ArticleScientific reports2016
β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 23 citations in OpenAlex.
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- Roles of post-translational modifications of UHRF1 in cancer.Epigenetics & chromatin · 2024Review
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- Aberrant splicing events caused by insertion of genes of interest into expression vectors.International journal of biological sciences · 2022Article
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- Suppression of JAK-STAT Signaling by Epstein-Barr Virus Tegument Protein BGLF2 through Recruitment of SHP1 Phosphatase and Promotion of STAT2 Degradation.Journal of virology · 2021Article
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- Severe acute respiratory syndrome coronavirus ORF3a protein activates the NLRP3 inflammasome by promoting TRAF3-dependent ubiquitination of ASC.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- The Role of Mammalian Creb3-Like Transcription Factors in Response to Nutrients.Frontiers in genetics · 2019Review
- Long Non-Coding RNAs in Obesity-Induced Cancer.Non-coding RNA · 2018Review
- Selective Activation of Type II Interferon Signaling by Zika Virus NS5 Protein.Journal of virology · 2017Article
- The Phosphorylation of PDX-1 by Protein Kinase CK2 Is Crucial for Its Stability.Pharmaceuticals (Basel, Switzerland) · 2016Article
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Authors and funding
7 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CREB-H is an endoplasmic reticulum-resident bZIP transcription factor which critically regulates lipid homeostasis and gluconeogenesis in the liver. CREB-H is proteolytically activated by regulated intramembrane proteolysis to generate a C-terminally truncated form known as CREB-H-ΔTC, which translocates to the nucleus to activate target gene expression. CREB-H-ΔTC is a fast turnover protein but the mechanism governing its destruction was not well understood. In this study, we report on β-TrCP-dependent ubiquitination and proteasomal degradation of CREB-H-ΔTC. The degradation of CREB-H-ΔTC was mediated by lysine 48-linked polyubiquitination and could be inhibited by proteasome inhibitor. CREB-H-ΔTC physically interacted with β-TrCP, a substrate recognition subunit of the SCF(β-TrCP) E3 ubiquitin ligase. Forced expression of β-TrCP increased the polyubiquitination and decreased the stability of CREB-H-ΔTC, whereas knockdown of β-TrCP had the opposite effect. An evolutionarily conserved sequence, SDSGIS, was identified in CREB-H-ΔTC, which functioned as the β-TrCP-binding motif. CREB-H-ΔTC lacking this motif was stabilized and resistant to β-TrCP-induced polyubiquitination. This motif was a phosphodegron and its phosphorylation was required for β-TrCP recognition. Furthermore, two inhibitory phosphorylation sites close to the phosphodegron were identified. Taken together, our work revealed a new intracellular signaling pathway that controls ubiquitination and degradation of the active form of CREB-H transcription factor.
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