumors.
- Genomic PCR and subsequent sequencing showed that the breakpoints were located in intron 23 of SEC31-like 1 protein-transport protein and intron 20 of ALK
- Potent and selective ALK inhibitors may have therapeutic application for anaplastic lymphoma kinase.
- Pseudosarcomatous myofibroblastic proliferations of the genitourinary tract may show ALK immunopositivity but do not show consistent ALK rearrangement by fluorescent in situ hybridization.
- can be adapted for the identification of known and unknown translocation partners of chimeric ALK fusion proteins involved in oncogenesis
- constitutive expression of C/EBPbeta in ALK-positive anaplastic large cell lymphoma and its relationship to NPM-ALK
- NPM/ALK-carrying T cell lymphoma (ALK+TCL) cells secrete IL-10 and TGF-beta and express FoxP3, indicating their T regulatory (Treg) cell phenotype.
- Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma.
- AUF1 was phosphorylated by ALK in vitro and was hyperphosphorylated in NPM-ALK-expressing cells.
- recruitment of insulin receptor substrate-1 to activated ALK and the activation of NF-kappaB are essential for the autocrine growth and survival signaling of midkine
- ALK has a proapoptotic activity in the absence of ligand, whereas it is antiapoptotic in the presence of its ligand and when the kinase is intrinsically activated.
- CD26 and cell surface adenosine deaminase are selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma
- molecular signature of ALK- anaplastic large-cell lymphoma included overexpression of CCR7, CNTFR, IL22, and IL21 genes
- A functional role for Shc and likely FRS2 in ALK-dependant MAP-kinase activation and neuronal differentiation of PC12 cells.
- This study thus supports the possibility that activated ALK may be important in human breast cancers and potentially activated either through the PTN/RPTPbeta/zeta signaling pathway.
- identify splicing factor as a novel nucleophosmin 1/anaplastic lymphoma kinase-binding protein and substrate
- phosphorylation of ALK in PTN-stimulated cells is mediated through the PTN/RPTPbeta/zeta signaling pathway
- JunB is a critical target of mTOR and is translationally regulated in NPM-ALK-positive lymphomas.
- Pleiotrophin failed to activate anaplastic lymphoma kinase (ALK) in neuroblastoma/glioblastoma cells expressing this receptor. ALK is still an orphan receptor in vertebrates.
- Oncogenic NPM1-ALK contains the ALK catalytic domain plus NPM1 oligomerization motif and mediates malignant cell transformation by epigenetic silencing of signal transducer and activator of transcription STAT5A in T-cell anaplastic large cell lymphomas.
- Fusion protein nucleophosmin (NPM)-ALK activates GTPase Rac1 via phosphatidylkinase 3-kinase (PI3K) and protein-tyrosine kinase c-src (Src) in anaplastic large cell lymphoma patients.
- findings indicate that phosphorylation of the first tyrosine of the YXXXYY motif is necessary for the autoactivation of the ALK kinase domain and the transforming activity of nucleoplasmin/ALK
- Translocations or deregulated expression of ALK contribute to oncogenesis and genetic or pharmacological tools, aimed at neutralizing its activity in anaplastic lymphoma [REVIEW]
- besides MYCN and ALK, other genes proximal and distal to MYCN are highly expressed in neuroblastoma
- ALK is part of a fusion protein linked to histological characteristics in a subset of lung neoplasms.
- different types of cytogenetic aberrations may involve the ALK gene in ALK-positive diffuse large B-cell lymphoma leading to peculiar immunohistochemical staining patterns [case reports]
- EML4-ALK fusion gene product is involved in the carcinogenesis in non-small cell lung carcinomas
- EML4-ALK fusions occur in less than 3% of non-small cell lung cancers samples; EML4 and/or ALK amplifications also occur.
- EML4-ALK fusion transcript is not present in gastrointestinal or breast cancers and is specific to NSCLC.
- A subset of lung cancers, lymphomas, and neuroblastomas that harbor genomic ALK alterations may be clinically responsive to pharmacologic ALK inhibition.
- Fluorescence in situ hybridization and molecular studies on the bone marrow aspirate specimens led to the detection of a clathrin (CLTC)/ALK rearrangement.
- A lung cancer cell line expressing endogenous variant 3 of EML4-ALK underwent cell death on exposure to a specific inhibitor of ALK catalytic activity.
- EML4-ALK fusion gene is expressed in lung cancer
- high prevalence of anti-ALK antibodies in pediatric ALK-positive ALCL and relationship between minimal residual disease and anti-ALK antibody response
- the spectrum of diseases exhibiting ALK translocation should be expanded to include ALK(+) histiocytosis
- results demonstrate that heritable mutations of ALK are the main cause of familial neuroblastoma, and that germline or acquired activation of this cell-surface kinase is a tractable therapeutic target for this lethal paediatric malignancy
- data identify ALK as a critical player in neuroblastoma development that may hence represent a very attractive therapeutic target in this disease that is still frequently fatal with current treatments
- the anaplastic lymphoma kinase, originally identified as a fusion kinase in a subtype of non-Hodgkin's lymphoma (NPM-ALK) and more recently in adenocarcinoma of lung (EML4-ALK), is also a frequent target of genetic alteration in advanced neuroblastoma
- detection of previously unknown mutations in the ALK gene, which encodes a receptor tyrosine kinase, in 8% of primary neuroblastomas
- concomitant inhibition of Cdc42 and NPM-ALK kinase acted synergistically to induce apoptosis of ALCL cells
- ALK protein contributes to NB(neuroblastoma) oncogenesis providing a highly interesting putative therapeutic target in a subset of unfavourable NB tumours.