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Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (zeige ERBB3 ELISA Kits) associated with alcohol dependence in humans and behavioral responses to ethanol in mice.
ALKR1275Q cooperated with MYCN (zeige MYCN ELISA Kits) in the development of aggressive NB, possibly by downregulating the expression of ECM (zeige MMRN1 ELISA Kits)/BM-associated genes and by conferring malignant potentials to MYCN (zeige MYCN ELISA Kits)-expressing cells.
ALK inhibitor alectinib inhibits tumor growth in a TH-MYCN (zeige MYCN ELISA Kits) transgenic neuroblastoma (zeige ARHGEF16 ELISA Kits) 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 ELISA Kits)) 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 ELISA Kits).
Th-MYCN (zeige MYCN ELISA Kits) genetically-engineered murine models of neuroblastoma (zeige ARHGEF16 ELISA Kits) using MRI (zeige C7ORF49 ELISA Kits), we have identified a marked ALK(F1174L)-driven vascular phenotype.
Mutation in ALK-fusion genes are associated with tyrosine kinase (zeige TXK ELISA Kits) inhibitor resistance in lung cancer.
ALK-positive lung adenocarcinoma who test immunohistochemistry-positive and FISH-negative may still respond to crizotinib therapy.
For intra-hepatic cholangiocarcinomas (IHCC)patients, ROS1 (zeige ROS1 ELISA Kits), ALK and c-MET expression levels have prognostic significance on clinical outcomes. Although this finding may require further validation, it has led to proposal of a new stratification or enriched biomarker for future phase III trial of anti-EGFR (zeige EGFR ELISA Kits) therapy in IHCC
Detection of the CAD (zeige CAD ELISA Kits)-ALK gene fusion in urine tr-DNA anticipated radiological confirmation of disease progression. Analysis of plasma ctDNA identified ALK kinase mutations that emerged during treatment with the ALK inhibitor entrectinib
data suggest a potential role of ALK in pediatric rhabdomyosarcoma
We report the first case of an ALK-positive Non Small Cell Lung Carcinoma patient who benefited from pemetrexed rechallenge after developing ALK inhibitor resistance. This strategy may be an option for some patients who suffer from acquired resistance to ALK inhibitors but responded to previous pemetrexed chemotherapy
ALK expression has different prognostic significance in patients with Anaplastic large cell lymphomas.
Anaplastic lymphoma kinase gene rearrangement is associated with non-small cell lung cancer.
The treatment of patients with anaplastic lymphoma receptor tyrosine kinase (ALK)-positive, metastatic non-small cell lung cancer.
The unique, potent, and pan-ALK mutant activity of brigatinib could be rationalized by structural analyses.
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