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The role of the postsynaptic density in the pathology of the fragile X syndrome.

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The role of the postsynaptic density in the pathology of the fragile X syndrome. / Kindler, Stefan; Kreienkamp, Hans-Jürgen.

in: Results Probl Cell Differ, Jahrgang 54, 2012, S. 61-80.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Kindler, S & Kreienkamp, H-J 2012, 'The role of the postsynaptic density in the pathology of the fragile X syndrome.', Results Probl Cell Differ, Jg. 54, S. 61-80. <http://www.ncbi.nlm.nih.gov/pubmed/22009348?dopt=Citation>

APA

Kindler, S., & Kreienkamp, H-J. (2012). The role of the postsynaptic density in the pathology of the fragile X syndrome. Results Probl Cell Differ, 54, 61-80. http://www.ncbi.nlm.nih.gov/pubmed/22009348?dopt=Citation

Vancouver

Kindler S, Kreienkamp H-J. The role of the postsynaptic density in the pathology of the fragile X syndrome. Results Probl Cell Differ. 2012;54:61-80.

Bibtex

@article{78e500ab01764a80acf93f6a0102f554,
title = "The role of the postsynaptic density in the pathology of the fragile X syndrome.",
abstract = "The protein repertoire of excitatory synapses controls dendritic spine morphology, synaptic plasticity and higher brain functions. In brain neurons, the RNA-associated fragile X mental retardation protein (FMRP) binds in vivo to various transcripts encoding key postsynaptic components and may thereby substantially regulate the molecular composition of dendritic spines. In agreement with this notion functional loss of FMRP in patients affected by the fragile X syndrome (FXS) causes cognitive impairment. Here we address our current understanding of the functional role of individual postsynaptic proteins. We discuss how FMRP controls the abundance of select proteins at postsynaptic sites, which signaling pathways regulate the local activity of FMRP at synapses, and how altered levels of postsynaptic proteins may contribute to FXS pathology.",
keywords = "Animals, Humans, Gene Expression Regulation, RNA, Messenger/metabolism, Membrane Proteins/genetics/metabolism, Fragile X Mental Retardation Protein/genetics/metabolism, Fragile X Syndrome/*pathology/*physiopathology, Post-Synaptic Density/*physiology/ultrastructure, Animals, Humans, Gene Expression Regulation, RNA, Messenger/metabolism, Membrane Proteins/genetics/metabolism, Fragile X Mental Retardation Protein/genetics/metabolism, Fragile X Syndrome/*pathology/*physiopathology, Post-Synaptic Density/*physiology/ultrastructure",
author = "Stefan Kindler and Hans-J{\"u}rgen Kreienkamp",
year = "2012",
language = "English",
volume = "54",
pages = "61--80",

}

RIS

TY - JOUR

T1 - The role of the postsynaptic density in the pathology of the fragile X syndrome.

AU - Kindler, Stefan

AU - Kreienkamp, Hans-Jürgen

PY - 2012

Y1 - 2012

N2 - The protein repertoire of excitatory synapses controls dendritic spine morphology, synaptic plasticity and higher brain functions. In brain neurons, the RNA-associated fragile X mental retardation protein (FMRP) binds in vivo to various transcripts encoding key postsynaptic components and may thereby substantially regulate the molecular composition of dendritic spines. In agreement with this notion functional loss of FMRP in patients affected by the fragile X syndrome (FXS) causes cognitive impairment. Here we address our current understanding of the functional role of individual postsynaptic proteins. We discuss how FMRP controls the abundance of select proteins at postsynaptic sites, which signaling pathways regulate the local activity of FMRP at synapses, and how altered levels of postsynaptic proteins may contribute to FXS pathology.

AB - The protein repertoire of excitatory synapses controls dendritic spine morphology, synaptic plasticity and higher brain functions. In brain neurons, the RNA-associated fragile X mental retardation protein (FMRP) binds in vivo to various transcripts encoding key postsynaptic components and may thereby substantially regulate the molecular composition of dendritic spines. In agreement with this notion functional loss of FMRP in patients affected by the fragile X syndrome (FXS) causes cognitive impairment. Here we address our current understanding of the functional role of individual postsynaptic proteins. We discuss how FMRP controls the abundance of select proteins at postsynaptic sites, which signaling pathways regulate the local activity of FMRP at synapses, and how altered levels of postsynaptic proteins may contribute to FXS pathology.

KW - Animals

KW - Humans

KW - Gene Expression Regulation

KW - RNA, Messenger/metabolism

KW - Membrane Proteins/genetics/metabolism

KW - Fragile X Mental Retardation Protein/genetics/metabolism

KW - Fragile X Syndrome/pathology/physiopathology

KW - Post-Synaptic Density/physiology/ultrastructure

KW - Animals

KW - Humans

KW - Gene Expression Regulation

KW - RNA, Messenger/metabolism

KW - Membrane Proteins/genetics/metabolism

KW - Fragile X Mental Retardation Protein/genetics/metabolism

KW - Fragile X Syndrome/pathology/physiopathology

KW - Post-Synaptic Density/physiology/ultrastructure

M3 - SCORING: Journal article

VL - 54

SP - 61

EP - 80

ER -