Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The cysteine-rich and C-terminal domains of dystrophin are not required for normal costameric localization in the mouse.

Transgenic research - 1 Mar 1996

Maconochie M K, Simpkins A H, Damien E, Coulton G, Greenfield A J, Brown S D

Abstract excerpt

Dystrophin has a modular structure and is believed to be critical for muscle cell cytoarchitecture by linking the cytoskeleton to the extracellular matrix. The N-terminus binds to actin and two domains at the C-terminus, the cysteine-rich and C-terminal domains, are associated with the sarcolemma indirectly via the dystroglycan complex. We have generated a mutation in mouse embryonic stem (ES) cells which serves...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alleles
Share to Cell Differentiation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Inbred C57BL

Share to Mutation

Share to Recombinant Fusion Proteins

Share to Sequence Deletion

Source

Identifiers

PMID: 8866894
DOI: 10.1007/BF01969430

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The cysteine-rich and C-terminal domains of dystrophin are not required for normal costameric localization in the mouse.PMID 8866894Read ↗

Chimaeric mice deficient in dystroglycans develop muscular dystrophy and have disrupted myoneural synapses.Semantic proximity Read ↗

Costamere proteins and their involvement in myopathic processes.Semantic proximity Read ↗

Removal of dystroglycan causes severe muscular dystrophy in zebrafish embryosSemantic proximity Read ↗

Truncated CASK does not alter skeletal muscle or protein interactors.Semantic proximity Read ↗

Dystrophin and utrophin: genetic analyses of their role in skeletal muscle.Semantic proximity Read ↗

Dystroglycan is not required for localization of dystrophin, syntrophin, and neuronal nitric-oxide synthase at the sarcolemma but regulates integrin alpha 7B expression and caveolin-3 distribution.Semantic proximity Read ↗

Complete deletion of all alpha-dystrobrevin isoforms does not reveal new neuromuscular junction phenotype.Semantic proximity Read ↗

Depletion of zebrafish Tcap leads to muscular dystrophy via disrupting sarcomere-membrane interaction, not sarcomere assembly.Semantic proximity Read ↗

Maturation and maintenance of the neuromuscular synapse: genetic evidence for roles of the dystrophin--glycoprotein complex.Semantic proximity Read ↗

Dystrophin is required for the formation of stable muscle attachments in the zebrafish embryo.Semantic proximity Read ↗

Muscular integrity--a matter of interlinking distinct structures via plectin.Semantic proximity Read ↗

Interaction of Axonal Chondrolectin with Collagen XIXa1 Is Necessary for Precise Neuromuscular Junction Formation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.