Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P62988 (
Ubiquitin
)
4,326
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Endemic arsenism is widely distributed in the world, which can damage multiple organs, especially in skin and liver. The etiology is clear, but the mechanisms involved remain unknown.
Ubiquitin
-proteasome pathway (UPP) is the main pathway regulating protein degradation of which proteasome subunit beta type-5(
PSMB5
) plays a dominant role. This paper aims to study the role and mechanism of
PSMB5
in sodium arsenite (NaAsO
2
)-induced oxidative stress liver injury in L-02 cells. Firstly, L-02 cells were exposed to different concentrations of NaAsO
2
to establish a liver injury model of oxidative stress, and then mechanisms of oxidative stress were studied with carbobenzoxyl-leucyl-leucl-leucll-line (MG132) and knockdown
PSMB5
(
PSMB5
-siRNA). The oxidative stress indicators, levels of 20S proteasome, the transcription and protein expression levels of
PSMB5
, Cu-Zn superoxide dismutase (SOD1), and glutathione peroxidase 1 (GPx1) were detected. The results demonstrated that NaAsO
2
could induce oxidative stress-induced liver injury and the activity of 20S proteasome and the protein expression of
PSMB5
, SOD1, and GPx1 decreased. After MG132 or
PSMB5
-siRNA pretreatment, the gene expression of PSMB decreased. After MG132 or
PSMB5
-siRNA pretreatment, and then L-02 cells were treated with NaAsO
2
, the gene expression of PSMB remarkably decreased; however, the protein expression of SOD1 and GPx1 increased. Overall, NaAsO
2
exposure could induce oxidative stress liver injury and low expression of
PSMB5
in L-02 cells, and
PSMB5
might play an important role in the regulation of oxidative stress by regulating the expression of SOD1 and Gpx1.
...
PMID:The role of PSMB5 in sodium arsenite-induced oxidative stress in L-02 cells. 3230 Oct 4
