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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Bromodomain containing 9

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Top mentioned proteins: BAF, SWI, BRD7, p53, Histone
Papers on BRD9
The mutational landscape of cutaneous T cell lymphoma and Sézary syndrome.
Palomero et al., New York City, United States. In Nat Genet, Dec 2015
Mutation analysis identified a broad spectrum of somatic mutations in key genes involved in epigenetic regulation (TET2, CREBBP, KMT2D (MLL2), KMT2C (MLL3), BRD9, SMARCA4 and CHD3) and signaling, including MAPK1, BRAF, CARD11 and PRKG1 mutations driving increased MAPK, NF-κB and NFAT activity upon T cell receptor stimulation.
A Subset of Human Bromodomains Recognizes Butyryllysine and Crotonyllysine Histone Peptide Modifications.
Cochran et al., San Francisco, United States. In Structure, Nov 2015
Profiling the nearly complete human bromodomain family revealed that while most human bromodomains bind only the shorter acetyl and propionyl marks, the bromodomains of BRD9, CECR2, and the second bromodomain of TAF1 also recognize the longer butyryl mark.
LP99: Discovery and Synthesis of the First Selective BRD7/9 Bromodomain Inhibitor.
Dixon et al., Madison, United States. In Angew Chem Int Ed Engl, Jun 2015
The bromodomain-containing proteins BRD9 and BRD7 are part of the human SWI/SNF chromatin-remodeling complexes BAF and PBAF.
Discovery of I-BRD9, a Selective Cell Active Chemical Probe for Bromodomain Containing Protein 9 Inhibition.
Humphreys et al., Cambridge, United Kingdom. In J Med Chem, May 2015
Herein, we report the discovery of I-BRD9, the first selective cellular chemical probe for bromodomain-containing protein 9 (BRD9).
9H-purine scaffold reveals induced-fit pocket plasticity of the BRD9 bromodomain.
Filippakopoulos et al., Salerno, Italy. In J Med Chem, Apr 2015
The 2-amine-9H-purine scaffold was identified as a weak bromodomain template and was developed via iterative structure based design into a potent nanomolar ligand for the bromodomain of human BRD9 with small residual micromolar affinity toward the bromodomain of BRD4.
Loss of function of SWI/SNF chromatin remodeling genes leads to genome instability of human lung cancer.
Ma et al., Suzhou, China. In Oncol Rep, 2015
Specifically, the mutant-typing of 6 BAF genes, SMARCA4, ARID2, ARID1B, BCL11A, BCL11B and BRD9 was associated with more overall mutations in the lung carcinoma samples.
[1,2,4]triazolo[4,3-a]phthalazines: inhibitors of diverse bromodomains.
Brennan et al., Oxford, United Kingdom. In J Med Chem, 2014
Commercially sourced and de novo synthesized substituted [1,2,4]triazolo[4,3-a]phthalazines are potent inhibitors of both the BET bromodomains such as BRD4 as well as bromodomains outside the BET family such as BRD9, CECR2, and CREBBP.
Proteomic and bioinformatic analysis of mammalian SWI/SNF complexes identifies extensive roles in human malignancy.
Crabtree et al., United States. In Nat Genet, 2013
To understand the full extent of their involvement, we conducted a proteomic analysis of endogenous mSWI/SNF complexes, which identified several new dedicated, stable subunits not found in yeast SWI/SNF complexes, including BCL7A, BCL7B and BCL7C, BCL11A and BCL11B, BRD9 and SS18.
SS18 together with animal-specific factors defines human BAF-type SWI/SNF complexes.
Logie et al., Nijmegen, Netherlands. In Plos One, 2011
Furthermore, SS18L1, DPF1, DPF2, DPF3, BRD9, BCL7A, BCL7B and BCL7C were identified.
Gain at chromosomal region 5p15.33, containing TERT, is the most frequent genetic event in early stages of non-small cell lung cancer.
Kim et al., South Korea. In Cancer Genet Cytogenet, 2008
Other potential candidate genes evidencing high numbers of genomic copy number changes (> or =40% of patients) included the following genes, encountered in >50% of 19 stage I (A+B) cancers: CEP72 and TPPP (14 of 19; 74%); AHRR, EXOC3 (previously SEC6L1), SLC9A3, LOC442126, ZDHHC11, BRD9, and TRIP13 (13/19; 68%); and CLPTM1L (alias CRR9), SLC6A3 (previously DAT1), and LOC401169 (10/19; 53%).
Integrative genomics analysis of chromosome 5p gain in cervical cancer reveals target over-expressed genes, including Drosha.
Murty et al., New York City, United States. In Mol Cancer, 2007
Other 5p genes identified as targets of CNI play a role in DNA repair and cell cycle regulation (BASP1, TARS, PAIP1, BRD9, RAD1, SKP2, and POLS), signal transduction (OSMR), and mitochondrial oxidative phosphorylation (NNT, SDHA, and NDUFS6), suggesting that disruption of pathways involving these genes may contribute to CC progression.
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