Suppressed disassembly of autolyzing p94/CAPN3 by N2A connectin/titin in a genetic reporter system.
about
Multiple molecular interactions implicate the connectin/titin N2A region as a modulating scaffold for p94/calpain 3 activity in skeletal muscleSkeletal muscle-specific calpain is an intracellular Na+-dependent proteaseMyogenic stage, sarcomere length, and protease activity modulate localization of muscle-specific calpain.Gene expression profiling in limb-girdle muscular dystrophy 2ADynamic distribution of muscle-specific calpain in mice has a key role in physical-stress adaptation and is impaired in muscular dystrophy.Comprehensive survey of p94/calpain 3 substrates by comparative proteomics--possible regulation of protein synthesis by p94.Non-proteolytic functions of calpain-3 in sarcoplasmic reticulum in skeletal muscles.The N- and C-terminal autolytic fragments of CAPN3/p94/calpain-3 restore proteolytic activity by intermolecular complementation.Muscle giants: molecular scaffolds in sarcomerogenesis.Calpain chronicle--an enzyme family under multidisciplinary characterizationTitin mutation segregates with hereditary myopathy with early respiratory failure.Screening of calpain-3 autolytic activity in LGMD muscle: a functional map of CAPN3 gene mutations.Calpain 3, the "gatekeeper" of proper sarcomere assembly, turnover and maintenance.Cardiac titin: a multifunctional giantOverview of the Muscle Cytoskeleton.Suppressor Mutations for Presenilin 1 Familial Alzheimer Disease Mutants Modulate γ-Secretase ActivitiesPLEIAD/SIMC1/C5orf25, a novel autolysis regulator for a skeletal-muscle-specific calpain, CAPN3, scaffolds a CAPN3 substrate, CTBP1.Interactions with M-band titin and calpain 3 link myospryn (CMYA5) to tibial and limb-girdle muscular dystrophiesNicastrin is dispensable for gamma-secretase protease activity in the presence of specific presenilin mutations.Anisotropic mechanosensitive pathways in the diaphragm and their implications in muscular dystrophies.Exploiting the CRISPR/Cas9 system to study alternative splicing in vivo: application to titin.CAPN3-mediated processing of C-terminal titin replaced by pathological cleavage in titinopathy.Muscle-specific calpain-3 is phosphorylated in its unique insertion region for enrichment in a myofibril fraction.
P2860
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P2860
Suppressed disassembly of autolyzing p94/CAPN3 by N2A connectin/titin in a genetic reporter system.
description
2006 nî lūn-bûn
@nan
2006 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Suppressed disassembly of auto ...... in a genetic reporter system.
@ast
Suppressed disassembly of auto ...... in a genetic reporter system.
@en
Suppressed disassembly of auto ...... in a genetic reporter system.
@nl
type
label
Suppressed disassembly of auto ...... in a genetic reporter system.
@ast
Suppressed disassembly of auto ...... in a genetic reporter system.
@en
Suppressed disassembly of auto ...... in a genetic reporter system.
@nl
prefLabel
Suppressed disassembly of auto ...... in a genetic reporter system.
@ast
Suppressed disassembly of auto ...... in a genetic reporter system.
@en
Suppressed disassembly of auto ...... in a genetic reporter system.
@nl
P2093
P2860
P356
P1476
Suppressed disassembly of auto ...... n in a genetic reporter system
@en
P2093
Dietmar Labeit
Fukuyo Torii
Katsuhide Yoshioka
Koichi Suzuki
Siegfried Labeit
Tatsuya Maeda
Yasuko Ono
Yukiko Kawabata
P2860
P304
18519-18531
P356
10.1074/JBC.M601029200
P407
P577
2006-04-20T00:00:00Z