The agrin/muscle‐specific kinase pathway: New targets for autoimmune and genetic disorders at the neuromuscular junction
Muscle & Nerve2001Vol. 25(1), pp. 4–16
Citations Over TimeTop 10% of 2001 papers
Abstract
The increasing understanding of the structural complexity of the neuromuscular junction (NMJ), and the processes that are important in its development, suggests many possible new disease targets. Here, we summarize briefly the genetic and autoimmune disorders that affect neuromuscular transmission, and the identified targets, including new evidence that antibodies to muscle-specific receptor tyrosine kinase (MuSK) are involved in the pathogenesis of acetylcholine receptor (AChR) antibody-negative myasthenia gravis. We then review the development of the NMJ, focusing on the important roles of nerve-derived agrin and MuSK in clustering of AChRs and other essential components of the NMJ.
Related Papers
- → Muscle-wide secretion of a miniaturized form of neural agrin rescues focal neuromuscular innervation in agrin mutant mice(2008)45 cited
- → The agrin/muscle‐specific kinase pathway: New targets for autoimmune and genetic disorders at the neuromuscular junction(2001)76 cited
- [Immunologic aspects of disorders of neuromuscular transmission. 2. Experimental autoimmune myasthenia gravis and the Lambert-Eaton myasthenic syndrome].(1994)
- → Relationship between clinical features and serum complements levels in anti-ACHR antibody-positive myasthenia gravis(2017)
- Anti-MuSK-positive myasthenia gravis patient antibody causes aberrant activation of MuSK and disassembly of acetylcholine receptor clusters(2009)