Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation.

Standard

Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation. / Leemhuis, Jost; Bouché, Elisabeth; Frotscher, Michael; Henle, Frank; Hein, Lutz; Herz, Joachim; Meyer, Dieter K; Pichler, Marina; Roth, Günter; Schwan, Carsten; Bock, Hans H.

in: J NEUROSCI, Jahrgang 30, Nr. 44, 44, 2010, S. 14759-14772.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Leemhuis, J, Bouché, E, Frotscher, M, Henle, F, Hein, L, Herz, J, Meyer, DK, Pichler, M, Roth, G, Schwan, C & Bock, HH 2010, 'Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation.', J NEUROSCI, Jg. 30, Nr. 44, 44, S. 14759-14772. <http://www.ncbi.nlm.nih.gov/pubmed/21048135?dopt=Citation>

APA

Leemhuis, J., Bouché, E., Frotscher, M., Henle, F., Hein, L., Herz, J., Meyer, D. K., Pichler, M., Roth, G., Schwan, C., & Bock, H. H. (2010). Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation. J NEUROSCI, 30(44), 14759-14772. [44]. http://www.ncbi.nlm.nih.gov/pubmed/21048135?dopt=Citation

Vancouver

Leemhuis J, Bouché E, Frotscher M, Henle F, Hein L, Herz J et al. Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation. J NEUROSCI. 2010;30(44):14759-14772. 44.

Bibtex

@article{b7938cb7fe544141862dc137044c7266,
title = "Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation.",
abstract = "Lipoprotein receptor signaling regulates the positioning and differentiation of postmitotic neurons during development and modulates neuronal plasticity in the mature brain. Depending on the contextual situation, the lipoprotein receptor ligand Reelin can have opposing effects on cortical neurons. We show that Reelin increases growth cone motility and filopodia formation, and identify the underlying signaling cascade. Reelin activates the Rho GTPase Cdc42, known for its role in neuronal morphogenesis and directed migration, in an apolipoprotein E receptor 2-, Disabled-1-, and phosphatidylinositol 3-kinase-dependent manner. We demonstrate that neuronal vesicle trafficking, a Cdc42-controlled process, is increased after Reelin treatment and further provide evidence that the peptidergic VIP/PACAP38 system and Reelin can functionally interact to promote axonal branching. In conclusion, Reelin-induced activation of Cdc42 contributes to the regulation of the cytoskeleton of individual responsive neurons and converges with other signaling cascades to orchestrate Rho GTPase activity and promote neuronal development. Our data link the observation that defects in Rho GTPases and Reelin signaling are responsible for developmental defects leading to neurological and psychiatric disorders.",
keywords = "Animals, Humans, Cells, Cultured, Mice, Mice, Knockout, Rats, Signal Transduction genetics, Animals, Newborn, Organ Culture Techniques, Cell Movement genetics, Cell Adhesion Molecules, Neuronal genetics, Cerebral Cortex embryology, Extracellular Matrix Proteins genetics, Growth Cones metabolism, HEK293 Cells, Nerve Tissue Proteins genetics, Phosphatidylinositol 3-Kinases genetics, Pseudopodia genetics, Receptors, Lipoprotein genetics, Serine Endopeptidases genetics, cdc42 GTP-Binding Protein genetics, Animals, Humans, Cells, Cultured, Mice, Mice, Knockout, Rats, Signal Transduction genetics, Animals, Newborn, Organ Culture Techniques, Cell Movement genetics, Cell Adhesion Molecules, Neuronal genetics, Cerebral Cortex embryology, Extracellular Matrix Proteins genetics, Growth Cones metabolism, HEK293 Cells, Nerve Tissue Proteins genetics, Phosphatidylinositol 3-Kinases genetics, Pseudopodia genetics, Receptors, Lipoprotein genetics, Serine Endopeptidases genetics, cdc42 GTP-Binding Protein genetics",
author = "Jost Leemhuis and Elisabeth Bouch{\'e} and Michael Frotscher and Frank Henle and Lutz Hein and Joachim Herz and Meyer, {Dieter K} and Marina Pichler and G{\"u}nter Roth and Carsten Schwan and Bock, {Hans H}",
year = "2010",
language = "Deutsch",
volume = "30",
pages = "14759--14772",
journal = "J NEUROSCI",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "44",

}

RIS

TY - JOUR

T1 - Reelin signals through apolipoprotein E receptor 2 and Cdc42 to increase growth cone motility and filopodia formation.

AU - Leemhuis, Jost

AU - Bouché, Elisabeth

AU - Frotscher, Michael

AU - Henle, Frank

AU - Hein, Lutz

AU - Herz, Joachim

AU - Meyer, Dieter K

AU - Pichler, Marina

AU - Roth, Günter

AU - Schwan, Carsten

AU - Bock, Hans H

PY - 2010

Y1 - 2010

N2 - Lipoprotein receptor signaling regulates the positioning and differentiation of postmitotic neurons during development and modulates neuronal plasticity in the mature brain. Depending on the contextual situation, the lipoprotein receptor ligand Reelin can have opposing effects on cortical neurons. We show that Reelin increases growth cone motility and filopodia formation, and identify the underlying signaling cascade. Reelin activates the Rho GTPase Cdc42, known for its role in neuronal morphogenesis and directed migration, in an apolipoprotein E receptor 2-, Disabled-1-, and phosphatidylinositol 3-kinase-dependent manner. We demonstrate that neuronal vesicle trafficking, a Cdc42-controlled process, is increased after Reelin treatment and further provide evidence that the peptidergic VIP/PACAP38 system and Reelin can functionally interact to promote axonal branching. In conclusion, Reelin-induced activation of Cdc42 contributes to the regulation of the cytoskeleton of individual responsive neurons and converges with other signaling cascades to orchestrate Rho GTPase activity and promote neuronal development. Our data link the observation that defects in Rho GTPases and Reelin signaling are responsible for developmental defects leading to neurological and psychiatric disorders.

AB - Lipoprotein receptor signaling regulates the positioning and differentiation of postmitotic neurons during development and modulates neuronal plasticity in the mature brain. Depending on the contextual situation, the lipoprotein receptor ligand Reelin can have opposing effects on cortical neurons. We show that Reelin increases growth cone motility and filopodia formation, and identify the underlying signaling cascade. Reelin activates the Rho GTPase Cdc42, known for its role in neuronal morphogenesis and directed migration, in an apolipoprotein E receptor 2-, Disabled-1-, and phosphatidylinositol 3-kinase-dependent manner. We demonstrate that neuronal vesicle trafficking, a Cdc42-controlled process, is increased after Reelin treatment and further provide evidence that the peptidergic VIP/PACAP38 system and Reelin can functionally interact to promote axonal branching. In conclusion, Reelin-induced activation of Cdc42 contributes to the regulation of the cytoskeleton of individual responsive neurons and converges with other signaling cascades to orchestrate Rho GTPase activity and promote neuronal development. Our data link the observation that defects in Rho GTPases and Reelin signaling are responsible for developmental defects leading to neurological and psychiatric disorders.

KW - Animals

KW - Humans

KW - Cells, Cultured

KW - Mice

KW - Mice, Knockout

KW - Rats

KW - Signal Transduction genetics

KW - Animals, Newborn

KW - Organ Culture Techniques

KW - Cell Movement genetics

KW - Cell Adhesion Molecules, Neuronal genetics

KW - Cerebral Cortex embryology

KW - Extracellular Matrix Proteins genetics

KW - Growth Cones metabolism

KW - HEK293 Cells

KW - Nerve Tissue Proteins genetics

KW - Phosphatidylinositol 3-Kinases genetics

KW - Pseudopodia genetics

KW - Receptors, Lipoprotein genetics

KW - Serine Endopeptidases genetics

KW - cdc42 GTP-Binding Protein genetics

KW - Animals

KW - Humans

KW - Cells, Cultured

KW - Mice

KW - Mice, Knockout

KW - Rats

KW - Signal Transduction genetics

KW - Animals, Newborn

KW - Organ Culture Techniques

KW - Cell Movement genetics

KW - Cell Adhesion Molecules, Neuronal genetics

KW - Cerebral Cortex embryology

KW - Extracellular Matrix Proteins genetics

KW - Growth Cones metabolism

KW - HEK293 Cells

KW - Nerve Tissue Proteins genetics

KW - Phosphatidylinositol 3-Kinases genetics

KW - Pseudopodia genetics

KW - Receptors, Lipoprotein genetics

KW - Serine Endopeptidases genetics

KW - cdc42 GTP-Binding Protein genetics

M3 - SCORING: Zeitschriftenaufsatz

VL - 30

SP - 14759

EP - 14772

JO - J NEUROSCI

JF - J NEUROSCI

SN - 0270-6474

IS - 44

M1 - 44

ER -