Article in Science signaling, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Keita UchidaDepartment of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.ORCID 0000-0001-8458-9796
Emily A ScarboroughDepartment of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.ORCID 0000-0001-5774-9731
Elizabeth PruzinskyPenn Cardiovascular Institute, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.ORCID 0000-0001-9330-5329
Kathlyene R StoneDepartment of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.ORCID 0009-0004-9460-9809
Hali HartmanDivision of Cardiology, Cardiac Center, the Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.ORCID 0009-0009-7520-9179
Daniel P KellyPenn Cardiovascular Institute, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.ORCID 0000-0002-3811-9491
Jonathan J EdwardsPenn Cardiovascular Institute, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.ORCID 0000-0002-8153-7066
Izhak KehatRappaport Institute and the Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, 1 Efron Street, P.O. Box 9697, Haifa 3109601, Israel.ORCID 0000-0002-4388-1579
Benjamin L ProsserDepartment of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.ORCID 0000-0003-3696-9131
Funding
Training Program in Cardiovascular Biology and MedicineT32HL007843 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI THOMAS P. CAPPOLA, Sharlene M Day · 1996 to 2026
$11.0M
Probing the Role of Mitochondrial Short-chain Carbon Homeostasis in the Hypertrophied and Failing HeartR01HL128349 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MUOIO, DEBORAH M · 2016 to 2024
$6.1M
Detyrosinated microtubules in cardiomyocyte mechanicsR01HL133080 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI Benjamin Lears Prosser · 2016 to 2026
$4.7M
Mechanical Stress-Dependent Remodeling of the Cardiac Microtubule NetworkR01HL149891 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI Kenneth Ber Margulies, Benjamin Lears Prosser · 2020 to 2026
$4.2M
Locking and Unlocking Cardiac MaturationR35HL177035 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DANIEL PATRICK KELLY · 2025 to 2026
$2.3M
Defining the Role of ROR2 in Right Ventricular Failure PathogenesisK08HL159311 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI EDWARDS, JONATHAN JOSEPH · 2021 to 2025
$657k
Role of the cardiac cytoskeleton in mRNA localization and hypertrophyF32HL158027 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI SCARBOROUGH, EMILY A · 2021 to 2022
$133k
Investigating the protective role of stress granules in cardiomyocytesF31HL182030 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI Katey Stone · 2025 to 2026
Cardiomyocytes depend on local translation for growth and can undergo directed growth in length or width in response to different stimuli. Protein synthesis is augmented during concentric hypertrophy, which leads to thickening of the heart muscle by increasing cardiomyocyte width. Protein synthesis is controlled at the translation initiation step, when ribosome loading onto transcripts is regulated by the sequential phosphorylation of the eukaryotic initiation factor 4E-binding protein 1 (4EBP1). Here, we identified a mode of 4EBP1 phosphorylation that was associated with concentric hypertrophy in cultured cardiomyocytes and mouse hearts. Whereas canonical phosphorylation of 4EBP1 by mTORC1 regulates global protein synthesis rates, mTORC1- and nuclear ERK-dependent phosphorylation of 4EBP1 was specifically activated during concentric but not eccentric hypertrophy. Nuclear ERK-dependent phosphorylation of 4EBP1 at Ser
Indexed as
Adaptor Proteins, Signal TransducingCell NucleusExtracellular Signal-Regulated MAP KinasesMultiprotein ComplexesMyocytes, CardiacPhosphoproteinsProtein BiosynthesisTOR Serine-Threonine KinasesAnimalsCell Cycle ProteinsCells, CulturedMechanistic Target of Rapamycin Complex 1MicePhosphorylationAdaptor Proteins, Signal TransducingCell Cycle ProteinsEif4ebp1 protein, mouseExtracellular Signal-Regulated MAP KinasesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesPhosphoproteinsTOR Serine-Threonine Kinases
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
mTORC1 and nuclear ERK spatially control translation in cardiomyocytes through 4EBP1 phosphorylation. · full record | OpenQuestion