ArticleCell cycle (Georgetown, Tex.)2010
Redundancy and variation in the ubiquitin-mediated proteolytic targeting of a transcription factor.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Praja1 RING-finger E3 ubiquitin ligase is a common suppressor of neurodegenerative disease-associated protein aggregation.Neuropathology : official journal of the Japanese Society of Neuropathology · 2022Article
- Targeting the E1 ubiquitin-activating enzyme (UBA1) improves elexacaftor/tezacaftor/ivacaftor efficacy towards F508del and rare misfolded CFTR mutants.Cellular and molecular life sciences : CMLS · 2022Article
- Identification of protein quality control regulators using a Drosophila model of TPI deficiency.Neurobiology of disease · 2021Article
- The ATF3 Transcription Factor Is a Short-Lived Substrate of the Arg/N-Degron Pathway.Biochemistry · 2020Article
- Slx5-Slx8 ubiquitin ligase targets active pools of the Yen1 nuclease to limit crossover formation.Nature communications · 2018Article
- Insights into the ubiquitin-proteasome system of human embryonic stem cells.Scientific reports · 2018Article
- DNA binding by the MATα2 transcription factor controls its access to alternative ubiquitin-modification pathways.Molecular biology of the cell · 2018Article
- Article
- STUbL-mediated degradation of the transcription factor MATα2 requires degradation elements that coincide with corepressor binding sites.Molecular biology of the cell · 2015Article
- Article
- The deubiquitylase USP15 stabilizes newly synthesized REST and rescues its expression at mitotic exit.Cell cycle (Georgetown, Tex.) · 2013Article
- Proteasome inhibitors suppress expression of NPM and ARF proteins.Cell cycle (Georgetown, Tex.) · 2011Article
- Terminating protein ubiquitination: Hasta la vista, ubiquitin.Cell cycle (Georgetown, Tex.) · 2011Article
- Degradation elements coincide with cofactor binding sites in a short-lived transcription factor.Cellular logisticsReview
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
As central components of the intricate networks of eukaryotic gene regulation, transcription factors are frequent targets of ubiquitin-dependent proteolysis. A well-known example is the budding yeast MATα2 (α2) transcriptional repressor, which functions as a master regulator of cell-type determination. Degradation of α2 by the ubiquitin-proteasome system is necessary for a phenotypic switch from one cell type to another. A surprisingly complex set of ubiquitin-protein conjugation mechanisms are involved. One pathway utilizes an integral-membrane ubiquitin ligase (E3) that also functions in endoplasmic reticulum-associated degradation (ERAD). Recently, we showed that a second α2 ubiquitylation pathway uses a heterodimeric E3 that, while able to bind the ubiquitin-like protein SUMO, directly recognizes non-sumoylated α2. Other transcription factors are now also known to be ubiquitylated by multiple mechanisms; as many as a dozen E3s have been implicated in degradation of the human p53 tumor suppressor, for example. We discuss general issues of redundancy and mechanistic variation in protein modification by ubiquitin.
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