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  • 1
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    The structural basis of protein acetylation by the p300/CBP transcriptional coactivator (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-02-15
    Description: The transcriptional coactivator p300/CBP (CREBBP) is a histone acetyltransferase (HAT) that regulates gene expression by acetylating histones and other transcription factors. Dysregulation of p300/CBP HAT activity contributes to various diseases including cancer. Sequence alignments, enzymology experiments and inhibitor studies on p300/CBP have led to contradictory results about its catalytic mechanism and its structural relation to the Gcn5/PCAF and MYST HATs. Here we describe a high-resolution X-ray crystal structure of a semi-synthetic heterodimeric p300 HAT domain in complex with a bi-substrate inhibitor, Lys-CoA. This structure shows that p300/CBP is a distant cousin of other structurally characterized HATs, but reveals several novel features that explain the broad substrate specificity and preference for nearby basic residues. Based on this structure and accompanying biochemical data, we propose that p300/CBP uses an unusual 'hit-and-run' (Theorell-Chance) catalytic mechanism that is distinct from other characterized HATs. Several disease-associated mutations can also be readily accounted for by the p300 HAT structure. These studies pave the way for new epigenetic therapies involving modulation of p300/CBP HAT activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Xin -- Wang, Ling -- Zhao, Kehao -- Thompson, Paul R -- Hwang, Yousang -- Marmorstein, Ronen -- Cole, Philip A -- England -- Nature. 2008 Feb 14;451(7180):846-50. doi: 10.1038/nature06546.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Gene Expression and Regulation, The Wistar Institute, 3601 Spruce Street, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18273021" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acid Sequence ; Catalysis ; Crystallography, X-Ray ; Dimerization ; Histone Acetyltransferases/antagonists & inhibitors/chemical ; synthesis/*chemistry/*metabolism ; Kinetics ; Models, Molecular ; Molecular Sequence Data ; Protein Structure, Tertiary ; Structure-Activity Relationship ; p300-CBP Transcription Factors/antagonists & inhibitors/chemical ; synthesis/*chemistry/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Drug discovery: Reader's block (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taverna, Sean D -- Cole, Philip A -- R01 DA025755/DA/NIDA NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1050-1. doi: 10.1038/4681050a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179160" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/metabolism ; Animals ; Antineoplastic Agents/pharmacology ; *Drug Discovery ; Enzyme Activation/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Histone Deacetylases/metabolism ; Humans ; Protein Binding/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Glucose and weight control in mice with a designed ghrelin O-acyltransferase inhibitor (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-26
    Description: Ghrelin is a gastric peptide hormone that stimulates weight gain in vertebrates. The biological activities of ghrelin require octanoylation of the peptide on Ser(3), an unusual posttranslational modification that is catalyzed by the enzyme ghrelin O-acyltransferase (GOAT). Here, we describe the design, synthesis, and characterization of GO-CoA-Tat, a peptide-based bisubstrate analog that antagonizes GOAT. GO-CoA-Tat potently inhibits GOAT in vitro, in cultured cells, and in mice. Intraperitoneal administration of GO-CoA-Tat improves glucose tolerance and reduces weight gain in wild-type mice but not in ghrelin-deficient mice, supporting the concept that its beneficial metabolic effects are due specifically to GOAT inhibition. In addition to serving as a research tool for mapping ghrelin actions, GO-CoA-Tat may help pave the way for clinical targeting of GOAT in metabolic diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068526/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068526/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnett, Brad P -- Hwang, Yousang -- Taylor, Martin S -- Kirchner, Henriette -- Pfluger, Paul T -- Bernard, Vincent -- Lin, Yu-yi -- Bowers, Erin M -- Mukherjee, Chandrani -- Song, Woo-Jin -- Longo, Patti A -- Leahy, Daniel J -- Hussain, Mehboob A -- Tschop, Matthias H -- Boeke, Jef D -- Cole, Philip A -- P01 CA016519/CA/NCI NIH HHS/ -- P01 CA016519-35/CA/NCI NIH HHS/ -- P30 DK079637/DK/NIDDK NIH HHS/ -- P60 DK079637/DK/NIDDK NIH HHS/ -- P60 DK079637-05/DK/NIDDK NIH HHS/ -- R01 DK081472/DK/NIDDK NIH HHS/ -- R01 DK081472-01A1/DK/NIDDK NIH HHS/ -- R01 DK081472-02/DK/NIDDK NIH HHS/ -- R01 DK081472-03/DK/NIDDK NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-04/GM/NIGMS NIH HHS/ -- R01 GM062437-11/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1689-92. doi: 10.1126/science.1196154. Epub 2010 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21097901" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Acyltransferases/*antagonists & inhibitors ; Animals ; Cell Survival/drug effects ; Drug Design ; Enzyme Inhibitors/chemical synthesis/*pharmacology/toxicity ; Ghrelin/deficiency/genetics/*metabolism ; Glucose/*metabolism ; Glucose Tolerance Test ; HeLa Cells ; Homeostasis ; Humans ; Insulin/metabolism ; Ion Channels/metabolism ; Islets of Langerhans/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondrial Proteins/metabolism ; Peptides/chemical synthesis/*pharmacology/toxicity ; Weight Gain/*drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-19
    Description: The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional regulatory properties. Although therapeutic targeting of most leukemia fusion proteins remains elusive, the posttranslational modifications that control their function could be targetable. We found that AML1-ETO, the fusion protein generated by the t(8;21) translocation, is acetylated by the transcriptional coactivator p300 in leukemia cells isolated from t(8;21) AML patients, and that this acetylation is essential for its self-renewal-promoting effects in human cord blood CD34(+) cells and its leukemogenicity in mouse models. Inhibition of p300 abrogates the acetylation of AML1-ETO and impairs its ability to promote leukemic transformation. Thus, lysine acetyltransferases represent a potential therapeutic target in AML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251012/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251012/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Lan -- Gural, Alexander -- Sun, Xiao-Jian -- Zhao, Xinyang -- Perna, Fabiana -- Huang, Gang -- Hatlen, Megan A -- Vu, Ly -- Liu, Fan -- Xu, Haiming -- Asai, Takashi -- Xu, Hao -- Deblasio, Tony -- Menendez, Silvia -- Voza, Francesca -- Jiang, Yanwen -- Cole, Philip A -- Zhang, Jinsong -- Melnick, Ari -- Roeder, Robert G -- Nimer, Stephen D -- GM62437/GM/NIGMS NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-12/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Aug 5;333(6043):765-9. doi: 10.1126/science.1201662. Epub 2011 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pharmacology and Chemistry Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764752" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cell Line ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Core Binding Factor Alpha 2 Subunit/chemistry/*metabolism ; E1A-Associated p300 Protein/antagonists & inhibitors/*metabolism ; Fetal Blood/cytology ; Gene Expression Profiling ; Hematopoietic Stem Cells/*cytology/physiology ; Humans ; Leukemia, Myeloid, Acute/*metabolism/pathology ; Lysine/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutant Proteins/metabolism ; Oncogene Proteins, Fusion/chemistry/*metabolism ; Preleukemia/metabolism/pathology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Processing, Post-Translational ; Transcriptional Activation ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Chemical rescue of a mutant enzyme in living cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-04
    Description: The restoration of catalytic activity to mutant enzymes by small molecules is well established for in vitro systems. Here, we show that the protein tyrosine kinase Src arginine-388--〉alanine (R388A) mutant can be rescued in live cells with the use of the small molecule imidazole. Cellular rescue of a viral Src homolog was rapid and reversible and conferred predicted oncogenic properties. Using chemical rescue in combination with mass spectrometry, we confirmed six known Src kinase substrates and identified several new protein targets. Chemical rescue data suggest that cellular Src is active under basal conditions. Rescue of R388A cellular Src provided insights into the mitogen-activated protein kinase pathway. This chemical rescue approach will likely have many applications in cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiao, Yingfeng -- Molina, Henrik -- Pandey, Akhilesh -- Zhang, Jin -- Cole, Philip A -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1293-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513984" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Fluorescence Resonance Energy Transfer ; Gene Expression Profiling ; Gene Expression Regulation ; Growth Substances/metabolism/pharmacology ; Humans ; Imidazoles/*metabolism/pharmacology ; Kinetics ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Nuclear Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Phosphorylation ; Phosphotyrosine/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins pp60(c-src)/*genetics/*metabolism ; Recombinant Proteins/metabolism ; Transfection ; src Homology Domains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Chromatin "prepattern" and histone modifiers in a fate choice for liver and pancreas (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-21
    Description: Transcriptionally silent genes can be marked by histone modifications and regulatory proteins that indicate the genes' potential to be activated. Such marks have been identified in pluripotent cells, but it is unknown how such marks occur in descendant, multipotent embryonic cells that have restricted cell fate choices. We isolated mouse embryonic endoderm cells and assessed histone modifications at regulatory elements of silent genes that are activated upon liver or pancreas fate choices. We found that the liver and pancreas elements have distinct chromatin patterns. Furthermore, the histone acetyltransferase P300, recruited via bone morphogenetic protein signaling, and the histone methyltransferase Ezh2 have modulatory roles in the fate choice. These studies reveal a functional "prepattern" of chromatin states within multipotent progenitors and potential targets to modulate cell fate induction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128430/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128430/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Cheng-Ran -- Cole, Philip A -- Meyers, David J -- Kormish, Jay -- Dent, Sharon -- Zaret, Kenneth S -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-12/GM/NIGMS NIH HHS/ -- R01 GM067718/GM/NIGMS NIH HHS/ -- R01 GM067718-08/GM/NIGMS NIH HHS/ -- R37 GM036477/GM/NIGMS NIH HHS/ -- R37 GM036477-28/GM/NIGMS NIH HHS/ -- R37GM36477/GM/NIGMS NIH HHS/ -- U01 DK072503/DK/NIDDK NIH HHS/ -- U01 DK072503-05/DK/NIDDK NIH HHS/ -- U01DK072503/DK/NIDDK NIH HHS/ -- U54MH084691/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2011 May 20;332(6032):963-6. doi: 10.1126/science.1202845.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Regenerative Medicine, Epigenetics Program, Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21596989" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Bone Morphogenetic Proteins/metabolism ; Cell Culture Techniques ; Cell Differentiation ; Cell Separation ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Embryonic Development ; Embryonic Induction ; Endoderm/*cytology ; *Gene Expression Regulation, Developmental ; Hepatocytes/cytology ; Histone-Lysine N-Methyltransferase/metabolism ; Histones/*metabolism ; Homeodomain Proteins/genetics/metabolism ; Liver/cytology/*embryology/metabolism ; Mice ; Multipotent Stem Cells/*cytology/metabolism ; Pancreas/cytology/*embryology/metabolism ; Polycomb Repressive Complex 2 ; Protein Processing, Post-Translational ; Regulatory Elements, Transcriptional ; Signal Transduction ; Trans-Activators/genetics/metabolism ; Transcription Factors/metabolism ; p300-CBP Transcription Factors/antagonists & inhibitors/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Electronic Resource
    Electronic Resource
    Preliminary examination of the crystal structure of l-proline (1949)
    Copenhagen : International Union of Crystallography (IUCr)
    Acta crystallographica 2 (1949), S. 129-130 
    Details
    ISSN: 0001-5520
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Geosciences
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1107/S0365110X4900031X
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    Paper (German National Licenses)
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  • 8
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    Altered pharmacology and distinct coactivator usage for estrogen receptor-dependent transcription through activating protein-1 (2005)
    National Academy of Sciences
    Details
    Publication Date: 2005-01-10
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    Electrophilic tuning of the chemoprotective natural product sulforaphane (2010)
    National Academy of Sciences
    Details
    Publication Date: 2010-05-03
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Phosphoproteomic analysis of Her2/neu signaling and inhibition (2006)
    National Academy of Sciences
    Details
    Publication Date: 2006-06-19
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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