Inhibition of Proteasome Activity Promotes the Correct Localization of Disease-Causing α-Sarcoglycan Mutants in HEK-293 Cells Constitutively Expressing β-, γ-, and δ-Sarcoglycan
- 31 July 2008
- journal article
- Published by Elsevier BV in The American Journal of Pathology
- Vol. 173 (1), 170-181
- https://doi.org/10.2353/ajpath.2008.071146
Abstract
No abstract availableKeywords
This publication has 59 references indexed in Scilit:
- SGCE missense mutations that cause myoclonus-dystonia syndrome impair ε-sarcoglycan trafficking to the plasma membrane: modulation by ubiquitination and torsinAHuman Molecular Genetics, 2007
- Sarcoglycanopathies: A clinico-pathological studyNeurology India, 2007
- ζ-Sarcoglycan is a functional homologue of γ-sarcoglycan in the formation of the sarcoglycan complexExperimental Cell Research, 2006
- Identification of functional domains in sarcoglycans essential for their interaction and plasma membrane targetingExperimental Cell Research, 2006
- LOVD: Easy creation of a locus-specific sequence variation database using an “LSDB-in-a-box” approachHuman Mutation, 2005
- The T‐tubule membrane ATP‐operated P2X4receptor influences contractility of skeletal muscleThe FASEB Journal, 2005
- Pharmacological chaperones: potential treatment for conformational diseasesTrends in Endocrinology & Metabolism, 2004
- Specific assembly pathway of sarcoglycans is dependent on beta‐ and delta‐sarcoglycanMuscle & Nerve, 2004
- Loss of sarcolemma nNOS in sarcoglycan‐deficient muscleThe FASEB Journal, 2002
- Limb-girdle Muscular Dystrophy (LGMD-1C) Mutants of Caveolin-3 Undergo Ubiquitination and Proteasomal DegradationOnline Journal of Public Health Informatics, 2000