PMID- 17915563
OWN - NLM
STAT- MEDLINE
DCOM- 20080206
LR  - 20211020
IS  - 1128-2460 (Print)
IS  - 1128-2460 (Linking)
VI  - 26
IP  - 1
DP  - 2007 Jul
TI  - The emerging diversity of neuromuscular junction disorders.
PG  - 5-10
AB  - Research advances over the last 30 years have shown that key transmembrane 
      proteins at the neuromuscular junction are vulnerable to antibody-mediated 
      autoimmune attack These targets are acetylcholine receptors (AChRs) and muscle 
      specific kinase (MuSK) in myasthenia gravis, voltage-gated calcium channels 
      (VGCCs) in the Lambert-Eaton myasthenic syndrome (LEMS), and voltage-gated 
      potassium channels (VGKCs) in neuromyotonia. In parallel with these immunological 
      advances, mutations identified in genes encoding pre-synaptic, synaptic and 
      postsynaptic proteins that are crucial to neuromuscular transmission have 
      revealed a similar diversity of congenital myasthenic syndromes (CMS). These 
      discoveries have had a major impact on diagnosis and management.
FAU - Newsom-Davis, J
AU  - Newsom-Davis J
AD  - Department of Clinical Neurology, University of Oxford, UK.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Italy
TA  - Acta Myol
JT  - Acta myologica : myopathies and cardiomyopathies : official journal of the 
      Mediterranean Society of Myology
JID - 9811169
SB  - IM
MH  - Female
MH  - Humans
MH  - Infant, Newborn
MH  - Lambert-Eaton Myasthenic Syndrome/physiopathology
MH  - Myasthenia Gravis/genetics/*physiopathology
MH  - Myasthenia Gravis, Neonatal/genetics
MH  - Neuromuscular Diseases/*classification/physiopathology
MH  - Neuromuscular Junction/*physiopathology
MH  - Pregnancy
MH  - Pregnancy Complications/physiopathology
PMC - PMC2949330
EDAT- 2007/10/06 09:00
MHDA- 2008/02/07 09:00
PMCR- 2007/07/01
CRDT- 2007/10/06 09:00
PHST- 2007/10/06 09:00 [pubmed]
PHST- 2008/02/07 09:00 [medline]
PHST- 2007/10/06 09:00 [entrez]
PHST- 2007/07/01 00:00 [pmc-release]
PST - ppublish
SO  - Acta Myol. 2007 Jul;26(1):5-10.