Page last updated: 2024-09-05

anacardic acid and Muscular Dystrophy, Duchenne

anacardic acid has been researched along with Muscular Dystrophy, Duchenne in 2 studies

Research

Studies (2)

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	0 (0.00)	29.6817
2010's	2 (100.00)	24.3611
2020's	0 (0.00)	2.80

Authors

Authors	Studies
Barish, GD; Bass, J; Demonbreun, AR; Haldar, SM; Jiang, Z; Kuntz, NL; McNally, EM; Peek, CB; Quattrocelli, M; Zelikovich, AS	1
Altucci, L; Berni, R; Capogrossi, MC; Castellano, S; Chimenti, C; Colussi, C; Frustaci, A; Gaetano, C; Macchi, E; Mai, A; Musso, E; Nebbioso, A; Rosati, J; Rossi, S; Sbardella, G; Spallotta, F; Stilli, D; Straino, S	1

Other Studies

2 other study(ies) available for anacardic acid and Muscular Dystrophy, Duchenne

Article	Year
Pulsed glucocorticoids enhance dystrophic muscle performance through epigenetic-metabolic reprogramming. JCI insight, 2019, 12-19, Volume: 4, Issue:24 Topics: Anacardic Acids; Animals; Biomarkers; Child; Cross-Sectional Studies; Disease Models, Animal; Drug Therapy, Combination; Epigenesis, Genetic; Epigenomics; Gene Expression Regulation; Glucocorticoids; Histone Acetyltransferases; Humans; Kruppel-Like Transcription Factors; Male; MEF2 Transcription Factors; Metabolomics; Mice; Mice, Inbred mdx; Muscle, Skeletal; Muscular Dystrophy, Duchenne; Nutrients; Prednisone; Pulse Therapy, Drug	2019
Nε-lysine acetylation determines dissociation from GAP junctions and lateralization of connexin 43 in normal and dystrophic heart. Proceedings of the National Academy of Sciences of the United States of America, 2011, Feb-15, Volume: 108, Issue:7 Topics: Acetylation; Anacardic Acids; Animals; Cardiomyopathies; Connexin 43; Gap Junctions; Histone Acetyltransferases; Hydroxamic Acids; Immunoprecipitation; Lysine; Mice; Mice, Inbred mdx; Microscopy, Fluorescence; Muscular Dystrophy, Duchenne; Myocytes, Cardiac; p300-CBP Transcription Factors; Vorinostat	2011

Article

Year

Pulsed glucocorticoids enhance dystrophic muscle performance through epigenetic-metabolic reprogramming.

JCI insight, 2019, 12-19, Volume: 4, Issue:24

Topics: Anacardic Acids; Animals; Biomarkers; Child; Cross-Sectional Studies; Disease Models, Animal; Drug Therapy, Combination; Epigenesis, Genetic; Epigenomics; Gene Expression Regulation; Glucocorticoids; Histone Acetyltransferases; Humans; Kruppel-Like Transcription Factors; Male; MEF2 Transcription Factors; Metabolomics; Mice; Mice, Inbred mdx; Muscle, Skeletal; Muscular Dystrophy, Duchenne; Nutrients; Prednisone; Pulse Therapy, Drug

2019

Nε-lysine acetylation determines dissociation from GAP junctions and lateralization of connexin 43 in normal and dystrophic heart.

Proceedings of the National Academy of Sciences of the United States of America, 2011, Feb-15, Volume: 108, Issue:7

Topics: Acetylation; Anacardic Acids; Animals; Cardiomyopathies; Connexin 43; Gap Junctions; Histone Acetyltransferases; Hydroxamic Acids; Immunoprecipitation; Lysine; Mice; Mice, Inbred mdx; Microscopy, Fluorescence; Muscular Dystrophy, Duchenne; Myocytes, Cardiac; p300-CBP Transcription Factors; Vorinostat

2011