Associated Papers
Correction: Investigating genotype-phenotype correlation of limb-girdle muscular dystrophy R8: association of clinical severity, protein biological function and protein oligomerization.
Liang X et al.
Acta Neuropathologica Communications, 2025
Investigating genotype-phenotype correlation of limb-girdle muscular dystrophy R8: association of clinical severity, protein biological function and protein oligomerization.
Liang X et al.
Acta Neuropathologica Communications, 2025
Tripartite Motif-Containing Protein 32 (TRIM32): What Does It Do for Skeletal Muscle?
Jeong SY et al.
Cells, 2023
TRIM32 biallelic defects cause limb-girdle muscular dystrophy R8: identification of two novel mutations and investigation of genotype-phenotype correlation.
Guan Y et al.
Skeletal Muscle, 2023
Case report: A novel patient presenting TRIM32-related limb-girdle muscular dystrophy.
Rimoldi M et al.
Frontiers in Neurology, 2023
TRIM32 and Malin in Neurological and Neuromuscular Rare Diseases.
Kumarasinghe L et al.
Cells, 2021
TRIM32: A Multifunctional Protein Involved in Muscle Homeostasis, Glucose Metabolism, and Tumorigenesis.
Bawa S et al.
Biomolecules, 2021
TRIM32, but not its muscular dystrophy-associated mutant, positively regulates and is targeted to autophagic degradation by p62/SQSTM1.
Overå KS et al.
Journal of Cell Science, 2019
Extending the clinical and mutational spectrum of TRIM32-related myopathies in a non-Hutterite population.
Johnson K et al.
Journal of Neurology, Neurosurgery, and Psychiatry, 2019
29921608 (PubMed )
Supplement: jnnp-2018-318288supp001.pdf
Altered myogenesis and premature senescence underlie human TRIM32-related myopathy.
Servián-Morilla E et al.
Acta Neuropathologica Communications, 2019
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