ArticleThe Journal of biological chemistry2010
GRIM-19 and p16(INK4a) synergistically regulate cell cycle progression and E2F1-responsive gene 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 13 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.
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.
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Who cites it
13 citing papers in PubMed, 38 citations in OpenAlex.
- Functional characterization of alleLife · 2025Article
- P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022Review
- Evaluation of 14-3-3 sigma as a potential partner of p16 in quiescence and differentiation.In vitro cellular & developmental biology. Animal · 2018Article
- Article
- Obesity and p16Molecular and cellular biology · 2017Article
- p16Molecular carcinogenesis · 2017Article
- GRIM-19: A master regulator of cytokine induced tumor suppression, metastasis and energy metabolism.Cytokine & growth factor reviews · 2017Review
- Overexpression of GRIM-19, a mitochondrial respiratory chain complex I protein, suppresses hepatocellular carcinoma growth.International journal of clinical and experimental pathology · 2014Article
- The cyclin-dependent kinase inhibitor p16INK4a physically interacts with transcription factor Sp1 and cyclin-dependent kinase 4 to transactivate microRNA-141 and microRNA-146b-5p spontaneously and in response to ultraviolet light-induced DNA damage.The Journal of biological chemistry · 2013Article
- p16(INK4A) represses the paracrine tumor-promoting effects of breast stromal fibroblasts.Oncogene · 2013Article
- p16INK4A represses breast stromal fibroblasts migration/invasion and their VEGF-A-dependent promotion of angiogenesis through Akt inhibition.Neoplasia (New York, N.Y.) · 2012Article
- Regulatory mechanisms of tumor suppressor P16(INK4A) and their relevance to cancer.Biochemistry · 2011Review
- GRIM-19 disrupts E6/E6AP complex to rescue p53 and induce apoptosis in cervical cancers.PloS one · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
GRIM-19 (Gene associated with Retinoid-IFN-induced Mortality-19) was originally isolated as a growth suppressor in a genome-wide knockdown screen with antisense libraries. Like classical tumor suppressors, mutations, and/or loss of GRIM-19 expression occur in primary human tumors; and it is inactivated by viral gene products. Our search for potential GRIM-19-binding proteins, using mass spectrometry, that permit its antitumor actions led to the inhibitor of cyclin-dependent kinase 4, CDKN2A. The GRIM-19/CDKN2A synergistically suppressed cell cycle progression via inhibiting E2F1-driven gene expression. The N terminus of GRIM-19 and the fourth ankyrin repeat of CDKN2A are crucial for their interaction. The biological relevance of these interactions is underscored by observations that GRIM-19 promotes the inhibitory effect of CDKN2A on CDK4; and mutations from primary tumors disrupt its ability to interact with GRIM-19 and suppress E2F1-driven gene expression.
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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.