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Shuang Cui
Researcher at Children's Hospital of Philadelphia
Publications - 10
Citations - 374
Shuang Cui is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: Zebrafish & Biliary atresia. The author has an hindex of 9, co-authored 9 publications receiving 329 citations. Previous affiliations of Shuang Cui include University of Pennsylvania.
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Journal ArticleDOI
Evidence from human and zebrafish that GPC1 is a biliary atresia susceptibility gene.
Shuang Cui,Melissa Leyva–Vega,Ellen A. Tsai,Steven F. EauClaire,Joseph T. Glessner,Hakon Hakonarson,Marcella Devoto,Marcella Devoto,Barbara Haber,Nancy B. Spinner,Randolph P. Matthews +10 more
TL;DR: Based on genetic analysis of patients with BA and zebrafish, GPC1 appears to be a BA susceptibility gene, and these findings support a role for Hedgehog signaling in the pathogenesis of BA.
BASIC AND TRANSLATIONAL—BILIARY Evidence From Human and Zebrafish That GPC1 Is a Biliary Atresia Susceptibility Gene
Shuang Cui,Ellen A. Tsai,Steven F. EauClaire,Joseph T. Glessner,Hakon Hakonarson,Marcella Devoto,Barbara Haber,Nancy B. Spinner,Randolph P. Matthews +8 more
TL;DR: GPC1 appears to be a BA susceptibility gene based on genetic analysis of patients with BA and zebrafish as mentioned in this paper, which supports a role for Hedgehog signaling in the pathogenesis of BA.
Journal ArticleDOI
DNA hypomethylation causes bile duct defects in zebrafish and is a distinguishing feature of infantile biliary atresia.
Randolph P. Matthews,Steven F. EauClaire,Monica R. Mugnier,Kristin Lorent,Shuang Cui,Megan M. Ross,Zhe Zhang,Pierre Russo,Michael Pack +8 more
TL;DR: Inhibition of DNA methylation leads to biliary defects and activation of IFN‐γ‐responsive genes, thus sharing features with BA, which is determined to be associated with DNA hypomethylation.
Journal ArticleDOI
Loss of a Candidate Biliary Atresia Susceptibility Gene, add3a, Causes Biliary Developmental Defects in Zebrafish.
Vivian Tang,Zenobia C. Cofer,Shuang Cui,Valerie Sapp,Kathleen M. Loomes,Randolph P. Matthews +5 more
TL;DR: The results of morpholino antisense oligonucleotide knockdown studies targeting add3a and xpnpep1 in zebrafish support previous studies identifying ADD3 as a putative genetic risk factor for BA susceptibility and provide evidence thatAdd3a may be affecting the Hh pathway, an important factor in BA pathogenesis.
Journal ArticleDOI
Disruption of planar cell polarity activity leads to developmental biliary defects.
TL;DR: It is reported that in zebrafish, morpholino antisense oligonucleotide-mediated knockdown of PCP genes including prickle-1a (pk1a) led to developmental biliary abnormalities, as well as localization defects of the liver and other digestive organs.