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Author Details

Oleg Tarnavski
Novartis Institutes for BioMedical Research, Inc. Cambridge
2003
14
13
PMIDPaper TitleJournal TitlePublished Year
34995278Lack of authentic atrial fibrillation in commonly used murine atrial fibrillation models.PLoS One2022
33495398Correction for McMullen et al., "Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy".Mol Cell Biol2021
22228770Transcription factor GATA4 is activated but not required for insulin-like growth factor 1 (IGF1)-induced cardiac hypertrophy.J Biol Chem2012
19763925Mouse surgical models in cardiovascular research.Methods Mol Biol2009
17660828Endothelial-to-mesenchymal transition contributes to cardiac fibrosis.Nat Med2007
16983087Gata4 is required for maintenance of postnatal cardiac function and protection from pressure overload-induced heart failure.Proc Natl Acad Sci U S A2006
15972800Haploinsufficiency of the cardiac transcription factor Nkx2-5 variably affects the expression of putative target genes.FASEB J2005
14597618The insulin-like growth factor 1 receptor induces physiological heart growth via the phosphoinositide 3-kinase(p110alpha) pathway.J Biol Chem2004
15226426Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy.Mol Cell Biol2004
15184287Inhibition of mTOR signaling with rapamycin regresses established cardiac hypertrophy induced by pressure overload.Circulation2004
15001440Alterations in apoptosis regulatory factors during hypertrophy and heart failure.Am J Physiol Heart Circ Physiol2004
14679301Mouse cardiac surgery: comprehensive techniques for the generation of mouse models of human diseases and their application for genomic studies.Physiol Genomics2004
12668503Rapamycin attenuates load-induced cardiac hypertrophy in mice.Circulation2003
14507992Phosphoinositide 3-kinase(p110alpha) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy.Proc Natl Acad Sci U S A2003
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Collaborators

Seigo Izumo
Beth Israel Deaconess Medical Center.
Co-authored papers 12
Julie R McMullen
Baker Heart and Diabetes Institute
Co-authored papers 10
Megan C Sherwood
Harvard Medical School, Boston Children's Hospital.
Co-authored papers 7
Tetsuo Shioi
Beth Israel Deaconess Medical Center.
Co-authored papers 6
Li Zhang
Brigham and Women's Hospital and Harvard Medical School
Co-authored papers 5
Peter M Kang
Beth Israel Deaconess Medical Center, Harvard Medical School
Co-authored papers 4
William T Pu
Boston Children's Hospital, Harvard Medical School
Co-authored papers 3
Sek Won Kong
Boston Children's Hospital, Seoul National University, Seoul National University Hospital
Co-authored papers 3
Egbert Bisping
Medical University of Graz
Co-authored papers 3
Natalya Bodyak
Beth Israel Deaconess Medical Center
Co-authored papers 2
Martina Schinke
Beth Israel Deaconess Medical Center
Co-authored papers 2
Sadakatsu Ikeda
Tokyo Medical and Dental University Hospital
Co-authored papers 2
Burkert Pieske
Charite University Medicine, Berlin Institute of Health (BIH)
Co-authored papers 1
Qing Ma
Boston Children's Hospital
Co-authored papers 1
Shaun R Coughlin
Co-authored papers 1
Satish K Rajagopal
Benioff Children's Hospital, University of California san francisco
Co-authored papers 1
Patrick Yue
Former employee of Portola Pharmaceuticals
Co-authored papers 1
Lauren Riggi
Co-authored papers 1
Jeffrey Brown
Co-authored papers 1
Jennifer K Son
Department of Radiology- Johns Hopkins University School of Medicine
Co-authored papers 1
Zhilin Liu
Wenzhou Medical University
Co-authored papers 1
Zhangli Springer
Co-authored papers 1
Weei-Yuarn Huang
Nova Scotia Health Authority
Co-authored papers 1
Release 1.2