J
Jennifer L. Moran
Researcher at Broad Institute
Publications - 119
Citations - 41227
Jennifer L. Moran is an academic researcher from Broad Institute. The author has contributed to research in topics: Genome-wide association study & Copy-number variation. The author has an hindex of 54, co-authored 114 publications receiving 33978 citations. Previous affiliations of Jennifer L. Moran include Scott & White Hospital & University of Illinois at Chicago.
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Journal ArticleDOI
Rescue of the mouse DDK syndrome by parent-of-origin-dependent modifiers.
Folami Y. Ideraabdullah,Kuikwon Kim,Daniel Pomp,Jennifer L. Moran,David R. Beier,Fernando Pardo-Manuel de Villena +5 more
TL;DR: The experiments demonstrate that PERA or PERC alleles at Rmod1 rescue lethality independently of allelic exclusion, and rescue of the lethal phenotype depends on the parental origin of the R mod1 alleles; transmission through the dam leads to rescue, while transmission throughThe sire has no effect.
Journal ArticleDOI
Latent TGF-β-binding protein 4 modifies muscular dystrophy in mice (The Journal of Clinical Investigation (2010) 120, 2, (645) DOI: 10.1172/JCI39845)
Journal ArticleDOI
A mouse model of Waardenburg syndrome type IV resulting from an ENU-induced mutation in endothelin 3.
Ivana Matera,Jody L. Cockroft,Jennifer L. Moran,David R. Beier,Dan Goldowitz,William J. Pavan +5 more
TL;DR: The power of using ENU mutagenesis screens to generate new animal models of human disease, and expands the spectrum of EDN3 mutant alleles, is demonstrated.
Journal ArticleDOI
An N-ethyl-N-nitrosourea mutagenesis recessive screen identifies two candidate regions for murine cardiomyopathy that map to chromosomes 1 and 15.
TL;DR: Using noninvasive echocardiography to screen for abnormalities in cardiac function, a heritable cardiomyopathic phenotype is identified in two families and the genes responsible for the observed phenotype will be strong candidates for disease-causing or disease-modifying genes in patients with heart failure.
Posted ContentDOI
Schizophrenia risk conferred by protein-coding de novo mutations
Daniel P. Howrigan,Samuel A. Rose,Samuel A. Rose,Kaitlin E. Samocha,Menachem Fromer,Menachem Fromer,Felecia Cerrato,Wei J. Chen,Claire Churchhouse,Kimberly Chambert,Sharon D. Chandler,Mark J. Daly,Ashley Dumont,Giulio Genovese,Hai-Gwo Hwu,Nan M. Laird,Jack A. Kosmicki,Jennifer L. Moran,Cheryl A. Roe,Tarjinder Singh,Shi-Heng Wang,Stephen V. Faraone,Stephen J. Glatt,Steven A. McCarroll,Steven A. McCarroll,Ming T. Tsuang,Benjamin M. Neale +26 more
TL;DR: Gene set analyses show that the modest increase in risk from DNMs in SCZ probands is concentrated in genes that are either highly brain expressed, under strong evolutionary constraint, and/or overlap with genes identified as DNM risk factors in other neurodevelopmental disorders.