ArticleThe Journal of biological chemistry2010
The transcriptional repressor ID2 can interact with the canonical clock components CLOCK and BMAL1 and mediate inhibitory effects on mPer1 expression.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- A prevalent disease-associated SNP in the humanNAR molecular medicine · 2026Article
- Genetic loci responsible for atrioventricular block in children.Frontiers in cell and developmental biology · 2026Review
- Circadian modulation by time-restricted feeding rescues brain pathology and improves memory in mouse models of Alzheimer's disease.Cell metabolism · 2023Article
- Photic Entrainment of the Circadian System.International journal of molecular sciences · 2022Review
- Transcriptome analysis of fat accumulation in 3T3-L1 adipocytes induced by chlorantraniliprole.Frontiers in nutrition · 2022Article
- Targeted Disruption of theInternational journal of molecular sciences · 2021Article
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- Early Transcriptomic Response to OxLDL in Human Retinal Pigment Epithelial Cells.International journal of molecular sciences · 2020Article
- Subcellular Localization Signals of bHLH-PAS Proteins: Their Significance, Current State of Knowledge and Future Perspectives.International journal of molecular sciences · 2019Review
- Inhibitor of DNA binding in heart development and cardiovascular diseases.Cell communication and signaling : CCS · 2019Review
- Lymphocyte innateness defined by transcriptional states reflects a balance between proliferation and effector functions.Nature communications · 2019Article
- Disease implication of hyper-Hippo signalling.Open biology · 2016Review
- Inflammatory properties of inhibitor of DNA binding 1 secreted by synovial fibroblasts in rheumatoid arthritis.Arthritis research & therapy · 2016Article
- Alterations of Hepatic Metabolism in Chronic Kidney Disease via D-box-binding Protein Aggravate the Renal Dysfunction.The Journal of biological chemistry · 2016Article
- Impaired Thermogenesis and a Molecular Signature for Brown Adipose Tissue in Id2 Null Mice.Journal of diabetes research · 2016Article
- Cancer/Testis Antigen PASD1 Silences the Circadian Clock.Molecular cell · 2015Article
- High fat diet rescues disturbances to metabolic homeostasis and survival in the Id2 null mouse in a sex-specific manner.Biochemical and biophysical research communications · 2014Article
- Circadian genes, xBmal1 and xNocturnin, modulate the timing and differentiation of somites in Xenopus laevis.PloS one · 2014Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
ID2 is a rhythmically expressed HLH transcriptional repressor. Deletion of Id2 in mice results in circadian phenotypes, highlighted by disrupted locomotor activity rhythms and an enhanced photoentrainment response. ID2 can suppress the transactivation potential of the positive elements of the clock, CLOCK-BMAL1, on mPer1 and clock-controlled gene (CCG) activity. Misregulation of CCGs is observed in Id2(-/-) liver, and mutant mice exhibit associated alterations in lipid homeostasis. These data suggest that ID2 contributes to both input and output components of the clock and that this may be via interaction with the bHLH clock proteins CLOCK and BMAL1. The aim of the present study was to explore this potential interaction. Coimmunoprecipitation analysis revealed the capability of ID2 to complex with both CLOCK and BMAL1, and mammalian two-hybrid analysis revealed direct interactions of ID2, ID1 and ID3 with CLOCK and BMAL1. Deletion of the ID2 HLH domain rendered ID2 ineffective at inhibiting CLOCK-BMAL1 transactivation, suggesting that interaction between the proteins is via the HLH region. Immunofluorescence analysis revealed overlapping localization of ID2 with CLOCK and BMAL1 in the cytoplasm. Overexpression of CLOCK and BMAL1 in the presence of ID2 resulted in a significant reduction in their nuclear localization, revealing that ID2 can sequester CLOCK and BMAL1 to the cytoplasm. Serum stimulation of Id2(-/-) mouse embryonic fibroblasts resulted in an enhanced induction of mPer1 expression. These data provide the basis for a molecular mechanism through which ID2 could regulate aspects of both clock input and output through a time-of-day specific interaction with CLOCK and BMAL1.
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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.