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ALKR1275Q cooperated with MYCN (show MYCN Antibodies) in the development of aggressive NB, possibly by downregulating the expression of ECM (show MMRN1 Antibodies)/BM-associated genes and by conferring malignant potentials to MYCN (show MYCN Antibodies)-expressing cells.
ALK inhibitor alectinib inhibits tumor growth in a TH-MYCN transgenic neurob (show ARHGEF16 Antibodies)lastoma mouse model.
Alk -/- mice initially consume more ethanol and have increased basal and ethanol-stimulated GABA release in the central nucleus of the amygdala when compared to Alk +/+ mice. After chronic ethanol exposure, Alk +/+ mice escalate their ethanol consumption, whereas Alk -/- mice do not. Basal GABA release in Alk -/- mice is not enhanced by chronic intermittent ethanol-two bottle choice drinking as it is in Alk +/+ mice.
An oral anaplastic lymphoma kinase (ALK) inhibitor.
ALK knock out male mice exhibit hypogonadotropic hypogonadism.
Ethanol activates ALK (and MDK (show MDK Antibodies)) signaling in the brain which regulates behaviors related to alcohol abuse.
Hyperactivation of Alk induces neonatal lethality in knock-in AlkF1178L mice.
Mutations in the ALK gene is associated with neuroblastoma (show ARHGEF16 Antibodies).
Th-MYCN (show MYCN Antibodies) genetically-engineered murine models of neuroblastoma (show ARHGEF16 Antibodies) using MRI (show C7ORF49 Antibodies), we have identified a marked ALK(F1174L)-driven vascular phenotype.
Reduced ALK1 (show ACVRL1 Antibodies) expression is associated with increased extracellular matrix protein expression, proliferation and migration in fibroblasts.
ALK-L1198F and ALK-G1201E mutations, originally identified in anaplastic thyroid cancer, do not result in ligand independent gain-of-function activity.
ALK+, LBCL cases display a dismal clinical outcome and can only be cured with conventional chemotherapy protocols at the stage of localized disease
Studies showed recurrent oncogenic alterations suche as chromosomal translocation and gene amplification of ALK in anaplastic large-cell lymphoma, inflammatory myofibroblastic tumor, and neuroblastoma (show ARHGEF16 Antibodies) and has highlighted the importance for ALK in histologically diverse pediatric cancers. [review]
Case Reports: inflammatory myofibroblastic tumors of the lung containing a chimeric A2M (show A2M Antibodies)-ALK gene categorized as a specific type of inflammatory myofibroblastic tumor that develops exclusively in neonates and infants.
ALK Rearrangement is associated with Lung Cancer.
Aberrant ALK expression is observed in ovarian serous carcinoma but not in mucinous carcinoma, is independent of gene translocation, and might be associated with progression and prognosis.
ALK gene Rearrangement is associated with Venous Thromboembolism in Non-Small-Cell Lung Cancer.
Our results suggest that the dynamic change in the numbers of circulating tumor cells (CTC) with ALK-CNG (show CNGA1 Antibodies) may be a predictive biomarker for crizotinib efficacy in ALK-rearranged non-small cell lung cancer (NSCLC)patients. Serial molecular analysis of CTC shows promise for real-time patient monitoring and clinical outcome prediction in this population.
Studies indicate that aberrant AXL receptor tyrosine kinase (AXL (show AXL Antibodies)) signaling and development of an epithelial-to-mesenchymal transition (EMT (show ITK Antibodies)) phenotype underlie resistance of anaplastic lymphoma kinase (ALK F1174L)-driven neuroblastoma (show ARHGEF16 Antibodies) (NB) cells to TAE684 and its derivatives.
Knockdown of SMYD2 (show SMYD2 Antibodies) as well as treatment with a SMYD2 (show SMYD2 Antibodies) inhibitor in two NSCLC cell lines with an EML4 (show EML4 Antibodies)-ALK gene significantly attenuated the phosphorylation levels of the EML4 (show EML4 Antibodies)-ALK protein.
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), ALK\\/KIF5B (chromosome 10), ALK\\/CLTC (chromosome 17), ALK\\/TPM4 (chromosome 19), and ALK\\/MSN (chromosome X).
ALK tyrosine kinase receptor
, anaplastic lymphoma kinase (Ki-1)
, CD246 antigen
, mutant anaplastic lymphoma kinase
, anaplastic lymphoma receptor tyrosine kinase
, anaplastic lymphoma kinase