About: Xuejun Wang

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

researcher (ORCID 0000-0001-9267-1343)

Attributes	Values
rdf:type	Item
description	ikertzailea (eu) 연구원 (ko) গবেষক (bn) 研究者 (ja) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy) onderzoeker (nl) researcher (ORCID 0000-0001-9267-1343) (en)
rdfs:label	Xuejun Wang (en) Xuejun Wang (es) Xuejun Wang (it) Xuejun Wang (nl) Xuejun Wang (sl) Xuejun Wang (ast)
skos:prefLabel	Xuejun Wang (en) Xuejun Wang (es) Xuejun Wang (it) Xuejun Wang (nl) Xuejun Wang (sl) Xuejun Wang (ast)
name	Xuejun Wang (en) Xuejun Wang (es) Xuejun Wang (it) Xuejun Wang (nl) Xuejun Wang (sl) Xuejun Wang (ast)
Scopus author ID	wds:Q38361109-5C483603-6FD4-4A7E-B87B-F5F542E8DF86
Scopus author ID	35235510300
instance of	wds:Q38361109-7024F0C7-0D3B-4CD6-8B64-C544B554D268
instance of	Homo sapiens
Loop ID	wds:Q38361109-EB422D41-81BA-45E1-BAB3-5505E0B47421
Loop ID	47177
Google Scholar author ID	wds:Q38361109-E2678614-39FC-43B6-95CD-D8766783FC19
Google Scholar author ID	ipQguqMAAAAJ
skos:altLabel	X. J. Wang (en) X.J. Wang (en) XJ Wang (en) Xiujie J Wang (en) Xiujie J. Wang (en)
occupation	wds:Q38361109-BD79A7E4-0478-427C-B582-07AB1AB5AD59
employer	wds:Q38361109-09931AB1-FEE5-441B-AF46-3758D1E620E7 wds:Q38361109-7CD5B304-7A90-4679-8E75-3621CB9E6F9A wds:Q38361109-805C2427-30F1-4178-9D05-72D31E7D3FB7 wds:Q38361109-E5B3611F-8EB5-45E3-97B1-75676E5DBB08
date of birth	wds:Q38361109-4D097949-88FC-491F-A19D-E354B8CA7596
educated at	wds:Q38361109-3BB06393-AC3E-4AB1-8AFE-8C1C17D1086F wds:Q38361109-3D70EF96-6F73-48B0-A705-F9B6D0EACE5F wds:Q38361109-7D119A36-F4D6-443E-8E13-F0FA17D761C1 wds:Q38361109-BCB9BCD5-39FA-4AB0-8E8C-35234221B07D
occupation	researcher
employer	University of South Dakota Sanford School of Medicine Cincinnati Children's Hospital Medical Center University of South Dakota Wuhan University School of Basic Medical Sciences
date of birth	2000-01-01 00:00:00Z (xsd:dateTime)
educated at	Wuhan University Cincinnati Children's Hospital Medical Center University of South Dakota
Springer Nature person ID	wds:Q38361109-96C13CB8-DFEC-4F00-B6E4-5281528A160B
ORCID iD	wds:Q38361109-2B472D29-8571-4F67-B5CC-1B5AC74DABD0
Dimensions author ID	wds:Q38361109-729A4116-A63D-45D8-B4F1-F4FA7A6EEDA4
ORCID iD	https://orcid.org/0000-0001-9267-1343
Springer Nature person ID	01246002307.76
ORCID iD	0000-0001-9267-1343
Dimensions author ID	01246002307.76
ResearcherID	wds:Q38361109-83D85268-CB13-4F39-A6E4-A9C3BED0C712
Publons author ID	wds:Q38361109-025d6095-de09-44fc-8a8d-35b154bf6118
ResearcherID	K-8874-2013
Publons author ID	2600987
Mendeley person ID	wds:Q38361109-0047ED67-EABE-4921-85C4-8A20A83F1838
Mendeley person ID	xuejun-wang5
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q38361109
is author of	Remodeling of gap junctions and slow conduction in a mouse model of desmin-related cardiomyopathy. Autophagic-lysosomal inhibition compromises ubiquitin-proteasome system performance in a p62 dependent manner in cardiomyocytes Hepatic deficiency of COP9 signalosome subunit 8 induces ubiquitin-proteasome system impairment and Bim-mediated apoptosis in murine livers. The COP9 signalosome and cullin-RING ligases in the heart The COP9 signalosome and vascular function: intriguing possibilities? The COP9 signalosome is required for autophagy, proteasome-mediated proteolysis, and cardiomyocyte survival in adult mice. COP9 signalosome regulates autophagosome maturation COP9 signalosome subunit 8 is required for postnatal hepatocyte survival and effective proliferation. Subcellular redistribution of focal adhesion kinase and its related nonkinase in hypertrophic myocardium Guidelines for the use and interpretation of assays for monitoring autophagy Increased myocardial Rab GTPase expression: a consequence and cause of cardiomyopathy COP9 signalosome subunit Csn8 is involved in maintaining proper duration of the G1 phase Perturbation of cullin deneddylation via conditional Csn8 ablation impairs the ubiquitin-proteasome system and causes cardiomyocyte necrosis and dilated cardiomyopathy in mice. Intrasarcoplasmic amyloidosis impairs proteolytic function of proteasomes in cardiomyocytes by compromising substrate uptake Proteasomal and lysosomal protein degradation and heart disease Heart failure and protein quality control Interplay between the ubiquitin-proteasome system and autophagy in proteinopathies. The ubiquitin-proteasome system in cardiac proteinopathy: a quality control perspective Altered ubiquitin-proteasome signaling in right ventricular hypertrophy and failure Rapid transition of cardiac myocytes from hyperplasia to hypertrophy during postnatal development Expression of R120G-alphaB-crystallin causes aberrant desmin and alphaB-crystallin aggregation and cardiomyopathy in mice Ubiquitin receptors and protein quality control Low thyroid function leads to cardiac atrophy with chamber dilatation, impaired myocardial blood flow, loss of arterioles, and severe systolic dysfunction Enhancement of proteasome function by PA28α overexpression protects against oxidative stress. Protein quality control and degradation in cardiomyocytes Sulforaphane enhances proteasomal and autophagic activities in mice and is a potential therapeutic reagent for Huntington's disease.

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