Редактирование: UBE2E3

Ubiquitin-conjugating enzyme E2 E3 (EC 2.3.2.23) (E2 ubiquitin-conjugating enzyme E3) (UbcH9) (Ubiquitin carrier protein E3) (Ubiquitin-conjugating enzyme E2-23 kDa) (Ubiquitin-protein ligase E3) [UBCE4] [UBCH9]

==Publications==

{{medline-entry
|title=Loss of the ubiquitin conjugating enzyme [[UBE2E3]] induces cellular senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29879550
|abstract=Cellular senescence plays essential roles in tissue homeostasis as well as a host of diseases ranging from cancers to age-related neurodegeneration. Various molecular pathways can induce senescence and these different pathways dictate the phenotypic and metabolic changes that accompany the transition to, and maintenance of, the senescence state. Here, we describe a novel senescence phenotype induced by depletion of [[UBE2E3]], a highly-conserved, metazoan ubiquitin conjugating enzyme. Cells depleted of [[UBE2E3]] become senescent in the absence of overt DNA damage and have a distinct senescence-associated secretory phenotype, increased mitochondrial and lysosomal mass, an increased sensitivity to mitochondrial and lysosomal poisons, and an increased basal autophagic flux. This senescence phenotype can be partially suppressed by co-depletion of either p53 or its cognate target gene, p21 , or by co-depleting the tumor suppressor p16 . Together, these data describe a direct link of a ubiquitin conjugating enzyme to cellular senescence and further underscore the consequences of disrupting the integration between the ubiquitin proteolysis system and the autophagy machinery.
|mesh-terms=* Autophagy
* Cellular Senescence
* Cyclin-Dependent Kinase Inhibitor p16
* Cyclin-Dependent Kinase Inhibitor p21
* DNA Damage
* Homeostasis
* Humans
* Mitochondria
* Tumor Suppressor Protein p53
* Ubiquitin
* Ubiquitin-Conjugating Enzymes
|keywords=* Autophagy
* Mitochondria
* Senescence
* UBE2E3
* Ubiquitin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6007080
}}