ArticleProceedings of the National Academy of Sciences of the United States of America2014
Novel INHAT repressor (NIR) is required for early lymphocyte development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. 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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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
7 citing papers in PubMed, 14 citations in OpenAlex.
- A post-translational regulatory map of chronic antigen-driven human T cell dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Drosophila and human cell studies reveal a conserved role for CEBPZ, NOC2L and NOC3L in rRNA processing and tumorigenesis.Journal of cell science · 2025Article
- Novel INHAT repressor drives glioblastoma growth by promoting ribosomal DNA transcription in glioma stem cells.Neuro-oncology · 2023Article
- Unmasking the biological function and regulatory mechanism of NOC2L: a novel inhibitor of histone acetyltransferase.Journal of translational medicine · 2023Review
- Interrogating cell type-specific cooperation of transcriptional regulators in 3D chromatin.iScience · 2021Article
- Knockdown of NIR Suppresses Breast Cancer Cell Proliferation via Promoting FOXO3.OncoTargets and therapy · 2021Article
- EZH2 Regulates the Developmental Timing of Effectors of the Pre-Antigen Receptor Checkpoints.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Novel inhibitor of histone acetyltransferase repressor (NIR) is a transcriptional corepressor with inhibitor of histone acetyltransferase activity and is a potent suppressor of p53. Although NIR deficiency in mice leads to early embryonic lethality, lymphoid-restricted deletion resulted in the absence of double-positive CD4(+)CD8(+) thymocytes, whereas bone-marrow-derived B cells were arrested at the B220(+)CD19(-) pro-B-cell stage. V(D)J recombination was preserved in NIR-deficient DN3 double-negative thymocytes, suggesting that NIR does not affect p53 function in response to physiologic DNA breaks. Nevertheless, the combined deficiency of NIR and p53 provided rescue of DN3L double-negative thymocytes and their further differentiation to double- and single-positive thymocytes, whereas B cells in the marrow further developed to the B220(+)CD19(+) pro-B-cell stage. Our results show that NIR cooperate with p53 to impose checkpoint for the generation of mature B and T lymphocytes.
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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.