R
Roberto Buccafusca
Researcher at Boston Children's Hospital
Publications - 18
Citations - 681
Roberto Buccafusca is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Inositol & Lithium (medication). The author has an hindex of 11, co-authored 13 publications receiving 604 citations. Previous affiliations of Roberto Buccafusca include Beth Israel Deaconess Medical Center & George Washington University.
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Journal ArticleDOI
Carbamylation of Serum Albumin as a Risk Factor for Mortality in Patients with Kidney Failure
Anders H. Berg,Christiane Drechsler,Julia Wenger,Roberto Buccafusca,Roberto Buccafusca,Tammy Hod,Sahir Kalim,Wenda Ramma,Samir M. Parikh,Hanno Steen,David J. Friedman,John Danziger,Christoph Wanner,Ravi Thadhani,S. Ananth Karumanchi,S. Ananth Karumanchi +15 more
TL;DR: Serum %C-Alb is identified as a risk factor for mortality in patients with ESRD and it is proposed that this risk factor may be modifiable with supplemental amino acid therapy.
Journal ArticleDOI
Glycogen synthase kinase-3 is essential for β-arrestin-2 complex formation and lithium-sensitive behaviors in mice.
W. Timothy O'Brien,Jian Huang,Roberto Buccafusca,Julie Garskof,Alexander J. Valvezan,Gerard T. Berry,Peter S. Klein +6 more
TL;DR: Findings show what is believed to be a new link between GSK-3 and the β-arrestin-2 complex in mice and propose an integrated mechanism that accounts for the effects of lithium on multiple behaviors, and demonstrate that Gsk-3 is a critical target of lithium in mammalian behaviors.
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Loss of Murine Na/myo-Inositol Cotransporter Leads to Brain myo-Inositol Depletion and Central Apnea*
Gerard T. Berry,Shuang Wu,Roberto Buccafusca,Jun Ren,Linda W. Gonzales,Philip L. Ballard,Jeffrey A. Golden,Martin J. Stevens,John J. Greer +8 more
TL;DR: The high affinity SMIT1 transporter is responsible for the Ins concentration gradient in the murine fetal-placental unit, and this model demonstrates the critical importance ofSMIT1 in the developing nervous system.
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KCNQ1, KCNE2, and Na(+)-coupled solute transporters form reciprocally regulating complexes that affect neuronal excitability
Geoffrey W. Abbott,Kwok Keung Tai,Daniel L. Neverisky,Alex Hansler,Zhaoyang Hu,Torsten K. Roepke,Daniel J. Lerner,Qiuying Chen,Li Liu,Bojana Zupan,Miklós Tóth,Robin L. Haynes,Xiaoping Huang,Didem Demirbas,Roberto Buccafusca,Steven S. Gross,Vikram A. Kanda,Gerard T. Berry +17 more
TL;DR: It is found that various solute transporters and potassium channel subunits formed complexes and reciprocally regulated each other in vitro and in vivo and channel-transporter signaling complexes may be a widespread mechanism to facilitate solute transport and electrochemical crosstalk.
Journal ArticleDOI
Phosphoinositide deficiency due to inositol depletion is not a mechanism of lithium action in brain
TL;DR: It is concluded that PtdIns deficiency due to "inositol depletion" is not a mechanism of lithium action in brain, and that Ins plays another unidentified role in the mammalian brain.