Редактирование: PSMD4

26S proteasome non-ATPase regulatory subunit 4 (26S proteasome regulatory subunit RPN10) (26S proteasome regulatory subunit S5A) (Antisecretory factor 1) (AF) (ASF) (Multiubiquitin chain-binding protein) [MCB1]

==Publications==

{{medline-entry
|title=Age-related decrease in proteasome expression contributes to defective nuclear factor-kappaB activation during hepatic ischemia/reperfusion.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19206148
|abstract=Hepatic ischemia/reperfusion (I/R) leads to liver injury and dysfunction through the initiation of a biphasic inflammatory response that is regulated by the transcription factor nuclear factor kappaB (NF-kappaB). We have previously shown that there is an age-dependent difference in the injury response to hepatic I/R in mice that correlates with divergent activation of NF-kappaB such that young mice have greater NF-kappaB activation, but less injury than old mice. In this study, we investigated the mechanism by which age alters the activation of NF-kappaB in the liver during I/R. Young (4-5 weeks) and old (12-14 months) mice underwent partial hepatic I/R. Livers were obtained for RNA microarray analysis and protein expression assays. Using microarray analysis, we identified age-dependent differences in the expression of genes related to protein ubiquitinylation and the proteasome. In old mice, genes that are involved in the ubiquitin-proteasome pathway were significantly down-regulated during I/R. Consistent with these findings, expression of a critical proteasome subunit, non-adenosine triphosphatase 4 ([[PSMD4]]), was reduced in old mice. Expression of the NF-kappaB inhibitory protein, IkappaB alpha, was increased in old mice and was greatly phosphorylated and ubiquitinylated. The data provide strong evidence that the age-related defect in hepatic NF-kappaB signaling during I/R is a result of decreased expression of [[PSMD4]], a proteasome subunit responsible for recognition and recruitment of ubiquitinylated substrates to the proteasome. It appears that decreased [[PSMD4]] expression prevents recruitment of phosphorylated and ubiquitinylated IkappaB alpha to the proteasome, resulting in a defect in NF-kappaB activation.
|mesh-terms=* Aging
* Animals
* Carrier Proteins
* Gene Expression Profiling
* Gene Regulatory Networks
* Hepatocytes
* I-kappa B Proteins
* Liver
* Male
* Mice
* Mice, Inbred C57BL
* NF-KappaB Inhibitor alpha
* NF-kappa B
* Oligonucleotide Array Sequence Analysis
* Proteasome Endopeptidase Complex
* RNA-Binding Proteins
* Reperfusion Injury
* Ubiquitination

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695826
}}