CREBBP lysine acetyltransferase domain mutations create zombie enzymes that alter chromatin loading dynamics and prevent EP300 redundancy
暂无分享,去创建一个
A. Haouz | L. Nastoupil | Haopeng Yang | Wenchao Zhang | Vida Ravanmehr | Ariel Mechaly | Leslie Regad | Ruidong Chen | Jared M. Henderson | E. Rojas | Ashley Wilson | Sydney Parsons | R. E. Davis | Qing Deng | Felipe Samaniego | Fernando Rodrigues-Lima | Michael R. Green
[1] A. Feinberg,et al. Epigenetics as a mediator of plasticity in cancer , 2023, Science.
[2] G. Slack,et al. BCL10 Mutations Define Distinct Dependencies Guiding Precision Therapy for DLBCL , 2022, Cancer discovery.
[3] Yihan Lin,et al. Co-condensation between transcription factor and coactivator p300 modulates transcriptional bursting kinetics. , 2021, Molecular cell.
[4] C. Chomienne,et al. Human CREBBP acetyltransferase is impaired by etoposide quinone, an oxidative and leukemogenic metabolite of the anticancer drug etoposide through modification of redox-sensitive zinc-finger cysteine residues. , 2020, Free radical biology & medicine.
[5] Jorja G. Henikoff,et al. Efficient chromatin accessibility mapping in situ by nucleosome-tethered tagmentation , 2020, eLife.
[6] S. Barrans,et al. Targeted sequencing in DLBCL, molecular subtypes, and outcomes: a Haematological Malignancy Research Network report. , 2020, Blood.
[7] Steven J. M. Jones,et al. Pan-cancer analysis of whole genomes , 2020, Nature.
[8] D. Gerlich,et al. Organization of Chromatin by Intrinsic and Regulated Phase Separation , 2019, Cell.
[9] K. Basso,et al. Unique and Shared Epigenetic Programs of the CREBBP and EP300 Acetyltransferases in Germinal Center B Cells Reveal Targetable Dependencies in Lymphoma. , 2019, Immunity.
[10] Steven Henikoff,et al. Improved CUT&RUN chromatin profiling tools , 2019, eLife.
[11] Michael R. Green,et al. Subtype-specific and co-occurring genetic alterations in B-cell non-Hodgkin lymphoma , 2019, bioRxiv.
[12] Michael R. Green,et al. Selective inhibition of HDAC3 targets synthetic vulnerabilities and activates immune surveillance in lymphoma , 2019, bioRxiv.
[13] Stefano Monti,et al. Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes , 2018, Nature Medicine.
[14] Roland Schmitz,et al. Genetics and Pathogenesis of Diffuse Large B‐Cell Lymphoma , 2018, The New England journal of medicine.
[15] Michael R. Green,et al. Chromatin modifying gene mutations in follicular lymphoma. , 2018, Blood.
[16] D. Dunson,et al. Genetic and Functional Drivers of Diffuse Large B Cell Lymphoma , 2017, Cell.
[17] S. Henikoff,et al. Targeted in situ genome-wide profiling with high efficiency for low cell numbers , 2018, Nature Protocols.
[18] Nicholas A. Sinnott-Armstrong,et al. An improved ATAC-seq protocol reduces background and enables interrogation of frozen tissues , 2017, Nature Methods.
[19] H. Dyson,et al. Role of the CBP catalytic core in intramolecular SUMOylation and control of histone H3 acetylation , 2017, Proceedings of the National Academy of Sciences.
[20] P. Eyers,et al. Bio-Zombie: the rise of pseudoenzymes in biology. , 2017, Biochemical Society transactions.
[21] Christopher A. Miller,et al. Recurrent somatic mutations affecting B-cell receptor signaling pathway genes in follicular lymphoma. , 2017, Blood.
[22] Steven Henikoff,et al. An efficient targeted nuclease strategy for high-resolution mapping of DNA binding sites , 2016, bioRxiv.
[23] L. Staudt,et al. Integrating genomic alterations in diffuse large B-cell lymphoma identifies new relevant pathways and potential therapeutic targets , 2016, Leukemia.
[24] Ali Bashashati,et al. Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study , 2016, PLoS medicine.
[25] P. Eyers,et al. The evolving world of pseudoenzymes: proteins, prejudice and zombies , 2016, BMC Biology.
[26] A. Rosenwald,et al. Clinicogenetic risk models predict early progression of follicular lymphoma after first-line immunochemotherapy. , 2016, Blood.
[27] Karen E Gascoigne,et al. Bromodomain inhibition of the transcriptional coactivators CBP/EP300 as a therapeutic strategy to target the IRF4 network in multiple myeloma , 2016, eLife.
[28] L. Fritsch,et al. An acetyltransferase assay for CREB-binding protein based on reverse phase-ultra-fast liquid chromatography of fluorescent histone H3 peptides. , 2015, Analytical biochemistry.
[29] M. Lunning,et al. Mutation of chromatin modifiers; an emerging hallmark of germinal center B-cell lymphomas , 2015, Blood Cancer Journal.
[30] Ash A. Alizadeh,et al. Mutations in early follicular lymphoma progenitors are associated with suppressed antigen presentation , 2015, Proceedings of the National Academy of Sciences.
[31] U. Klein,et al. Dynamics of B cells in germinal centres , 2015, Nature Reviews Immunology.
[32] O. Griffith,et al. COSMIC (Catalogue of Somatic Mutations in Cancer) , 2014 .
[33] L. Staudt,et al. Genome-wide copy-number analyses reveal genomic abnormalities involved in transformation of follicular lymphoma. , 2014, Blood.
[34] A. Andrews,et al. Differences in Specificity and Selectivity Between CBP and p300 Acetylation of Histone H3 and H3/H4 , 2013, Biochemistry.
[35] David A. Orlando,et al. Master Transcription Factors and Mediator Establish Super-Enhancers at Key Cell Identity Genes , 2013, Cell.
[36] Kenneth H. Buetow,et al. CREBBP mutations in relapsed acute lymphoblastic leukaemia , 2011, Nature.
[37] Raul Rabadan,et al. Inactivating mutations of acetyltransferase genes in B-cell lymphoma , 2010, Nature.
[38] M. Esteller,et al. Aberrant epigenetic landscape in cancer: how cellular identity goes awry. , 2010, Developmental cell.
[39] Ling Wang,et al. The structural basis of protein acetylation by the p300/CBP transcriptional coactivator , 2008, Nature.
[40] R. Roeder,et al. Regulation of the p300 HAT domain via a novel activation loop , 2004, Nature Structural &Molecular Biology.
[41] Shicai Wang,et al. COSMIC: the Catalogue Of Somatic Mutations In Cancer , 2018, Nucleic Acids Res..
[42] Yingming Zhao,et al. Structure of p300 in complex with acyl-CoA variants. , 2017, Nature chemical biology.
[43] M. Hung,et al. Phosphorylation of CBP by IKKalpha promotes cell growth by switching the binding preference of CBP from p53 to NF-kappaB. , 2007, Molecular cell.