ArticleCell cycle (Georgetown, Tex.)2011
Selective targeting of histone methylation.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 35 citations in OpenAlex.
- Dysregulation of Central-Medial Amygdala Histone Modifiers in Preclinical Models of Ethanol Exposure.Addiction biology · 2025Review
- The KDM5A/HOXA5 axis regulates osteosarcoma progression via activating the Wnt/β-catenin pathway.European journal of medical research · 2025Article
- Prognostic importance of NUP98-rearrangements in acute myeloid leukemia: A systematic review and meta-analysis.Caspian journal of internal medicine · 2024Review
- Protein modification regulated autophagy inFrontiers in physiology · 2023Review
- KDM5A and KDM5B histone-demethylases contribute to HU-induced replication stress response and tolerance.Biology open · 2021Article
- LncRNA HOTAIR regulates lipopolysaccharide-induced cytokine expression and inflammatory response in macrophages.Scientific reports · 2018Article
- Rethinking the Epigenetic Framework to Unravel the Molecular Pathology of Schizophrenia.International journal of molecular sciences · 2017Review
- Enhancer-promoter interactions are encoded by complex genomic signatures on looping chromatin.Nature genetics · 2016Article
- Review
- Article
- Reversible inhibition of lysine specific demethylase 1 is a novel anti-tumor strategy for poorly differentiated endometrial carcinoma.BMC cancer · 2014Article
- Reversible LSD1 inhibition interferes with global EWS/ETS transcriptional activity and impedes Ewing sarcoma tumor growth.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Histone demethylase jumonji AT-rich interactive domain 1B (JARID1B) controls mammary gland development by regulating key developmental and lineage specification genes.The Journal of biological chemistry · 2014Article
- Histone lysine-specific methyltransferases and demethylases in carcinogenesis: new targets for cancer therapy and prevention.Current cancer drug targets · 2013Review
- JNK and STAT3 signaling pathways converge on Akt-mediated phosphorylation of EZH2 in bronchial epithelial cells induced by arsenic.Cell cycle (Georgetown, Tex.) · 2013Article
- Maintenance of gene silencing by the coordinate action of the H3K9 methyltransferase G9a/KMT1C and the H3K4 demethylase Jarid1a/KDM5A.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Coordinated repression of cell cycle genes by KDM5A and E2F4 during differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Histone demethylase KDM5B collaborates with TFAP2C and Myc to repress the cell cycle inhibitor p21(cip) (CDKN1A).Molecular and cellular biology · 2012Article
- Article
- Co-regulation of histone-modifying enzymes in cancer.PloS one · 2011Article
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 2 institutions in 3 countries.
Funding
Abstract
Histones are post-translationally modified by multiple histone-modifying enzymes, which in turn influences gene expression. Much of the work in the field to date has focused on genetic, biochemical and structural characterization of these enzymes. The most recent genome-wide methods provide insights into specific recruitment of histone-modifying enzymes in vivo and, therefore, onto mechanisms of establishing a differential expression pattern. Here we focus on the recruitment mechanisms of the enzymes involved in the placement of two contrasting histone marks, histone H3 lysine 4 (H3K4) methylation and histone H3 lysine 27 (H3K27) methylation. We describe distribution of their binding sites and show that recruitment of different histone-modifying proteins can be coordinated, opposed, or alternating. Specifically, genomic sites of the H3K4 histone demethylase KDM5A become accessible to its homolog KDM5B in cells with a lowered KDM5A level. The currently available data on recruitment of H3K4/H3K27 modifying enzymes suggests that the formed protein complexes are targeted in a sequential and temporal manner, but that additional, still unknown, interactions contribute to targeting specificity.
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.