gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

SH3 and multiple ankyrin repeat domains 1

Shank1, SSTRIP, Synamon, Shank1a
a scaffold protein in the post synaptic density that forms a complex with GKAP and PSD-95 [RGD, Feb 2006] (from NCBI)
Sponsored links
Top mentioned proteins: Shank, CAN, PSD-95, V1a, somatostatin
Papers on Shank1
Developmental neurogenetics and multimodal neuroimaging of sex differences in autism.
GENDAAR Research Consortium et al., Los Angeles, United States. In Brain Imaging Behav, Feb 2016
DRD1, NLGN3, MAOA, and SHANK1 deletion have been discovered in ASD.
Mice with Shank3 Mutations Associated with ASD and Schizophrenia Display Both Shared and Distinct Defects.
Feng et al., Cambridge, United States. In Neuron, Feb 2016
Furthermore, we found differential Shank3 mRNA stability and SHANK1/2 upregulation in these two lines.
SHANK1 and autism spectrum disorders.
Wang et al., Shanghai, China. In Sci China Life Sci, Oct 2015
Recently, deletions and point mutations of the SHANK1 gene have been detected in ASD individuals, indicating the involvement of SHANK1 in ASD.
Early communication deficits in the Shank1 knockout mouse model for autism spectrum disorder: Developmental aspects and effects of social context.
Wöhr et al., Marburg an der Lahn, Germany. In Autism Res, Oct 2015
Here, we studied communication by means of isolation-induced pup ultrasonic vocalizations (USV) in the Shank1 mouse model for ASD by comparing Shank1(-/-) null mutant, Shank1(+/-) heterozygous, and Shank1(+/+) wildtype littermate controls.
Shank1 regulates excitatory synaptic transmission in mouse hippocampal parvalbumin-expressing inhibitory interneurons.
Futai et al., Worcester, United States. In Eur J Neurosci, Apr 2015
The Shank genes (SHANK1, 2, 3) encode scaffold proteins highly enriched in postsynaptic densities where they regulate synaptic structure in spiny neurons.
The JNK1/JNK3 interactome--contributions by the JNK3 unique N-terminus and JNK common docking site residues.
Bogoyevitch et al., Melbourne, Australia. In Biochem Biophys Res Commun, 2014
ΔN JNK3α1), and interaction evaluation in the yeast two-hybrid system defined the interacting partners as either JNK1-specific interactors (ATF7, FUS, KCNE4, PIAS1, SHANK1, TKT), typical JBD-dependent interactors shared by JNK1α1 and JNK3α1 (AKAP6, BMPR2, EEF1A1, GFAP, GRIP2, GTF2F1, HDAC2, MAP1B, MYO9B, PTPN2, RABGAP1, RUSC2, SUMO1, SYPL1, TOPBP1, ZNF668), or JNK3-specific partners (ATXN1, NNAT, PTGDS) dependent on interaction with the JNK3 N-terminal extension.
Meta-analysis of SHANK Mutations in Autism Spectrum Disorders: a gradient of severity in cognitive impairments.
Bourgeron et al., Paris, France. In Plos Genet, 2014
In neurons, SHANK2 and SHANK3 have a positive effect on the induction and maturation of dendritic spines, whereas SHANK1 induces the enlargement of spine heads.
Repetitive behaviors in the Shank1 knockout mouse model for autism spectrum disorder: developmental aspects and effects of social context.
Wöhr et al., Marburg an der Lahn, Germany. In J Neurosci Methods, 2014
Several ASD candidate genes have been identified, including the SHANK gene family with its three family members SHANK1, SHANK2, and SHANK3.
Ultrasonic vocalizations in Shank mouse models for autism spectrum disorders: detailed spectrographic analyses and developmental profiles.
Wöhr, Marburg an der Lahn, Germany. In Neurosci Biobehav Rev, 2014
Among the most promising candidate genes for ASD is the SHANK gene family, including SHANK1, SHANK2 (ProSAP1), and SHANK3 (ProSAP2).
The emerging role of SHANK genes in neuropsychiatric disorders.
Bourgeron et al., Paris, France. In Dev Neurobiol, 2014
This review focuses on the disorders associated with mutations in SHANK3 and the other members of its family, SHANK1 and SHANK2.
A subset of genomic alterations detected in rolandic epilepsies contains candidate or known epilepsy genes including GRIN2A and PRRT2.
Sanlaville et al., Lyon, France. In Epilepsia, 2014
The CNVs of highest interest comprised or disrupted strong candidate or confirmed genes for epileptic and other neurodevelopmental disorders, including BRWD3, GRIN2A, KCNC3, PRKCE, PRRT2, SHANK1, and TSPAN7.
Dysfunction of SHANK2 and CHRNA7 in a patient with intellectual disability and language impairment supports genetic epistasis of the two loci.
Kutsche et al., Hamburg, Germany. In Clin Genet, 2013
They have been associated with mutations in genes encoding proteins important for the formation and stabilization of synapses, such as SHANK1-3.
Modeling autism by SHANK gene mutations in mice.
Ehlers et al., Durham, United States. In Neuron, 2013
Shank family proteins (Shank1, Shank2, and Shank3) are synaptic scaffolding proteins that organize an extensive protein complex at the postsynaptic density (PSD) of excitatory glutamatergic synapses.
SHANK1 Deletions in Males with Autism Spectrum Disorder.
Scherer et al., Toronto, Canada. In Am J Hum Genet, 2012
A hemizygous SHANK1 deletion segregates in a four-generation family in which male carriers--but not female carriers--have autism spectrum disorder with higher functioning.
A promoter variant of SHANK1 affects auditory working memory in schizophrenia patients and in subjects clinically at risk for psychosis.
Mössner et al., Bonn, Germany. In Eur Arch Psychiatry Clin Neurosci, 2012
The results of this study suggested a role of SHANK1 in working memory deficits in schizophrenia.
The structural flexibility of the shank1 PDZ domain is important for its binding to different ligands.
Eom et al., Inch'ŏn, South Korea. In Biochem Biophys Res Commun, 2011
this study provides a new level of understanding of the specificity and structural plasticity of the shank PDZ domain.
Sociability and motor functions in Shank1 mutant mice.
Crawley et al., Bethesda, United States. In Brain Res, 2011
Shank1 null mice do not demonstrate autism-relevant social interaction deficits, but confirm and extend a role for Shank1 in motor functions.
Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
Crawley et al., Bethesda, United States. In Plos One, 2010
The reduced levels of ultrasonic vocalizations and scent marking behavior in Shank1(-/-) mice are consistent with a phenotype relevant to social communication deficits in autism.
Interaction of G-protein-coupled receptors with synaptic scaffolding proteins.
Böckers et al., Hamburg, Germany. In Biochem Soc Trans, 2002
By yeast two-hybrid screening, we have identified the intracellular C-termini of CIRL1 and CIRL2 as interaction partners of the PDZ domain of the proline-rich synapse-associated protein (ProSAP)/somatostatin receptor-interacting protein (SSTRIP) family of postsynaptic proteins (SSTRIP, ProSAP1 and ProSAP2, also known as shank1-shank3 respectively).
share on facebooktweetadd +1mail to friends