ArticleDNA and cell biology2021
The Long-Lost Ligase: CRL4
Article in DNA and cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- The evolving landscape of CDK inhibitor use in breast cancer therapy and beyond.Nature reviews. Drug discovery · 2026Review
- AMBRA1 Inhibits Non-Small Cell Lung Cancer Progression Through miR-1178/p53/CDK2-Regulated Cell Cycle Arrest.Journal of cellular and molecular medicine · 2025Article
- Mechanism of D-type cyclin recognition by the AMBRA1 E3 ligase receptor.Science advances · 2025Article
- Rab40 GTPases regulate AMBRA1-mediated transcription and cell migration.Journal of cell science · 2025Article
- Ambra1 Deficiency Inhibits the Proliferation of Breast Cancer Cells Through the Akt-FoxO1-p27 Pathway.Breast cancer (Dove Medical Press) · 2025Article
- D-Type Cyclins in Development and Disease.Genes · 2023Review
- Ambra1 in cancer: implications for clinical oncology.Apoptosis : an international journal on programmed cell death · 2022Review
- Cancer cell cycle dystopia: heterogeneity, plasticity, and therapy.Trends in cancer · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
D-type cyclins (cyclin D1, D2, and D3, together cyclin D) are central drivers of the cell division cycle and well-described proto-oncoproteins. Rapid turnover of cyclin D is critical for its regulation, but the underlying mechanism has remained a matter of debate. Recently, AMBRA1 was identified as the major regulator of the stability of all three D-type cyclins. AMBRA1 serves as the substrate receptor for one of ∼40 CUL4-RING E3 ubiquitin ligase (CRL4) complexes to mediate the polyubiquitylation and subsequent degradation of cyclin D. Consequently, AMBRA1 regulates cell proliferation to impact tumor growth and the cellular response to cell cycle-targeted cancer therapies. Here we discuss the findings that implicate AMBRA1 as a core member of the cell cycle machinery.
Indexed as
Identifiers
What OpenQuestion holds
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.