ArticleProceedings of the National Academy of Sciences of the United States of America2001
Id1 regulation of cellular senescence through transcriptional repression of p16/Ink4a.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 227 citations in OpenAlex.
- Reduced osteogenic factors and early osteoblast senescence in SOD1(G93A) ALS mouse model.JCI insight · 2026Article
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- An attractor state zone precedes neural crest fate in melanoma initiation.bioRxiv : the preprint server for biology · 2024Article
- Single-Cell Transcriptomic Profiling of Cholangiocyte Organoids Derived from Bile Ducts of Primary Sclerosing Cholangitis Patients.Digestive diseases and sciences · 2024Article
- Transcriptomic analysis of cellular senescence induced by ectopic expression of ATF6α in human breast cancer cells.PloS one · 2024Article
- Effect of aging on the formation and growth of colonic epithelial organoids by changes in cell cycle arrest through TGF-β-Smad3 signaling.Inflammation and regeneration · 2023Article
- Heterogenous Differences in Cellular Senescent Phenotypes in Pre-Eclampsia and IUGR following Quantitative Assessment of Multiple Biomarkers of Senescence.International journal of molecular sciences · 2023Article
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- Delineating the Switch between Senescence and Apoptosis in Cervical Cancer Cells under Ciclopirox Treatment.Cancers · 2021Article
- The Involvement of Ubiquitination Machinery in Cell Cycle Regulation and Cancer Progression.International journal of molecular sciences · 2021Review
- The importance of CDC27 in cancer: molecular pathology and clinical aspects.Cancer cell international · 2021Review
- HIF1 and ID1 Interplay Confers Adaptive Survival to HIF1α-Inhibition.Frontiers in cell and developmental biology · 2021Article
- Alterations in TGFβ signaling during prostate cancer progression.American journal of clinical and experimental urology · 2021Review
- Id1 expression in kidney endothelial cells protects against diabetes-induced microvascular injury.FEBS open bio · 2020Article
- ACVR1 Function in Health and Disease.Cells · 2019Review
- Growth suppression by dual BRAF(V600E) and NRAS(Q61) oncogene expression is mediated by SPRY4 in melanoma.Oncogene · 2019Article
- ID1-induced p16/IL6 axis activation contributes to the resistant of hepatocellular carcinoma cells to sorafenib.Cell death & disease · 2018Article
- ER stress and distinct outputs of the IRE1α RNase control proliferation and senescence in response to oncogenic Ras.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Id1 Promotes Obesity by Suppressing Brown Adipose Thermogenesis and White Adipose Browning.Diabetes · 2017Article
42 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The Id family of helix-loop-helix (HLH) transcriptional regulatory proteins does not possess a basic DNA-binding domain and functions as a negative regulator of basic HLH transcription factors. Id proteins coordinate cell growth and differentiation pathways within mammalian cells and have been shown to regulate G(1)-S cell-cycle transitions. Although much recent data has implicated Id1 in playing a critical role in modulating cellular senescence, no direct genetic evidence has been reported to substantiate such work. Here we show that Id1-null primary mouse embryo fibroblasts undergo premature senescence despite normal growth profiles at early passage. These cells possess increased expression of the tumor-suppressor protein p16/Ink4a but not p19/ARF, and have decreased cyclin-dependent kinase (cdk) 2 and cdk4 kinase activity. We also show that Id1 is able to directly inhibit p16/Ink4a but not p19/ARF promoter activity via its HLH domain, and that Id1 inhibits transcriptional activation at E-boxes within the p16/Ink4a promoter. Our data provide, to our knowledge, the first genetic evidence for a role for Id1 as an inhibitor of cellular senescence and suggest that Id1 functions to delay cellular senescence through repression of p16/Ink4a. Because epigenetic and genetic abrogation of p16/Ink4a function has been implicated in the evolution of several human malignancies, we propose that transcriptional regulation of p16/Ink4a may also provide a mechanism for the dysregulation of normal cellular growth controls during the evolution of human malignancies.
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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.