scholarly journals The Caenorhabditis elegans matrix non-peptidase MNP-1 is required for neuronal cell migration and interacts with the Ror receptor tyrosine kinase CAM-1

2017 ◽  
Vol 424 (1) ◽  
pp. 18-27 ◽  
Author(s):  
Teresa R. Craft ◽  
Wayne C. Forrester
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Neuronal Cell

scholarly journals Multiple functions of let-23, a Caenorhabditis elegans receptor tyrosine kinase gene required for vulval induction.

Genetics ◽  
1991 ◽  
Vol 128 (2) ◽  
pp. 251-267 ◽  
Author(s):  
R V Aroian ◽  
P W Sternberg
Keyword(s):  
Caenorhabditis Elegans ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Egf Receptor ◽  
Kinase Gene ◽  
Multiple Functions ◽  
Tyrosine Kinase Gene ◽  
Receptor Tyrosine Kinase Gene ◽  
Epidermal Growth ◽  
Mutant Phenotypes

Abstract The let-23 gene, which encodes a putative tyrosine kinase of the epidermal growth factor (EGF) receptor subfamily, has multiple functions during Caenorhabditis elegans development. We show that let-23 function is required for vulval precursor cells (VPCs) to respond to the signal that induces vulval differentiation: a complete loss of let-23 function results in no induction. However, some let-23 mutations that genetically reduce but do not eliminate let-23 function result in VPCs apparently hypersensitive to inductive signal: as many as five of six VPCs can adopt vulval fates, in contrast to the three that normally do. These results suggest that the let-23 receptor tyrosine kinase controls two opposing pathways, one that stimulates vulval differentiation and another that negatively regulates vulval differentiation. Furthermore, analysis of 16 new let-23 mutations indicates that the let-23 kinase functions in at least five tissues. Since various let-23 mutant phenotypes can be obtained independently, the let-23 gene is likely to have tissue-specific functions.

scholarly journals CLIP‐170 spatially modulates receptor tyrosine kinase recycling to coordinate cell migration

Traffic ◽  
2019 ◽  
Vol 20 (3) ◽  
pp. 187-201
Author(s):  
Kossay Zaoui ◽  
Stephanie Duhamel ◽  
Christine A. Parachoniak ◽  
Morag Park
Keyword(s):  
Cell Migration ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase

scholarly journals Receptor Tyrosine Kinase Ror2 Mediates Wnt5a-induced Polarized Cell Migration by Activating c-Jun N-terminal Kinase via Actin-binding Protein Filamin A

2008 ◽  
Vol 283 (41) ◽  
pp. 27973-27981 ◽  
Author(s):  
Akira Nomachi ◽  
Michiru Nishita ◽  
Daisuke Inaba ◽  
Masahiro Enomoto ◽  
Mayumi Hamasaki ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Binding Protein ◽  
Actin Binding ◽  
Filamin A ◽  
Actin Binding Protein

scholarly journals Non-receptor tyrosine kinase Src is required for ischemia-stimulated neuronal cell proliferation via Raf/ERK/CREB activation in the dentate gyrus

2009 ◽  
Vol 10 (1) ◽  
pp. 139 ◽  
Author(s):  
He-Ping Tian ◽  
Bao-Sheng Huang ◽  
Jie Zhao ◽  
Xiao-Han Hu ◽  
Jun Guo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tyrosine Kinase ◽  
Dentate Gyrus ◽  
Receptor Tyrosine Kinase ◽  
Neuronal Cell ◽  
Creb Activation

scholarly journals Receptor tyrosine kinase signaling required for integrin alpha v beta 5-directed cell motility but not adhesion on vitronectin.

1994 ◽  
Vol 127 (3) ◽  
pp. 859-866 ◽  
Author(s):  
R L Klemke ◽  
M Yebra ◽  
E M Bayna ◽  
D A Cheresh
Keyword(s):  
Cell Migration ◽  
Tyrosine Kinase ◽  
Cell Motility ◽  
Receptor Tyrosine Kinase ◽  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
De Novo ◽  
Growth Factor Receptor ◽  
Dependent Manner ◽  
Pkc Activation

FG human pancreatic carcinoma cells adhere to vitronectin using integrin alpha v beta 5 yet are unable to migrate on this ligand whereas they readily migrate on collagen in an alpha 2 beta 1-dependent manner. We report here that epidermal growth factor receptor (EGFR) activation leads to de novo alpha v beta 5-dependent FG cell migration on vitronectin. The EGFR specific tyrosine kinase inhibitor tyrphostin 25 selectively prevents EGFR autophosphorylation thereby preventing the EGF-induced FG cell migration response on vitronectin without affecting constitutive migration on collagen. Protein kinase C (PKC) activation also leads to alpha v beta 5-directed motility on vitronectin; however, this is not blocked by tyrosine kinase inhibitors. In this case, PKC activation appears to be associated with and downstream of EGFR signaling since calphostin C, an inhibitor of PKC, blocks FG cell migration on vitronectin induced by either PKC or EGF. These findings represent the first report implicating a receptor tyrosine kinase in a specific integrin mediated cell motility event independent of adhesion.

scholarly journals Inhibition of Integrin-mediated Cell Adhesion but Not Directional Cell Migration Requires Catalytic Activity of EphB3 Receptor Tyrosine Kinase

2004 ◽  
Vol 280 (2) ◽  
pp. 923-932 ◽  
Author(s):  
Hui Miao ◽  
Klaus Strebhardt ◽  
Elena B. Pasquale ◽  
Tang-Long Shen ◽  
Jun-Lin Guan ◽  
...  
Keyword(s):  
Cell Migration ◽  
Catalytic Activity ◽  
Cell Adhesion ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Directional Cell Migration
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