A role for anaplastic lymphoma kinase (ALK) function in zebrafish neural crest development

2006 ◽  
Vol 295 (1) ◽  
pp. 410
Author(s):  
Robert N. Kelsh ◽  
Xueyan Yang ◽  
Jeanette Mueller ◽  
Andrew Ward
Keyword(s):  
Neural Crest ◽  
Anaplastic Lymphoma Kinase ◽  
Anaplastic Lymphoma ◽  
Neural Crest Development

scholarly journals ALKALs are in vivo ligands for ALK family Receptor Tyrosine Kinases in the neural crest and derived cells

2017 ◽  
Author(s):  
Andrey Fadeev ◽  
Patricia Mendoza Garcia ◽  
Uwe Irion ◽  
Jikui Guan ◽  
Kathrin Pfeifer ◽  
...  
Keyword(s):  
Neural Crest ◽  
Tyrosine Kinases ◽  
Pigment Cells ◽  
Loss Of Function ◽  
Receptor Complexes ◽  
Anaplastic Lymphoma ◽  
Zebrafish Larvae ◽  
Neural Crest Development ◽  
Biochemical Analyses

AbstractMutations in Anaplastic Lymphoma Kinase (ALK) are implicated in somatic and familial neuroblastoma, a paediatric tumour of neural crest-derived tissues. Recently, biochemical analyses have identified secreted small ALKAL proteins (FAM150, AUG) as potential ligands for human ALK and the related Leukocyte Tyrosine Kinase (LTK). In the zebrafish Danio rerio, DrLtk, which is similar to human ALK in sequence and domain structure, controls the development of iridophores, neural crest-derived pigment cells. Hence, the zebrafish system allows studying Alk/Ltk and Alkals involvement in neural crest regulation in vivo. Using zebrafish pigment pattern formation, Drosophila eye patterning, and cell culture-based assays, we show that zebrafish Alkals potently activate zebrafish Ltk and human ALK driving downstream signalling events. Overexpression of the three Dr Alkals cause ectopic iridophore development whereas loss of function alleles lead to spatially distinct patterns of iridophore loss in zebrafish larvae and adults. alkal loss of function triple mutants completely lack iridophores and are larval lethal as is the case for ltk null mutants. Our results provide the first in vivo evidence of (i) activation of ALK/LTK family receptors by ALKALs and (ii) an involvement of these ligand-receptor complexes in neural crest development.

scholarly journals GSK3 Controls Migration of the Neural Crest Lineage

2018 ◽  
Author(s):  
Sandra G. Gonzalez Malagon ◽  
Anna M. Lopez Muñoz ◽  
Daniel Doro ◽  
Triòna G. Bolger ◽  
Evon Poon ◽  
...  
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Glycogen Synthase ◽  
Neuroblastoma Cells ◽  
Neural Crest Cells ◽  
Anaplastic Lymphoma ◽  
Neural Crest Development ◽  
And Migration ◽  
Neural Crest Migration

AbstractMigration of the neural crest lineage is critical to its physiological function. Mechanisms controlling neural crest migration are comparatively unknown, due to difficulties accessing this cell population in vivo. Here, we uncover novel requirements of glycogen synthase kinase 3 (GSK3) in regulating the neural crest. We demonstrate that GSK3 is tyrosine phosphorylated (pY) in neural crest cells and that this activation depends on anaplastic lymphoma kinase (ALK), a protein associated with neuroblastoma. Consistent with this, neuroblastoma cells with pathologically increased ALK activity express high levels of pY-GSK3 and migration of these cells can be inhibited by GSK3 or ALK blockade. In normal neural crest cells, loss of GSK3 leads to increased pFAK and misregulation of Rac1 and lamellipodin, key regulators of cell migration. Genetic reduction of GSK-3 results in failure of migration. All together, this work identifies a role for GSK3 in cell migration during neural crest development and cancer.

Anaplastic Lymphoma Kinase in Human Cancer

2012 ◽  
Vol 17 (2) ◽  
pp. 123-143 ◽  
Author(s):  
Christina Schonherr ◽  
Bengt Hallberg ◽  
Ruth Palmer
Keyword(s):  
Anaplastic Lymphoma Kinase ◽  
Human Cancer ◽  
Anaplastic Lymphoma
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