scholarly journals A Novel Membrane Peptide that Inhibits Cell Migration by Activation of the Receptor Tyrosine Kinase EphA2

2018 ◽  
Vol 114 (3) ◽  
pp. 265a
Author(s):  
Justin M. Westerfield ◽  
Daiane S. Alves ◽  
Xiaojun Shi ◽  
Vanessa P. Nguyen ◽  
Robert H. Pullen ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Membrane Peptide

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 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

scholarly journals Filopodia formation mediated by receptor tyrosine kinase Ror2 is required for Wnt5a-induced cell migration

2006 ◽  
Vol 175 (4) ◽  
pp. 555-562 ◽  
Author(s):  
Michiru Nishita ◽  
Sa Kan Yoo ◽  
Akira Nomachi ◽  
Shuichi Kani ◽  
Nagako Sougawa ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tyrosine Kinase ◽  
Wnt Signaling ◽  
Receptor Tyrosine Kinase ◽  
Cultured Cells ◽  
Actin Binding ◽  
Filamin A ◽  
Jnk Pathway ◽  
Actin Reorganization ◽  
Rich Domain

The receptor tyrosine kinase Ror2 plays important roles in developmental morphogenesis. It has recently been shown that Ror2 mediates Wnt5a-induced noncanonical Wnt signaling by activating the Wnt–JNK pathway and inhibiting the β-catenin–TCF pathway. However, the function of Ror2 in noncanonical Wnt signaling leading to cell migration is largely unknown. We show, using genetically different or manipulated cultured cells, that Ror2 is critical for Wnt5a-induced, but not Wnt3a-induced, cell migration. Ror2-mediated cell migration requires the extracellular cysteine-rich domain (CRD), which is the binding site for Wnt5a, and the cytoplasmic proline-rich domain (PRD) of Ror2. Furthermore, Ror2 can mediate filopodia formation via actin reorganization, irrespective of Wnt5a, and this Ror2-mediated filopodia formation requires the actin-binding protein filamin A, which associates with the PRD of Ror2. Intriguingly, disruption of filopodia formation by suppressing the expression of either Ror2 or filamin A inhibits Wnt5a-induced cell migration, indicating that Ror2-mediated filopodia formation is essential for Wnt5a-induced cell migration.

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