Enteroviral protease 2A directly cleaves dystrophin and is inhibited by a dystrophin-based substrate analogue.
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Coronavirus 3CLpro proteinase cleavage sites: possible relevance to SARS virus pathologyDystrophin deficiency markedly increases enterovirus-induced cardiomyopathy: a genetic predisposition to viral heart disease.Cardiac myosin and the TH1/TH2 paradigm in autoimmune myocarditisStructure and dynamics of coxsackievirus B4 2A proteinase, an enyzme involved in the etiology of heart diseaseEndophilin A1 regulates dendritic spine morphogenesis and stability through interaction with p140Cap.Multiple pathogenetic mechanisms in X linked dilated cardiomyopathy.Ex vivo and in vivo inhibition of human rhinovirus replication by a new pseudosubstrate of viral 2A protease.Contractile function, sarcolemma integrity, and the loss of dystrophin after skeletal muscle eccentric contraction-induced injuryRecent progress in understanding coxsackievirus replication, dissemination, and pathogenesis.Therapy insight: cardiovascular complications associated with muscular dystrophies.Picornavirus modification of a host mRNA decay protein.Challenges and opportunities in dystrophin-deficient cardiomyopathy gene therapy.SNIP/p140Cap mRNA expression is an unfavourable prognostic factor in breast cancer and is not expressed in normal breast tissueGenetics of dilated cardiomyopathy.Postmortem diagnosis of infectious heart diseases: A mystifying cause of Sudden Infant DeathInhibition of Coxsackievirus-associated dystrophin cleavage prevents cardiomyopathy.Viral and host proteins involved in picornavirus life cycleEnteroviral proteases: structure, host interactions and pathogenicity.p140Cap dual regulation of E-cadherin/EGFR cross-talk and Ras signalling in tumour cell scatter and proliferation.Functional Consequences of RNA 5'-Terminal Deletions on Coxsackievirus B3 RNA Replication and Ribonucleoprotein Complex Formation.Role of virus-induced myocardial affections in sudden infant death syndrome: a prospective postmortem study.Severe dystrophic cardiomyopathy caused by the enteroviral protease 2A-mediated C-terminal dystrophin cleavage fragment.Immunological and pathological consequences of coxsackievirus RNA persistence in the heart.Stability of dystrophin STR fragments in relation to junction helicity.Dominant-negative function of the C-terminal fragments of NBR1 and SQSTM1 generated during enteroviral infection.SNAP-25 regulates spine formation through postsynaptic binding to p140Cap.Synergistic inhibition of enterovirus 71 replication by interferon and rupintrivir.
P2860
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P2860
Enteroviral protease 2A directly cleaves dystrophin and is inhibited by a dystrophin-based substrate analogue.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
@zh
2000年论文
@zh-cn
name
Enteroviral protease 2A direct ...... phin-based substrate analogue.
@en
type
label
Enteroviral protease 2A direct ...... phin-based substrate analogue.
@en
prefLabel
Enteroviral protease 2A direct ...... phin-based substrate analogue.
@en
P2093
P2860
P356
P1476
Enteroviral protease 2A direct ...... phin-based substrate analogue.
@en
P2093
P2860
P304
11191-11197
P356
10.1074/JBC.275.15.11191
P407
P577
2000-04-01T00:00:00Z