Judith S Eisen, James C Smith. Development 2008
Times Cited: 437
Times Cited: 437
Times Cited
Times Co-cited
Similarity
Guidelines for morpholino use in zebrafish.
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Genetic compensation induced by deleterious mutations but not gene knockdowns.
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A primer for morpholino use in zebrafish.
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p53 activation by knockdown technologies.
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The zebrafish reference genome sequence and its relationship to the human genome.
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Genetic compensation triggered by mutant mRNA degradation.
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Estrogens Suppress a Behavioral Phenotype in Zebrafish Mutants of the Autism Risk Gene, CNTNAP2.
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Disruptive CHD8 mutations define a subtype of autism early in development.
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Lessons from morpholino-based screening in zebrafish.
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Genetic compensation: A phenomenon in search of mechanisms.
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Fiji: an open-source platform for biological-image analysis.
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Morpholino antisense oligomers: design, preparation, and properties.
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CHD8 regulates neurodevelopmental pathways associated with autism spectrum disorder in neural progenitors.
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The first mecp2-null zebrafish model shows altered motor behaviors.
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Two knockdown models of the autism genes SYNGAP1 and SHANK3 in zebrafish produce similar behavioral phenotypes associated with embryonic disruptions of brain morphogenesis.
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Highly efficient CRISPR/Cas9-mediated knock-in in zebrafish by homology-independent DNA repair.
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Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2.
Michael I Love, Wolfgang Huber, Simon Anders. Genome Biol 2014
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A meckelin-filamin A interaction mediates ciliogenesis.
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A genetic screen for mutations affecting embryogenesis in zebrafish.
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6
Number of inadvertent RNA targets for morpholino knockdown in Danio rerio is largely underestimated: evidence from the study of Ser/Arg-rich splicing factors.
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CRISPR/Cas9-induced shank3b mutant zebrafish display autism-like behaviors.
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A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity.
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Zebrafish knockout of Down syndrome gene, DYRK1A, shows social impairments relevant to autism.
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Heritable gene targeting in zebrafish using customized TALENs.
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Function and regulation of AUTS2, a gene implicated in autism and human evolution.
Nir Oksenberg, Laurie Stevison, Jeffrey D Wall, Nadav Ahituv. PLoS Genet 2013
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Reverse Genetics in Zebrafish: Mutants, Morphants, and Moving Forward.
Nathan D Lawson. Trends Cell Biol 2016
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Drug screening in Scn1a zebrafish mutant identifies clemizole as a potential Dravet syndrome treatment.
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Precise and efficient genome editing in zebrafish using the CRISPR/Cas9 system.
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HTSeq--a Python framework to work with high-throughput sequencing data.
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A genetic screen in zebrafish identifies cilia genes as a principal cause of cystic kidney.
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Convergent extension movements and ciliary function are mediated by ofd1, a zebrafish orthologue of the human oral-facial-digital type 1 syndrome gene.
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De novo loss-of-function mutations in CHD2 cause a fever-sensitive myoclonic epileptic encephalopathy sharing features with Dravet syndrome.
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Morpholino antisense oligonucleotides: tools for investigating vertebrate development.
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Zebrafish models of autism spectrum disorder.
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Methyl-CpG Binding Protein 2 (Mecp2) Regulates Sensory Function Through Sema5b and Robo2.
Wan Y Leong, Zhi H Lim, Vladimir Korzh, Thomas Pietri, Eyleen L K Goh. Front Cell Neurosci 2015
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In vivo imaging of embryonic vascular development using transgenic zebrafish.
Nathan D Lawson, Brant M Weinstein. Dev Biol 2002
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Efficient mutagenesis by Cas9 protein-mediated oligonucleotide insertion and large-scale assessment of single-guide RNAs.
James A Gagnon, Eivind Valen, Summer B Thyme, Peng Huang, Laila Akhmetova, Andrea Pauli, Tessa G Montague, Steven Zimmerman, Constance Richter, Alexander F Schier. PLoS One 2014
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5
Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.