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Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (zeige ERBB3 Antikörper) associated with alcohol dependence in humans and behavioral responses to ethanol in mice.
ALKR1275Q cooperated with MYCN (zeige MYCN Antikörper) in the development of aggressive NB, possibly by downregulating the expression of ECM (zeige MMRN1 Antikörper)/BM-associated genes and by conferring malignant potentials to MYCN (zeige MYCN Antikörper)-expressing cells.
ALK inhibitor alectinib inhibits tumor growth in a TH-MYCN (zeige MYCN Antikörper) transgenic neuroblastoma (zeige ARHGEF16 Antikörper) 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 (zeige MDK Antikörper)) 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 (zeige ARHGEF16 Antikörper).
Th-MYCN (zeige MYCN Antikörper) genetically-engineered murine models of neuroblastoma (zeige ARHGEF16 Antikörper) using MRI (zeige C7ORF49 Antikörper), we have identified a marked ALK(F1174L)-driven vascular phenotype.
However, toxicity issues remain a problem for ceritinib, and another next-generation ALK inhibitor, alectinib, is more likely to become the drug of choice for untreated patients
ALK Rearrangement is associated with resistant to crizotinib therapy in a metastatic abdominal nodule with Small Cell Carcinoma.
ALK Fusion Patterns are associated with Response to Crizotinib Treatment in Lung cancer.
High ALK expression is associated with Merkel cell carcinoma.
The aim was to investigate the prevalence of ALK fusion variants and to compare clinical outcomes according to ALK fusion variants.
Results demonstrate that the frequency and spectrum of ALK resistance mutations differs depending on the ALK inhibitor. Moreover, resistance profiles may evolve over time and in response to sequential ALK inhibitors.
Detection of Gene Rearrangements in Circulating Tumor Cells: Examples of ALK-, ROS1 (zeige ROS1 Antikörper)-, RET (zeige RET Antikörper)-Rearrangements in Non-Small-Cell Lung Cancer and ERG (zeige ERG Antikörper)-Rearrangements in Prostate Cancer.(
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 (zeige ARHGEF16 Antikörper) and has highlighted the importance for ALK in histologically diverse pediatric cancers. [review]
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