In one paragraphArticle in Communications chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from itWhat 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 registryThe 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.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
5 · Who and what moneyAuthors and funding
9 authors.
Rama Reddy GoluguriDepartment of Biochemistry, Stanford University School of Medicine, Stanford, CA, USA.
Timothy S McMillenDepartment of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, USA.
Joseph D PowersCenter for Translational Muscle Research, University of Washington, Seattle, WA, USA.
Kathleen M RuppelDepartment of Biochemistry, Stanford University School of Medicine, Stanford, CA, USA.
Funding
From proteins to cells to tissues: A multi-scale assessment of biomechanical regulation by the myosin molecular motorRM1GM131981 · NIGMS · STANFORD UNIVERSITY · PI BERNSTEIN, DANIEL, MACK, DAVID LEE · 2019 to 2023
$10.3MCARDIOVASCULAR RESEARCH TRAINING PROGRAMT32HL007828 · NHLBI · UNIVERSITY OF WASHINGTON · PI Francis Kim, Farid Moussavi-Harami · 1997 to 2026
$10.2MUW Center for Translational Muscle Research (Overall Application)P30AR074990 · NIAMS · UNIVERSITY OF WASHINGTON · PI Jennifer Michelle Davis · 2019 to 2026
$7.5MEngineered Stem Cells for Cardiac RepairR01HL128368 · NHLBI · UNIVERSITY OF WASHINGTON · PI REGNIER, MICHAEL · 2018 to 2025
$6.1MComputational and Experimental Models of Myosin VariantsR01HL179584 · NHLBI · UNIVERSITY OF WASHINGTON · PI Farid Moussavi-Harami, MICHAEL REGNIER · 2026 to 2026
$1.8MBioengineering Cardiovascular Training Grant (BCTG)T32EB032787 · NIBIB · UNIVERSITY OF WASHINGTON · PI MICHAEL REGNIER, Ying Zheng · 2022 to 2026
$969kDysregulated mechanosignaling in dilated cardiomyopathy caused by defective Filamin CR00HL159224 · NHLBI · UNIVERSITY OF WASHINGTON · PI POWERS, JOSEPH D. · 2023 to 2025
$747kA multiscale computational and experimental platform to investigate cardiomyopathies and targeted therapeuticsK99HL173646 · NHLBI · UNIVERSITY OF WASHINGTON · PI CHILDERS, MATTHEW CARTER · 2024 to 2025
$272kNHLBI NIH HHS K99 HL173646NHLBI NIH HHS R00 HL159224NHLBI NIH HHS R01 HL128368NHLBI NIH HHS R01 HL179584NHLBI NIH HHS T32 HL007828NIAMS NIH HHS P30 AR074990NIBIB NIH HHS T32 EB032787NIGMS NIH HHS RM1 GM131981U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R00HL159224U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL128368U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) T32HL007828U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) P30AR074990U.S. Department of Health & Human Services | NIH | National Institute of Biomedical Imaging and Bioengineering (NIBIB) T32EB032787U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) 1RM1 GM131981-03
6 · The paper itselfAbstract
Mutations in myosin alter its motor functions in diverse ways by affecting different structural and chemo-mechanical events. Multidisciplinary strategies can be used to understand how varying alterations in motor function converge to common phenotypes like hypercontractility and hypertrophic cardiomyopathy (HCM). We combined molecular dynamics (MD) simulations with protein biochemical and myofibril mechanical analyses to study the HCM-causing myosin variant G256E. MD simulations demonstrated that G256E induces structural changes that increase the work required to displace ADP.Mg
Identifiers
PMID42086861
PMCPMC13350965
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