Mitogenesis and endocytosis: What's at the INTERSECTIoN?

O’Bryan, John P.; Mohney, Robert P.; Oldham, Carla E.

doi:10.1038/sj.onc.1204773

Cited by 52 publications

(59 citation statements)

References 80 publications

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“…For example, synaptojanin 1, a polyphosphoinositide phosphatase, is involved in uncoating of clathrin-coated vesicles and in the downregulation of actin polymerization at endocytic zones (Slepnev and De Camilli, 2000). Similarly, intersectin 1 is a scaffolding protein that interacts with a number of proteins needed either for clathrinmediated endocytosis or for actin assembly (O'Bryan et al, 2001;Schafer, 2002) and appears to link membrane-trafficking events with downstream signaling. Grik1, the gene encoding the GluR5 (glutamate receptor 5) subunit of kainate receptors, is also present in three copies in Ts65Dn.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal Long-Term Potentiation Suppressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down Syndrome

Kleschevnikov¹,

Belichenko²,

Villar³

et al. 2004

J. Neurosci.

434

399

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Although many genetic disorders are characterized by cognitive failure during development, there is little insight into the neurobiological basis for the abnormalities. Down syndrome (DS), a disorder caused by the presence of three copies of chromosome 21 (trisomy 21), is characterized by impairments in learning and memory attributable to dysfunction of the hippocampus. We explored the cellular basis for these abnormalities in Ts65Dn mice, a genetic model for DS. Although basal synaptic transmission in the dentate gyrus was normal, there was severe impairment of long-term potentiation (LTP) as a result of reduced activation of NMDA receptors. After suppressing inhibition with picrotoxin, a GABA A receptor antagonist, NMDA receptor-mediated currents were normalized and induction of LTP was restored. Several lines of evidence suggest that inhibition in the Ts65Dn dentate gyrus was enhanced, at least in part, because of presynaptic abnormalities. These findings raise the possibility that similar changes contribute to abnormalities in learning and memory in people with DS and, perhaps, in other developmental disorders with cognitive failure.

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Section: Discussionmentioning

confidence: 99%

Hippocampal Long-Term Potentiation Suppressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down Syndrome

Kleschevnikov¹,

Belichenko²,

Villar³

et al. 2004

J. Neurosci.

434

399

View full text Add to dashboard Cite

show abstract

“…Intersectin is a component of clathrin-coated vesicles, and has been termed an ' endocytic scaffold ' for its ability to cluster key endocytic components, including Eps15 (epidermal-growth-factor-receptor-pathway substrate 15) and dynamin [56]. The two mammalian intersectins are each produced as two splice variants, with the long forms gaining an exchange-factor domain specific for Cdc42 [57].…”

Section: Cdc42 and Intersectinmentioning

confidence: 99%

Regulation of endocytic traffic by Rho GTPases

Qualmann

Mellor

2003

Biochemical Journal

115

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The members of the Rho subfamily of small GTPases are key regulators of the actin cytoskeleton. However, recent studies have provided evidence for multiple additional roles for these signalling proteins in controlling endocytic traffic. Here we review our current understanding of Rho GTPase action within the endocytic pathway and examine the potential points of convergence with the more established, actin-based functions of these signalling proteins.

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“…3 Cellular functions 3.1 Endocytosis and exocytosis Intersectin 1 is regarded as an adaptor protein, according that it has the ability to bind different kinds of proteins and can interact to each other by its various domains [15] . Recent research has indicated that intersectin 1 participates in both endocytosis and exocytosis and regulates different intra-cellular signaling transduction pathways.…”

Section: Distribution In the Central Nervous Systemmentioning

confidence: 99%

“…Northern blotting analysis reported that the ratio of mRNA of intersectin 1-L to intersectin 1-S expression in the brain increased after birth. Therefore, the expressions of intersectin 1-L and intersectin 1-S are strictly regulated in each cell or tissue type [15] .…”

Section: Isoform Specificitymentioning

confidence: 99%

Intersectin 1: a molecular linker in the central nervous system

Niu

Jie

2008

Neurosci. Bull.

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Down syndrome (DS) is the most common cause of cognitive impairment associated with a congenital chromosomal abnormality, trisomy of chromosome 21. Mental retardation and congenital heart defects are key features of DS. All DS individuals develop early-onset Alzheimer's disease-like neuropathology. Intersectin 1 gene is localized on human chromosome 21, the critical region of DS, and it has higher expression in the brain of DS patients than in normal individuals. So fully understanding functions of intersectin 1 is critical for revealing the pathogenesis of DS. Intersectin 1 protein has two isoforms: intersectin 1-L and intersectin 1-S. This review will focus on the distribution, expression characters and functions of intersectin 1 in the central nervous system.

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Mitogenesis and endocytosis: What's at the INTERSECTIoN?

Cited by 52 publications

References 80 publications

Hippocampal Long-Term Potentiation Suppressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down Syndrome

Hippocampal Long-Term Potentiation Suppressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down Syndrome

Regulation of endocytic traffic by Rho GTPases

Intersectin 1: a molecular linker in the central nervous system

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