acetyl coenzyme a has been researched along with Autism Spectrum Disorder in 3 studies
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 (66.67) | 24.3611 |
2020's | 1 (33.33) | 2.80 |
Authors | Studies |
---|---|
Denu, JM; Dieterich, IA; Frelka, A; Lawton, AJ; Li, L; Ma, M; Miles, HN; Orefice, NS; Pearce, RA; Puglielli, L; Rigby, MJ; Shapiro, SL; Yi, SY; Yu, JPJ | 1 |
Guo, WX; He, XX; He, ZX; Huang, BQ; Jian, YL; Lu, J; Ma, J; Mei, L; Qiu, DL; Su, C; Wang, GY; Wang, X; Wang, YJ; Xiong, WC; Zhang, BB; Zhang, LQ; Zhang, Y; Zheng, YW; Zhu, XJ | 1 |
Bomba-Warczak, E; Burger, C; Chapman, ER; Denu, JM; Dowell, JA; Hullinger, R; Li, L; Li, M; Mitchell, HA; Peng, Y; Puglielli, L; Wang, J | 1 |
3 other study(ies) available for acetyl coenzyme a and Autism Spectrum Disorder
Article | Year |
---|---|
Increased expression of SLC25A1/CIC causes an autistic-like phenotype with altered neuron morphology.
Topics: Acetyl Coenzyme A; Animals; Autism Spectrum Disorder; Autistic Disorder; Citric Acid; Humans; Mice; Mitochondrial Proteins; Neurons; Organic Anion Transporters; Phenotype; Proteomics | 2022 |
Autism candidate gene DIP2A regulates spine morphogenesis via acetylation of cortactin.
Topics: Acetyl Coenzyme A; Acetylation; Amino Acid Motifs; Animals; Animals, Newborn; Autism Spectrum Disorder; Binding Sites; Cortactin; Dendritic Spines; Disease Models, Animal; Embryo, Mammalian; Gene Expression Regulation, Developmental; Genetic Complementation Test; Mice; Mice, Knockout; Morphogenesis; Nuclear Proteins; Post-Synaptic Density; Protein Binding; Protein Interaction Domains and Motifs; Protein Processing, Post-Translational; Pyramidal Cells; Synaptic Transmission | 2019 |
Increased expression of AT-1/SLC33A1 causes an autistic-like phenotype in mice by affecting dendritic branching and spine formation.
Topics: Acetyl Coenzyme A; Animals; Autism Spectrum Disorder; Dendritic Spines; Epigenesis, Genetic; Histones; Humans; Membrane Transport Proteins; Mice; Mice, Transgenic; Mitochondria; Phenotype | 2016 |