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most_recent_publications_2018-10-11_test.xml
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most_recent_publications_2018-10-11_test.xml
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<?xml version="1.0" ?>
<!DOCTYPE PubmedArticleSet PUBLIC "-//NLM//DTD PubMedArticle, 1st June 2018//EN" "https://dtd.nlm.nih.gov/ncbi/pubmed/out/pubmed_180601.dtd">
<PubmedArticleSet>
<PubmedArticle>
<MedlineCitation Status="In-Data-Review" Owner="NLM">
<PMID Version="1">30268145</PMID>
<DateRevised>
<Year>2018</Year>
<Month>10</Month>
<Day>03</Day>
</DateRevised>
<Article PubModel="Electronic">
<Journal>
<ISSN IssnType="Electronic">1466-609X</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>22</Volume>
<Issue>1</Issue>
<PubDate>
<Year>2018</Year>
<Month>Sep</Month>
<Day>29</Day>
</PubDate>
</JournalIssue>
<Title>Critical care (London, England)</Title>
<ISOAbbreviation>Crit Care</ISOAbbreviation>
</Journal>
<ArticleTitle>The glucocorticoid receptor and cortisol levels in pediatric septic shock.</ArticleTitle>
<Pagination>
<MedlinePgn>244</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1186/s13054-018-2177-8</ELocationID>
<Abstract>
<AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">There is controversy around the prescription of adjunct corticosteroids in patients with fluid-refractory septic shock, and studies provide mixed results, showing benefit, no benefit, and harm. Traditional means for evaluating whether a patient receives corticosteroids relied on anecdotal experience or measurement of serum cortisol production following stimulation. We set out to measure both serum cortisol and the intracellular signaling receptor for cortisol, the glucocorticoid receptor (GCR), in this group of patients.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">We enrolled pediatric patients admitted to the pediatric intensive care unit with a diagnosis of systemic inflammatory response syndrome (SIRS), sepsis, or septic shock as well as healthy controls. We measured serum cortisol concentration and GCR expression by flow cytometry in peripheral blood leukocytes on the day of admission and day 3.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">We enrolled 164 patients for analysis. There was no difference between GCR expression comparing SIRS, sepsis, and septic shock. When all patients with septic shock were compared, those patients with a complicated course, defined as two or more organ failures at day 7 or death by day 28, had lower expression of GCR in all peripheral blood leukocytes. Further analysis suggested that patients with the combination of low GCR and high serum cortisol had higher rates of complicated course (75%) compared with the other three possible combinations of GCR and cortisol levels: low GCR and low cortisol (33%), high GCR and high cortisol (33%), and high GCR and low cortisol (13%; P <0.05).</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">We show that decreased expression of the GCR correlated with poor outcome from septic shock, particularly in those patients with high serum cortisol. This is consistent with findings from transcriptional studies showing that downregulation of GCR signaling genes portends worse outcome.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Alder</LastName>
<ForeName>Matthew N</ForeName>
<Initials>MN</Initials>
<AffiliationInfo>
<Affiliation>Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, Children's Hospital Research Foundation, 3333 Burnet Avenue, MLC 2005, Cincinnati, OH, 45229, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Opoka</LastName>
<ForeName>Amy M</ForeName>
<Initials>AM</Initials>
<AffiliationInfo>
<Affiliation>Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, Children's Hospital Research Foundation, 3333 Burnet Avenue, MLC 2005, Cincinnati, OH, 45229, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Wong</LastName>
<ForeName>Hector R</ForeName>
<Initials>HR</Initials>
<AffiliationInfo>
<Affiliation>Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, Children's Hospital Research Foundation, 3333 Burnet Avenue, MLC 2005, Cincinnati, OH, 45229, USA. hector.wong@cchmc.org.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y">
<Grant>
<GrantID>K08GM124298</GrantID>
<Agency>National Institute of General Medical Sciences</Agency>
<Country/>
</Grant>
<Grant>
<GrantID>R35GM126943</GrantID>
<Agency>National Institute of General Medical Sciences</Agency>
<Country/>
</Grant>
<Grant>
<GrantID>R01GM108025</GrantID>
<Agency>National Institute of General Medical Sciences (US)</Agency>
<Country/>
</Grant>
</GrantList>
<PublicationTypeList>
<PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic">
<Year>2018</Year>
<Month>09</Month>
<Day>29</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo>
<Country>England</Country>
<MedlineTA>Crit Care</MedlineTA>
<NlmUniqueID>9801902</NlmUniqueID>
<ISSNLinking>1364-8535</ISSNLinking>
</MedlineJournalInfo>
<CommentsCorrectionsList>
<CommentsCorrections RefType="Cites">
<RefSource>JAMA. 2002 Aug 21;288(7):862-71</RefSource>
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<RefSource>Crit Care Med. 2016 Jun;44(6):1034-41</RefSource>
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<RefSource>N Engl J Med. 2018 Mar 01;378(9):809-818</RefSource>
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<RefSource>Am J Respir Crit Care Med. 2015 Feb 1;191(3):309-15</RefSource>
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<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Cortisol</Keyword>
<Keyword MajorTopicYN="N">Glucocorticoid receptor</Keyword>
<Keyword MajorTopicYN="N">Sepsis</Keyword>
<Keyword MajorTopicYN="N">Septic shock</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="received">
<Year>2018</Year>
<Month>05</Month>
<Day>24</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2018</Year>
<Month>09</Month>
<Day>04</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2018</Year>
<Month>10</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed">
<Year>2018</Year>
<Month>10</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2018</Year>
<Month>10</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>epublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">30268145</ArticleId>
<ArticleId IdType="doi">10.1186/s13054-018-2177-8</ArticleId>
<ArticleId IdType="pii">10.1186/s13054-018-2177-8</ArticleId>
<ArticleId IdType="pmc">PMC6162875</ArticleId>
</ArticleIdList>
</PubmedData>
</PubmedArticle>
<PubmedArticle>
<MedlineCitation Status="In-Process" Owner="NLM">
<PMID Version="1">29752280</PMID>
<DateRevised>
<Year>2018</Year>
<Month>08</Month>
<Day>03</Day>
</DateRevised>
<Article PubModel="Electronic">
<Journal>
<ISSN IssnType="Electronic">1754-8411</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>11</Volume>
<Issue>5</Issue>
<PubDate>
<Year>2018</Year>
<Month>05</Month>
<Day>10</Day>
</PubDate>
</JournalIssue>
<Title>Disease models & mechanisms</Title>
<ISOAbbreviation>Dis Model Mech</ISOAbbreviation>
</Journal>
<ArticleTitle><i>Drosophila</i> Insulin receptor regulates the persistence of injury-induced nociceptive sensitization.</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">dmm034231</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1242/dmm.034231</ELocationID>
<Abstract>
<AbstractText>Diabetes-associated nociceptive hypersensitivity affects diabetic patients with hard-to-treat chronic pain. Because multiple tissues are affected by systemic alterations in insulin signaling, the functional locus of insulin signaling in diabetes-associated hypersensitivity remains obscure. Here, we used <i>Drosophila</i> nociception/nociceptive sensitization assays to investigate the role of Insulin receptor (Insulin-like receptor, InR) in nociceptive hypersensitivity. <i>InR</i> mutant larvae exhibited mostly normal baseline thermal nociception (absence of injury) and normal acute thermal hypersensitivity following UV-induced injury. However, their acute thermal hypersensitivity persists and fails to return to baseline, unlike in controls. Remarkably, injury-induced persistent hypersensitivity is also observed in larvae that exhibit either type 1 or type 2 diabetes. Cell type-specific genetic analysis indicates that <i>InR</i> function is required in multidendritic sensory neurons including nociceptive class IV neurons. In these same nociceptive sensory neurons, only modest changes in dendritic morphology were observed in the <i>InR<sup>RNAi</sup></i> -expressing and diabetic larvae. At the cellular level, <i>InR</i>-deficient nociceptive sensory neurons show elevated calcium responses after injury. Sensory neuron-specific expression of InR rescues the persistent thermal hypersensitivity of <i>InR</i> mutants and constitutive activation of InR in sensory neurons ameliorates the hypersensitivity observed with a type 2-like diabetic state. Our results suggest that a sensory neuron-specific function of InR regulates the persistence of injury-associated hypersensitivity. It is likely that this new system will be an informative genetically tractable model of diabetes-associated hypersensitivity.</AbstractText>
<CopyrightInformation>© 2018. Published by The Company of Biologists Ltd.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Im</LastName>
<ForeName>Seol Hee</ForeName>
<Initials>SH</Initials>
<Identifier Source="ORCID">0000-0002-0777-3466</Identifier>
<AffiliationInfo>
<Affiliation>Department of Genetics, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA seolheeim@mdanderson.org mjgalko@mdanderson.org.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Patel</LastName>
<ForeName>Atit A</ForeName>
<Initials>AA</Initials>
<AffiliationInfo>
<Affiliation>Neuroscience Institute, Georgia State University, P.O. Box 5030, Atlanta, GA 30303, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Cox</LastName>
<ForeName>Daniel N</ForeName>
<Initials>DN</Initials>
<Identifier Source="ORCID">0000-0001-9191-9212</Identifier>
<AffiliationInfo>
<Affiliation>Neuroscience Institute, Georgia State University, P.O. Box 5030, Atlanta, GA 30303, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Galko</LastName>
<ForeName>Michael J</ForeName>
<Initials>MJ</Initials>
<Identifier Source="ORCID">0000-0002-3759-2017</Identifier>
<AffiliationInfo>
<Affiliation>Department of Genetics, University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA seolheeim@mdanderson.org mjgalko@mdanderson.org.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Genetics and Epigenetics Graduate Program, University of Texas Graduate School of Biomedical Sciences, 6767 Bertner Avenue, Houston, TX 77030, USA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y">
<Grant>
<GrantID>R01 NS086082</GrantID>
<Acronym>NS</Acronym>
<Agency>NINDS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant>
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<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="Y">Diabetes</Keyword>
<Keyword MajorTopicYN="Y">Drosophila</Keyword>
<Keyword MajorTopicYN="Y">Hyperalgesia</Keyword>
<Keyword MajorTopicYN="Y">Insulin receptor</Keyword>
<Keyword MajorTopicYN="Y">Nociceptive sensitization</Keyword>
<Keyword MajorTopicYN="Y">Sensory neurons</Keyword>
</KeywordList>
<CoiStatement>Competing interestsThe authors declare no competing or financial interests.</CoiStatement>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="received">
<Year>2018</Year>
<Month>02</Month>
<Day>15</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2018</Year>
<Month>03</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2018</Year>
<Month>5</Month>
<Day>13</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="pubmed">
<Year>2018</Year>
<Month>5</Month>
<Day>13</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<Minute>0</Minute>
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<ArticleId IdType="pii">11/5/dmm034231</ArticleId>
<ArticleId IdType="doi">10.1242/dmm.034231</ArticleId>
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<PMID Version="1">29932900</PMID>
<DateRevised>
<Year>2018</Year>
<Month>09</Month>
<Day>16</Day>
</DateRevised>
<Article PubModel="Print">
<Journal>
<ISSN IssnType="Electronic">1097-4164</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>70</Volume>
<Issue>6</Issue>
<PubDate>
<Year>2018</Year>
<Month>Jun</Month>
<Day>21</Day>
</PubDate>
</JournalIssue>
<Title>Molecular cell</Title>
<ISOAbbreviation>Mol. Cell</ISOAbbreviation>
</Journal>
<ArticleTitle>Spt6 Association with RNA Polymerase II Directs mRNA Turnover During Transcription.</ArticleTitle>
<Pagination>
<MedlinePgn>1054-1066.e4</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S1097-2765(18)30394-0</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.molcel.2018.05.020</ELocationID>
<Abstract>
<AbstractText>Spt6 is an essential histone chaperone that mediates nucleosome reassembly during gene transcription. Spt6 also associates with RNA polymerase II (RNAPII) via a tandem Src2 homology domain. However, the significance of Spt6-RNAPII interaction is not well understood. Here, we show that Spt6 recruitment to genes and the nucleosome reassembly functions of Spt6 can still occur in the absence of its association with RNAPII. Surprisingly, we found that Spt6-RNAPII association is required for efficient recruitment of the Ccr4-Not de-adenylation complex to transcribed genes for essential degradation of a range of mRNAs, including mRNAs required for cell-cycle progression. These findings reveal an unexpected control mechanism for mRNA turnover during transcription facilitated by a histone chaperone.</AbstractText>
<CopyrightInformation>Copyright © 2018 Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Dronamraju</LastName>
<ForeName>Raghuvar</ForeName>
<Initials>R</Initials>
<AffiliationInfo>
<Affiliation>Department of Biochemistry & Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Hepperla</LastName>
<ForeName>Austin J</ForeName>
<Initials>AJ</Initials>
<AffiliationInfo>
<Affiliation>Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Shibata</LastName>
<ForeName>Yoichiro</ForeName>
<Initials>Y</Initials>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Adams</LastName>
<ForeName>Alexander T</ForeName>
<Initials>AT</Initials>
<AffiliationInfo>
<Affiliation>Department of Biochemistry & Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Magnuson</LastName>
<ForeName>Terry</ForeName>
<Initials>T</Initials>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Genetics, The Carolina Center for Genome Sciences, University of North Carolina, Chapel Hill, NC 27599, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Davis</LastName>
<ForeName>Ian J</ForeName>
<Initials>IJ</Initials>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Genetics, The Carolina Center for Genome Sciences, University of North Carolina, Chapel Hill, NC 27599, USA; Departments of Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Strahl</LastName>
<ForeName>Brian D</ForeName>
<Initials>BD</Initials>
<AffiliationInfo>
<Affiliation>Department of Biochemistry & Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: brian_strahl@med.unc.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y">
<Grant>
<GrantID>R01 GM110058</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant>
<GrantID>R35 GM126900</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList>
<PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo>
<Country>United States</Country>
<MedlineTA>Mol Cell</MedlineTA>
<NlmUniqueID>9802571</NlmUniqueID>
<ISSNLinking>1097-2765</ISSNLinking>
</MedlineJournalInfo>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Ccr4-Not</Keyword>
<Keyword MajorTopicYN="N">RNA polymerase II</Keyword>
<Keyword MajorTopicYN="N">Spt6</Keyword>
<Keyword MajorTopicYN="N">cell cycle</Keyword>
<Keyword MajorTopicYN="N">chromatin</Keyword>
<Keyword MajorTopicYN="N">histones</Keyword>
<Keyword MajorTopicYN="N">mRNA stability</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="received">
<Year>2017</Year>
<Month>10</Month>
<Day>16</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised">
<Year>2018</Year>
<Month>03</Month>
<Day>23</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2018</Year>
<Month>05</Month>
<Day>17</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2018</Year>
<Month>6</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed">
<Year>2018</Year>
<Month>6</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2018</Year>
<Month>6</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
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<PublicationStatus>ppublish</PublicationStatus>
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<Year>2018</Year>
<Month>09</Month>
<Day>15</Day>
</DateRevised>
<Article PubModel="Print-Electronic">
<Journal>
<ISSN IssnType="Electronic">1083-351X</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>293</Volume>
<Issue>35</Issue>
<PubDate>
<Year>2018</Year>
<Month>Aug</Month>
<Day>31</Day>
</PubDate>
</JournalIssue>
<Title>The Journal of biological chemistry</Title>
<ISOAbbreviation>J. Biol. Chem.</ISOAbbreviation>
</Journal>
<ArticleTitle>PBRM1 bromodomains variably influence nucleosome interactions and cellular function.</ArticleTitle>
<Pagination>
<MedlinePgn>13592-13603</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.RA118.003381</ELocationID>
<Abstract>
<AbstractText>Chromatin remodelers use bromodomains (BDs) to recognize histones. Polybromo 1 (PBRM1 or BAF180) is hypothesized to function as the nucleosome-recognition subunit of the PBAF chromatin-remodeling complex and is frequently mutated in clear cell renal cell carcinoma (ccRCC). Previous studies have applied <i>in vitro</i> methods to explore the binding specificities of the six individual PBRM1 BDs. However, BD targeting to histones and the influence of neighboring BD on nucleosome recognition have not been well characterized. Here, using histone microarrays and intact nucleosomes to investigate the histone-binding characteristics of the six PBRM1 BDs individually and combined, we demonstrate that BD2 and BD4 of PBRM1 mediate binding to acetylated histone peptides and to modified recombinant and cellular nucleosomes. Moreover, we show that neighboring BDs variably modulate these chromatin interactions, with BD1 and BD5 enhancing nucleosome interactions of BD2 and BD4, respectively, whereas BD3 attenuated these interactions. We also found that binding pocket missense mutations in BD4 observed in ccRCC disrupt PBRM1-chromatin interactions and that these mutations in BD4, but not similar mutations in BD2, in the context of full-length PBRM1, accelerate ccRCC cell proliferation. Taken together, our biochemical and mutational analyses have identified BD4 as being critically important for maintaining proper PBRM1 function and demonstrate that BD4 mutations increase ccRCC cell growth. Because of the link between PBRM1 status and sensitivity to immune checkpoint inhibitor treatment, these data also suggest the relevance of BD4 as a potential clinical target.</AbstractText>
<CopyrightInformation>© 2018 Slaughter et al.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Slaughter</LastName>
<ForeName>Mariesa J</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo>
<Affiliation>From the Department of Genetics, Curriculum in Genetics and Molecular Biology.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Shanle</LastName>
<ForeName>Erin K</ForeName>
<Initials>EK</Initials>
<AffiliationInfo>
<Affiliation>Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599 and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>McFadden</LastName>
<ForeName>Andrew W</ForeName>
<Initials>AW</Initials>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Hollis</LastName>
<ForeName>Emily S</ForeName>
<Initials>ES</Initials>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Suttle</LastName>
<ForeName>Lindsey E</ForeName>
<Initials>LE</Initials>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Strahl</LastName>
<ForeName>Brian D</ForeName>
<Initials>BD</Initials>
<AffiliationInfo>
<Affiliation>From the Department of Genetics, Curriculum in Genetics and Molecular Biology.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599 and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Davis</LastName>
<ForeName>Ian J</ForeName>
<Initials>IJ</Initials>
<AffiliationInfo>
<Affiliation>From the Department of Genetics, Curriculum in Genetics and Molecular Biology, ian_davis@med.unc.edu.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Lineberger Comprehensive Cancer Center.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>the Department of Pediatrics, University of North Carolina, Chapel Hill, North Carolina 27514.</Affiliation>
</AffiliationInfo>
</Author>