Article in Communications biology, 2025. 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.
Muthukumar KaruppasamyDepartment of Pediatrics, Division of Neurology at the University of Alabama at Birmingham and Children's of Alabama, Birmingham, AL, USA.ORCID http://orcid.org/0000-0003-0034-9950
Katherine G EnglishDepartment of Pediatrics, Division of Neurology at the University of Alabama at Birmingham and Children's of Alabama, Birmingham, AL, USA.ORCID http://orcid.org/0000-0003-2757-5157
Shelby N RorrerDepartment of Pediatrics, Division of Neurology at the University of Alabama at Birmingham and Children's of Alabama, Birmingham, AL, USA.ORCID http://orcid.org/0009-0009-5640-9669
Michael A LopezDepartment of Pediatrics, Division of Neurology at the University of Alabama at Birmingham and Children's of Alabama, Birmingham, AL, USA.ORCID http://orcid.org/0000-0002-3029-0761
Matthew S AlexanderDepartment of Pediatrics, Division of Neurology at the University of Alabama at Birmingham and Children's of Alabama, Birmingham, AL, USA. matthewalexander@uabmc.edu.ORCID http://orcid.org/0000-0001-7406-5171
Funding
UAB Pilot Center for Precision Animal Modeling (C-PAM) - Resource and Service SectionU54OD030167 · OD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Bradley K. Yoder · 2020 to 2026
$15.3M
Interdisciplinary Training in Pathobiology and Rehabilitation Medicine.T32HD071866 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAMES RIMMER, Anna E. Thalacker-Mercer · 2012 to 2026
$4.8M
Circadian dysfunction and neurodegenerative diseaseR01NS082413 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GAMBLE, KAREN L · 2013 to 2022
$4.6M
Modulation of Jagged1/Pitpna in DMD as a means of therapyR01AR064300 · NIAMS · BOSTON CHILDREN'S HOSPITAL · PI KUNKEL, LOUIS M · 2014 to 2023
$3.9M
Circadian and sleep mechanisms among racial groups for nicotine dependence, craving, and withdrawalR01DA046096 · NIDA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CROPSEY, KAREN L, GAMBLE, KAREN L · 2020 to 2024
$2.8M
Muscle clock and weakness: diversity supplementR01AR079220 · NIAMS · UNIVERSITY OF FLORIDA · PI ESSER, KARYN A · 2021 to 2025
$2.8M
Muscle clock disruption accelerates the onset and progression of neurodegenerationR01AR066082 · NIAMS · UNIVERSITY OF KENTUCKY · PI ESSER, KARYN A · 2014 to 2018
$2.0M
The essentiality of serine and glycine for skeletal muscle regeneration in agingR01AG075059 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THALACKER-MERCER, ANNA E. · 2022 to 2025
$1.5M
Smad8 is a driver of Duchenne muscular dystrophy pathology via myomiR repressionK08NS120812 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LOPEZ, MICHAEL ALONZO · 2021 to 2025
$1.1M
Dystrophin as a novel regulator of the circadian clock in skeletal muscle and the brainR21NS140497 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATTHEW Scott ALEXANDER · 2025 to 2026
$424k
NIAMS NIH HHS R01 AR064300NIAMS NIH HHS R01 AR066082NIAMS NIH HHS R01 AR079220NIA NIH HHS R01 AG075059NICHD NIH HHS T32 HD071866NIDA NIH HHS R01 DA046096NIH HHS U54 OD030167NINDS NIH HHS K08 NS120812NINDS NIH HHS R01 NS082413NINDS NIH HHS R21 NS140497United States Department of Defense | United States Army | Army Medical Command | Congressionally Directed Medical Research Programs (CDMRP) MD240021U.S. Department of Health & Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) T32HD071866U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) K08NS120812U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) R01AR064300U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) R01AR066082U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) R01AR079220U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) R21NS140497U.S. Department of Health & Human Services | NIH | National Institute on Drug Abuse (NIDA) R01DA046096U.S. Department of Health & Human Services | NIH | National Institute on Drug Abuse (NIDA) R01NS082413U.S. Department of Health & Human Services | NIH | NIH Office of the Director (OD) U54OD030167
6 · The paper itself
Abstract
Duchenne muscular dystrophy (DMD) patients suffer from skeletal and cardiopulmonary weakness, and up to one third are diagnosed on the autism spectrum. Dystrophin is an essential protein for regulating intracellular force transmission to the extracellular matrix (ECM) within the skeletal muscle, but also plays key roles in neurobehavior and cognitive function. The mouse Dmd gene is X-linked and has several isoforms with enriched tissue expression in the skeletal muscle, heart, and the brain. Constitutive and inducible deletion of muscle dystrophin resulted in a skeletal muscle myopathy, dystrophic histopathology, and functional deficits compared to the mdx mouse. Transcriptomic analysis of Dmd mKO muscles revealed dysregulation of ECM and cytokine pathways. Purkinje dystrophin knockout (Dmd:Pcp2 KO) mice displayed neurobehavioral deficits in social approach, social memory, and spatial memory. These studies reveal the essential requirement for dystrophin expression in both the skeletal muscle and brain for normal physiological and neurobehavioral function.
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.
Conditional Dmd ablation in muscle and brain causes profound effects on muscle function and neurobehavior. · full record | OpenQuestion