The isopeptide bonds formed by ubiquitin or its relatives are cleaved by hydrolases with active site cysteines. Recent studies have revealed that similar metalloprotease motifs--JAMMs--in the Rpn11 subunit of the 26S proteasome lid and in the Csn5 subunit of the COP9 signalosome are involved in deubiquitination and deneddylation, respectively.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0960-9822(02)01317-9 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Activators of the 26S proteasome when protein degradation increases.
Exp Mol Med
January 2025
Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA, 02115, USA.
In response to extra- and intracellular stimuli that constantly challenge and disturb the proteome, cells rapidly change their proteolytic capacity to maintain proteostasis. Failure of such efforts often becomes a major cause of diseases or is associated with exacerbation. Increase in protein breakdown occurs at multiple steps in the ubiquitin-proteasome system, and the regulation of ubiquitination has been extensively studied.
View Article and Find Full Text PDFHypoxia-induced conversion of sensory Schwann cells into repair cells is regulated by HDAC8.
Nat Commun
January 2025
Institute of Developmental Biology and Neurobiology, Faculty of Biology, Johannes Gutenberg University Mainz, Mainz, Germany.
After a peripheral nerve injury, Schwann cells (SCs), the myelinating glia of the peripheral nervous system, convert into repair cells that foster axonal regrowth, and then remyelinate or re-ensheath regenerated axons, thereby ensuring functional recovery. The efficiency of this mechanism depends however on the time needed for axons to regrow. Here, we show that ablation of histone deacetylase 8 (HDAC8) in SCs accelerates the regrowth of sensory axons and sensory function recovery.
View Article and Find Full Text PDFStress responses induced by perturbation of the ubiquitin-proteasome system.
Trends Biochem Sci
January 2025
Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA. Electronic address:
The ubiquitin-proteasome system is key for proteostasis and its disruption can induce several cellular adaptations. Here, we summarize the range of cellular responses that are induced by perturbation of distinct components of the ubiquitin-proteasome system, and how proteasome stress in a tissue can induce systemic responses in distant tissues.
View Article and Find Full Text PDFTargeting p97/Valosin-Containing Protein Promotes Hepatic Stellate Cell Senescence and Mitigates Liver Fibrosis.
DNA Cell Biol
January 2025
Research Center of Integrated Traditional Chinese and Western Medicine, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou 646000, China.
Liver fibrosis, one of the main histological determinants of various chronic liver diseases, currently lacks effective treatment. Hepatic stellate cells (HSCs) are pivotal in the production of extracellular matrix and amplify the fibrogenic response. Inhibiting the activation of HSCs or promoting the senescence of activated HSCs is crucial for the regression of liver fibrosis.
View Article and Find Full Text PDFThe Role and Mechanisms of Ubiquitin-Proteasome System-Mediated Ferroptosis in Neurological Disorders.
Neurosci Bull
January 2025
Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, 250117, China.
Ferroptosis is a form of cell death elicited by an imbalance in intracellular iron concentrations, leading to enhanced lipid peroxidation. In neurological disorders, both oxidative stress and mitochondrial damage can contribute to ferroptosis, resulting in nerve cell dysfunction and death. The ubiquitin-proteasome system (UPS) refers to a cellular pathway in which specific proteins are tagged with ubiquitin for recognition and degradation by the proteasome.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!