Anaplastic Lymphoma Kinase and Leukocyte Tyrosine Kinase: Functions and genetic interactions in learning, memory and adult neurogenesis

@article{Weiss2012AnaplasticLK,
  title={Anaplastic Lymphoma Kinase and Leukocyte Tyrosine Kinase: Functions and genetic interactions in learning, memory and adult neurogenesis},
  author={Joseph B. Weiss and Changhui Xue and Ted S. Benice and Liquan Xue and Stephan W. Morris and Jacob Raber},
  journal={Pharmacology Biochemistry and Behavior},
  year={2012},
  volume={100},
  pages={566-574}
}

Figures from this paper

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Effects of Pharmacologic and Genetic Inhibition of Alk on Cognitive Impairments in NF1 Mutant Mice
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TLDR
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Neuronal leucine-rich repeat 1 negatively regulates anaplastic lymphoma kinase in neuroblastoma
TLDR
It is shown that NLRR1 appears to be an extracellular negative regulator of ALK signalling in NB and neuronal development and may be beneficial to comprehend NB heterogeneity and to develop a novel therapy against unfavourable NB.
Transcriptome Regulation by Oncogenic ALK Pathway in Mammalian Cortical Development Revealed by Single-Cell RNA Sequencing.
TLDR
It is found that transient embryonic ALK inactivation caused long-lasting abnormalities in the adult mouse brain, including impaired neuronal connectivity and cognition, along with delayed neuronal migration and decreased neuronal proliferation during neurodevelopment.
Jelly belly trans‐synaptic signaling to anaplastic lymphoma kinase regulates neurotransmission strength and synapse architecture
TLDR
Novel roles for Jeb–Alk signaling in the modulation of synaptic function and structure have potential implications for recently reported Alk functions in human addiction, retention of spatial memory, cognitive dysfunction in neurofibromatosis, and pathogenesis of amyotrophic lateral sclerosis.
ALKALs are in vivo ligands for ALK family receptor tyrosine kinases in the neural crest and derived cells
TLDR
In vivo evidence is provided of activation of ALK/LTK family receptors by ALKALs and an involvement of these ligand–receptor complexes in neural crest development and in vivo evidence of loss-of-function alleles lead to spatially distinct patterns of iridophore loss in zebrafish larvae and adults.
Loss of RET Promotes Mesenchymal Identity in Neuroblastoma Cells
TLDR
It is shown here that ALK activation in response to ALKAL2 ligand results in the rapid phosphorylation of RET in NB cells, providing additional insight into the contribution of RET to the ALK-driven gene signature in NB.
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References

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The Receptor Tyrosine Kinase Alk Controls Neurofibromin Functions in Drosophila Growth and Learning
TLDR
dAlk is identified as an upstream activator of dNf1-regulated Ras signaling responsible for several dNF1 defects, and human Alk is implicate as a potential therapeutic target in NF1.
Behavioral and Neurochemical Alterations in Mice Deficient in Anaplastic Lymphoma Kinase Suggest Therapeutic Potential for Psychiatric Indications
TLDR
It is suggested that ALK functions in the adult brain to regulate the function of the frontal cortex and hippocampus and identifies ALK as a new target for psychiatric indications, such as schizophrenia and depression, with an underlying deregulated monoaminergic signalling.
An Evolutionary Conserved Role for Anaplastic Lymphoma Kinase in Behavioral Responses to Ethanol
TLDR
The results suggest that Alk plays an evolutionary conserved role in ethanol-related behaviors and may be a novel candidate gene conferring risk for AUDs as well as a potential target for pharmacological intervention.
ALK (Anaplastic Lymphoma Kinase) expression in DRG neurons and its involvement in neuron–Schwann cells interaction
TLDR
It is shown that ALK is specifically present in a subtype of neurons during DRG development, and that the majority of these neurons co‐expressed TrkA and Ret, and it is hypothesized that the presence of satellite Schwann cells was involved in the absence of truncated ALK.
Jeb signals through the Alk receptor tyrosine kinase to drive visceral muscle fusion
TLDR
It is shown that Drosophila Alk is the receptor for Jeb in the developing visceral mesoderm, and that Jeb binding stimulates an Alk-driven, extracellular signal-regulated kinase-mediated signalling pathway, which results in the expression of the downstream gene duf—needed for muscle fusion.
Anaplastic lymphoma kinase is dynamically expressed on subsets of motor neurons and in the peripheral nervous system
TLDR
The data presented here identify ALK as a novel candidate receptor for regulating critical events in the development of neurons in both the central and the peripheral nervous systems.
Molecular characterization of ALK, a receptor tyrosine kinase expressed specifically in the nervous system
TLDR
Molecular cloning of cDNAs for both the human and mouse ALK proteins reveal that ALK is a novel receptor protein-tyrosine kinase having a putative transmembrane domain and an extracellular domain and shows the greatest sequence similarity to LTK (leukocyte tyrosine Kinase) whose biological function is presently unknown.
ALK, the chromosome 2 gene locus altered by the t(2;5) in non-Hodgkin's lymphoma, encodes a novel neural receptor tyrosine kinase that is highly related to leukocyte tyrosine kinase (LTK)
Anaplastic Lymphoma Kinase (ALK) was originally identified as a member of the insulin receptor subfamily of receptor tyrosine kinases that acquires transforming capability when truncated and fused to
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