About: James S. Sutcliffe

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

molecular physiologist

Attributes	Values
rdf:type	Item
description	forskare (sv) 연구원 (ko) 研究者 (ja) araştırmacı (tr) wetenschapper (nl) дослідник (uk) वैज्ञानिक (hi) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy) hulumtues (sq) molecular physiologist (en)
rdfs:label	James S Sutcliffe (nl) James S Sutcliffe (sl) James S. Sutcliffe (en)
skos:prefLabel	James S Sutcliffe (nl) James S Sutcliffe (sl) James S. Sutcliffe (en)
name	James S Sutcliffe (nl) James S Sutcliffe (sl) James S. Sutcliffe (en)
affiliation	wds:Q37651326-45F97D48-C527-4E07-A0D1-7870008A58CF
affiliation	Vanderbilt Department of Molecular Physiology and Biophysics
Scopus author ID	wds:Q37651326-D2FB630F-2F6E-4A63-AD70-32A41847DE72
Scopus author ID	7101638712
given name	wds:Q37651326-C8AB1F66-A5D4-430A-886D-22278F0C2886
given name	James
instance of	wds:Q37651326-3CDE61BA-35BB-4455-A742-54C6CDC8FDA1
instance of	Homo sapiens
Loop ID	wds:Q37651326-8DF320B4-97B6-4C5E-8D3F-28CD60DC85B3
Loop ID	683697
skos:altLabel	JS Sutcliffe (en) James Sutcliffe (en) Sutcliffe, JS (en)
occupation	wds:Q37651326-60A1365F-95DD-4ED8-90C0-3201CBCBD86F
employer	wds:Q37651326-78A90C44-3578-4AF4-B305-229FA1254096 wds:Q37651326-B9674749-0CBF-48B6-8905-00EF5C73B242 wds:Q37651326-E334A2DB-A26F-4702-A7D7-C35A67FAAF3A wds:Q37651326-F11937B6-E6DC-46B1-AC02-ED914929C3CB
sex or gender	wds:Q37651326-68F4538C-CE3D-4E97-8800-8E18EC86F9CB
educated at	wds:Q37651326-1CB21118-3488-4664-B930-D362B635FB74 wds:Q37651326-7492480B-7E32-46CD-A9E0-A2981F6DABD3
family name	wds:Q37651326-19A60C59-16EB-4D2B-858E-088395C0F498
occupation	researcher
employer	Vanderbilt University Vanderbilt University School of Medicine Baylor College of Medicine Emory University School of Medicine
sex or gender	male
educated at	Auburn University Baylor College of Medicine
family name	Sutcliffe
ORCID iD	wds:Q37651326-95102537-0E60-4061-A94B-A14FB50E961D
ORCID iD	https://orcid.org/0000-0001-5200-6007
ORCID iD	0000-0001-5200-6007
ResearcherID	wds:Q37651326-C459B2FD-91E4-4335-8E0A-BACA21D6B010
Publons author ID	wds:Q37651326-826c0883-be3e-40e7-9260-d1307f21326b
ResearcherID	C-1348-2012
Publons author ID	2748759
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q37651326
is author of	Allelic heterogeneity at the serotonin transporter locus (SLC6A4) confers susceptibility to autism and rigid-compulsive behaviors Genome-wide and Ordered-Subset linkage analyses provide support for autism loci on 17q and 19p with evidence of phenotypic and interlocus genetic correlates Exploratory subsetting of autism families based on savant skills improves evidence of genetic linkage to 15q11-q13 Distinct genetic risk based on association of MET in families with co-occurring autism and gastrointestinal conditions A linkage disequilibrium map of the 1-Mb 15q12 GABA(A) receptor subunit cluster and association to autism. Human serotonin transporter variants display altered sensitivity to protein kinase G and p38 mitogen-activated protein kinase Loci nominally associated with autism from genome-wide analysis show enrichment of brain expression quantitative trait loci but not lymphoblastoid cell line expression quantitative trait loci Genetics. Insights into the pathogenesis of autism. Rare familial 16q21 microdeletions under a linkage peak implicate cadherin 8 (CDH8) in susceptibility to autism and learning disability Rare complete knockouts in humans: population distribution and significant role in autism spectrum disorders Autism genome-wide copy number variation reveals ubiquitin and neuronal genes Genome-wide analyses of exonic copy number variants in a family-based study point to novel autism susceptibility genes A framework for the interpretation of de novo mutation in human disease Microduplications of 16p11.2 are associated with schizophrenia Contribution of SHANK3 mutations to autism spectrum disorder A genetic variant that disrupts MET transcription is associated with autism De novo truncating mutations in E6-AP ubiquitin-protein ligase gene (UBE3A) in Angelman syndrome. Individual common variants exert weak effects on the risk for autism spectrum disorders Functional impact of global rare copy number variation in autism spectrum disorders Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome Tissue specific expression of FMR-1 provides evidence for a functional role in fragile X syndrome. Deletions of a differentially methylated CpG island at the SNRPN gene define a putative imprinting control region Autism gene variant causes hyperserotonemia, serotonin receptor hypersensitivity, social impairment and repetitive behavior A novel approach of homozygous haplotype sharing identifies candidate genes in autism spectrum disorder The spectrum of mutations in UBE3A causing Angelman syndrome Strong association of de novo copy number mutations with autism Recurrent rearrangements of chromosome 1q21.1 and variable pediatric phenotypes Mapping autism risk loci using genetic linkage and chromosomal rearrangements Patterns and rates of exonic de novo mutations in autism spectrum disorders A genome-wide scan for common alleles affecting risk for autism Synaptic, transcriptional and chromatin genes disrupted in autism Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism Common genetic variants on 5p14.1 associate with autism spectrum disorders Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs Convergence of genes and cellular pathways dysregulated in autism spectrum disorders Insights into Autism Spectrum Disorder Genomic Architecture and Biology from 71 Risk Loci Parent-of-origin effects of the serotonin transporter gene associated with autism Molecular genetics of the platelet serotonin system in first-degree relatives of patients with autism Genetic analysis of biological pathway data through genomic randomization

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