ArticleCommunications biology2024
TRAF7 determines circadian period through ubiquitination and degradation of DBP.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed.
- Elevated levels of Ube2g1 in hematopoietic stem cells lead to segmental aging of the hematopoietic system.Haematologica · 2026Article
- Article
- D-Box Binding Protein (DBP) as a Circadian Output Regulator: Molecular Mechanisms, Tissue-Specific Functions, and Disease Relevance.International journal of molecular sciences · 2026Review
- Biology and Time Course of Obstruction-Induced Detrusor Underactivity Causing Postvoid Residual Urine.International neurourology journal · 2026Article
- Article
- TRAF7 in signaling and disease: emerging mechanisms and clinical implications.Molecular medicine (Cambridge, Mass.) · 2025Review
- The ubiquitin-proteasome system in circadian regulation.Frontiers in neuroscience · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
D-site binding protein, DBP, is a clock-controlled transcription factor and drives daily rhythms of physiological processes through the regulation of an array of genes harboring a DNA binding motif, D-box. DBP protein levels show a circadian oscillation with an extremely robust peak/trough ratio, but it is elusive how the temporal pattern is regulated by post-translational regulation. In this study, we show that DBP protein levels are down-regulated by the ubiquitin-proteasome pathway. Analysis using 19 dominant-negative forms of E2 enzymes have revealed that UBE2G1 and UBE2T mediate the degradation of DBP. A proteomic analysis of DBP-interacting proteins and database screening have identified Tumor necrosis factor Receptor-Associated Factor 7 (TRAF7), a RING-type E3 ligase, that forms a complex with UBE2G1 and/or UBE2T. Ubiquitination analysis have revealed that TRAF7 enhances K48-linked polyubiquitination of DBP in cultured cells. Overexpression of TRAF7 down-regulates DBP protein level, while knockdown of TRAF7 up-regulates DBP in cultured cells. Knockout of TRAF7 in NIH3T3 cells have revealed that TRAF7 mediates the time-of-the-day-dependent regulation of DBP levels. Furthermore, TRAF7 has a period-shortening effect on the cellular clock. Together, TRAF7 plays an important role in circadian clock oscillation through destabilization of DBP.
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Registered trials
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.