ArticleThe Biochemical journal1992
Evolutionary conservation of the dystrophin central rod domain.
Article in The Biochemical journal, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 58 citations in OpenAlex.
- Systemic MyoAAV-saRNA delivery activates endogenous utrophin and rescues dystrophic pathology in mdx mice.Regenerative therapy · 2025Article
- Review
- Dual Myostatin and Dystrophin Exon Skipping by Morpholino Nucleic Acid Oligomers Conjugated to a Cell-penetrating Peptide Is a Promising Therapeutic Strategy for the Treatment of Duchenne Muscular Dystrophy.Molecular therapy. Nucleic acids · 2012Article
- Article
- Massive idiosyncratic exon skipping corrects the nonsense mutation in dystrophic mouse muscle and produces functional revertant fibers by clonal expansion.The Journal of cell biology · 2000Article
- Enhanced expression of recombinant dystrophin following intramuscular injection of Epstein-Barr virus (EBV)-based mini-chromosome vectors in mdx mice.Gene therapy · 1999Article
- Genetic correction of dystrophin deficiency and skeletal muscle remodeling in adult MDX mouse via transplantation of retroviral producer cells.The Journal of clinical investigation · 1997Article
- Deletions in the 5' region of dystrophin and resulting phenotypes.Journal of medical genetics · 1994Article
- A novel point mutation (G-1 to T) in a 5' splice donor site of intron 13 of the dystrophin gene results in exon skipping and is responsible for Becker muscular dystrophy.American journal of human genetics · 1994Article
- Exon skipping and translation in patients with frameshift deletions in the dystrophin gene.American journal of human genetics · 1993Article
- Assignment of laminin heavy chains using the lectin Ricinus communis agglutinin-1.The Biochemical journal · 1993Article
- Dystrophin-related protein, utrophin, in normal and dystrophic human fetal skeletal muscle.The Histochemical journal · 1993Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystrophin cDNA fragments encoding the C-terminal repeats of the central rod region have been expressed as fusion proteins. The polyclonal antisera raised to the purified fusion proteins have been characterized and neither antiserum cross-reacted with dystrophin-related protein. Antisera detected dystrophin with molecular mass close to that of the human in all terrestrial vertebrates and amphibia studied. Experiments with antisera to the N-terminal region of the dystrophin rod confirmed that epitopes to the rod region were conserved during this evolutionary period and the length of this domain remained unaltered.
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Registered trials
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.