ArticleProceedings of the National Academy of Sciences of the United States of America2018
ZFAND5/ZNF216 is an activator of the 26S proteasome that stimulates overall protein degradation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 58 citations in OpenAlex.
- Stimulating proteasomal degradation in human proteinopathies.The FEBS journal · 2026Review
- Comprehensive transcriptomic profiling reveals impaired polyamine metabolism as a contributor to age-related muscle decline.iScience · 2026Article
- Zfand5 terminates TLR3/4 signaling and necroptosis by targeting TRIF to the proteasome for degradation.Cell death & disease · 2026Article
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- Emerging tools and methods to study cell signalling mediated by branched ubiquitin chains.Biochemical Society transactions · 2025Review
- Molecular insights into region-specific sexual dichromatism: Comparative transcriptome analysis of red cheek pigmentation in zebra finches.PLoS genetics · 2025Article
- Activators of the 26S proteasome when protein degradation increases.Experimental & molecular medicine · 2025Review
- Activation of the 26S Proteasome to Reduce Proteotoxic Stress and Improve the Efficacy of PROTACs.ACS pharmacology & translational science · 2025Review
- Importance of Zinc Homeostasis for Normal Cardiac Rhythm.Current cardiology reviews · 2025Review
- Proteasome: Role in T Cell Function Regulation.International journal of biological sciences · 2025Review
- Genomic variations associated with risk and protection against vincristine-induced peripheral neuropathy in pediatric cancer patients.NPJ genomic medicine · 2024Article
- Understanding neurodevelopmental proteasomopathies as new rare disease entities: A review of current concepts, molecular biomarkers, and perspectives.Genes & diseases · 2024Review
- Multi-omics profiling of DNA methylation and gene expression alterations in human cocaine use disorder.Translational psychiatry · 2024Article
- Noncanonical inheritance of phenotypic information by protein amyloids.Nature cell biology · 2024Article
- Rice A20/AN1 protein, OsSAP10, confers water-deficit stress tolerance via proteasome pathway and positive regulation of ABA signaling in Arabidopsis.Plant cell reports · 2024Article
- Person-specific differences in ubiquitin-proteasome mediated proteostasis in human neurons.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Ursolic Acid Induces Beneficial Changes in Skeletal Muscle mRNA Expression and Increases Exercise Participation and Performance in Dogs with Age-Related Muscle Atrophy.Animals : an open access journal from MDPI · 2024Article
- Enhanced understanding of cinnamaldehyde's therapeutic potential in osteoarthritis through bioinformatics and mechanistic validation of its anti-apoptotic effect.Frontiers in medicine · 2024Article
- Molecular mechanism for activation of the 26S proteasome by ZFAND5.Molecular cell · 2023Article
- Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
ZFAND5/ZNF216, a member of the zinc finger AN1-type domain family, is abundant in heart and brain, but is induced in skeletal muscle during atrophy (although not in proteotoxic stress). Because mice lacking ZFAND5 exhibit decreased atrophy, a role in stimulating protein breakdown seemed likely. Addition of recombinant ZFAND5 to purified 26S proteasomes stimulated hydrolysis of ubiquitinated proteins, short peptides, and ATP. Mutating its C-terminal AN1 domain abolished the stimulation of proteasomal peptidase activity. Mutating its N-terminal zinc finger A20 domain, which binds ubiquitin chains, prevented the enhanced degradation of ubiquitinated proteins without affecting peptidase activity. Mouse embryonic fibroblast (MEF) cells lacking ZFAND5 had lower rates of protein degradation and proteasomal activity than WT MEFs. ZFAND5 addition to cell lysates stimulated proteasomal activity and protein degradation. Unlike other proteasome regulators, ZFAND5 enhances multiple 26S activities and overall cellular protein breakdown.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.