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DMD — NOS1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Gücüyener et al., Brain Dev 2000
(Cerebral Palsy...) :
Nitric oxide is formed in skeletal muscle by the neuronal type
nitric oxide synthase and the signalling function of
dystrophin and related compounds are in part
mediated by nitric oxide
Sander et al., Proc Natl Acad Sci U S A 2000
(Ischemia...) :
In both mouse and human skeletal muscle,
dystrophin deficiency
results in loss of neuronal
nitric oxide synthase , which normally is localized to the sarcolemma as part of the dystrophin-glycoprotein complex
Minatel et al., Muscle Nerve 2001
:
We investigated whether the changes in acetylcholine receptor ( AChR ) distribution and
neuronal nitric oxide synthase (nNOS) expression reported for the skeletal muscle of mdx mice were a
consequence of muscle fiber regeneration rather than of the absence of
dystrophin
Crosbie et al., FASEB J 2002
(Muscular Dystrophies...) :
We report that loss of the sarcoglycan-sarcospan complex in muscle causes a dramatic reduction in the levels of
nNOS expression at the membrane, even in the
presence of normal
dystrophin and syntrophin expression
Adams et al., J Cell Sci 2008
(Muscular Dystrophy, Animal) :
Despite restoration of sarcolemmal alpha-syntrophin, neuronal nitric oxide synthase (nNOS) was not localized to the sarcolemma, suggesting that
nNOS requires both
dystrophin and alpha-syntrophin for correct localization
Thomas et al., PloS one 2012
(Disease Models, Animal...) :
In patients with Duchenne muscular dystrophy (DMD) and the standard mdx mouse model of DMD,
dystrophin deficiency
causes loss of neuronal
nitric oxide synthase ( nNOSµ ) from the sarcolemma, producing functional ischemia when the muscles are exercised
Grozdanovic et al., Histol Histopathol 1999
:
The association of
nNOS with the sarcolemma is
mediated by the
dystrophin-glycoprotein complex