Proteomics

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Chronological proteomic analysis of skeletal muscle of limb-girdle muscular dystrophy R1 model mouse

ABSTRACT: Comparative analysis of soluble proteomes in skeletal muscle from calpain-3 knock-out mouse or proteolytically inactive calpain-3 knock-in mouse to that of wild type mouse.

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Yasuko Ono 

PROVIDER: PXD036420 | JPOST Repository | Mon Jul 14 00:00:00 BST 2025

REPOSITORIES: jPOST

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A14023_100mM_5ug_8uL_125min_003.wiff Wiff
A14023_100mM_5ug_8uL_125min_003.wiff.scan Wiff
A14023_175mM_5ug_8uL_125min_005.wiff Wiff
A14023_175mM_5ug_8uL_125min_005.wiff.scan Wiff
A14023_1M_4ug_8uL_125min_009.wiff Wiff
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Publications

Distinct systemic metabolic features in limb-girdle muscular dystrophy type R1 mouse models as a potential early pathogenic signature.

Shinkai-Ouchi Fumiko F   Itoh Yoshiki Y   Shindo Mayumi M   Mikami Kyohei K   Iguchi Yoshinobu Y   Hata Shoji S   Tsutsumi Rie R   Izumi-Mishima Yuna Y   Machida Kyoka K   Suzuki Yuki Y   Sakaue Hiroshi H   Ono Yasuko Y  

Biochimica et biophysica acta. Molecular basis of disease 20250709 7

Limb-girdle muscular dystrophy type R1 (LGMDR1, formerly LGMD2A) is a genetic disorder caused by mutations in CAPN3 and is characterized by progressive proximal limb muscle weakness. The CAPN3 gene product, calpain-3/CAPN3/p94, is a member of the intracellular cysteine protease superfamily predominantly expressed in the skeletal muscle. LGMDR1 pathogenesis has been investigated separately using mouse models: CAPN3:C129S [knock-in (KI)] mice, which express a proteolytically inactive variant, and  ...[more]

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