-
Je něco špatně v tomto záznamu ?
The molecular mechanisms of calpains action on skeletal muscle atrophy
J. Huang, X. Zhu
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články, přehledy
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- hypertrofie MeSH
- interakce mezi receptory a ligandy MeSH
- kalpain metabolismus MeSH
- lidé MeSH
- proteasomový endopeptidasový komplex metabolismus MeSH
- proteolýza * MeSH
- protoonkogenní proteiny c-akt metabolismus MeSH
- signální transdukce MeSH
- svalová atrofie metabolismus MeSH
- svalové proteiny metabolismus MeSH
- ubikvitin metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
Skeletal muscle atrophy is associated with a loss of muscle protein which may result from both increased proteolysis and decreased protein synthesis. Investigations on cell signaling pathways that regulate muscle atrophy have promoted our understanding of this complicated process. Emerging evidence implicates that calpains play key roles in dysregulation of proteolysis seen in muscle atrophy. Moreover, studies have also shown that abnormally activated calpain results muscle atrophy via its downstream effects on ubiquitin-proteasome pathway (UPP) and Akt phosphorylation. This review will discuss the role of calpains in regulation of skeletal muscle atrophy mainly focusing on its collaboration with either UPP or Akt in atrophy conditions in hope to stimulate the interest in development of novel therapeutic interventions for skeletal muscle atrophy.
Citace poskytuje Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc17012760
- 003
- CZ-PrNML
- 005
- 20170424110711.0
- 007
- ta
- 008
- 170412s2016 xr d f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.933087 $2 doi
- 035 __
- $a (PubMed)26988155
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Huang, Jiaru $u Ningxia Medical University, Yinchuan, Ningxia, China
- 245 14
- $a The molecular mechanisms of calpains action on skeletal muscle atrophy / $c J. Huang, X. Zhu
- 520 9_
- $a Skeletal muscle atrophy is associated with a loss of muscle protein which may result from both increased proteolysis and decreased protein synthesis. Investigations on cell signaling pathways that regulate muscle atrophy have promoted our understanding of this complicated process. Emerging evidence implicates that calpains play key roles in dysregulation of proteolysis seen in muscle atrophy. Moreover, studies have also shown that abnormally activated calpain results muscle atrophy via its downstream effects on ubiquitin-proteasome pathway (UPP) and Akt phosphorylation. This review will discuss the role of calpains in regulation of skeletal muscle atrophy mainly focusing on its collaboration with either UPP or Akt in atrophy conditions in hope to stimulate the interest in development of novel therapeutic interventions for skeletal muscle atrophy.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a kalpain $x metabolismus $7 D002154
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a hypertrofie $7 D006984
- 650 _2
- $a svalové proteiny $x metabolismus $7 D009124
- 650 _2
- $a svalová atrofie $x metabolismus $7 D009133
- 650 _2
- $a proteasomový endopeptidasový komplex $x metabolismus $7 D046988
- 650 12
- $a proteolýza $7 D059748
- 650 _2
- $a protoonkogenní proteiny c-akt $x metabolismus $7 D051057
- 650 _2
- $a interakce mezi receptory a ligandy $7 D020239
- 650 _2
- $a signální transdukce $7 D015398
- 650 _2
- $a ubikvitin $x metabolismus $7 D025801
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a přehledy $7 D016454
- 700 1_
- $a Zhu, Xiaoping $u Department of Respiratory Diseases, YangPu Hospital of Tongji University, Shanghai, China
- 773 0_
- $w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 65, č. 4 (2016), s. 547-560
- 856 41
- $u http://www.biomed.cas.cz/physiolres/ $y domovská stránka časopisu
- 910 __
- $a ABA008 $b A 4120 $c 266 $y 4 $z 0
- 990 __
- $a 20170412 $b ABA008
- 991 __
- $a 20170421082115 $b ABA008
- 999 __
- $a ok $b bmc $g 1201695 $s 973533
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2016 $b 65 $c 4 $d 547-560 $e 20160315 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
- LZP __
- $b NLK118 $a Pubmed-20170412