ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Publication Date: 2015-06-24
    Description: Despite the rapid accumulation of tumor-profiling data and transcription factor (TF) ChIP-seq profiles, efforts integrating TF binding with the tumor-profiling data to understand how TFs regulate tumor gene expression are still limited. To systematically search for cancer-associated TFs, we comprehensively integrated 686 ENCODE ChIP-seq profiles representing 150 TFs with 7484...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2012-10-03
    Description: B cells and plasma cells possess distinct RNA processing environments that respectively promote the expression of membrane-associated Ig by B cells versus the secretion of Ig by plasma cells. Through a combination of transcriptional profiling and screening using a lentiviral short-hairpin RNA interference library, we show that both the splicing...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2010-03-26
    Description: After fertilization the embryonic genome is inactive until transcription is initiated during the maternal-zygotic transition. This transition coincides with the formation of pluripotent cells, which in mammals can be used to generate embryonic stem cells. To study the changes in chromatin structure that accompany pluripotency and genome activation, we mapped the genomic locations of histone H3 molecules bearing lysine trimethylation modifications before and after the maternal-zygotic transition in zebrafish. Histone H3 lysine 27 trimethylation (H3K27me3), which is repressive, and H3K4me3, which is activating, were not detected before the transition. After genome activation, more than 80% of genes were marked by H3K4me3, including many inactive developmental regulatory genes that were also marked by H3K27me3. Sequential chromatin immunoprecipitation demonstrated that the same promoter regions had both trimethylation marks. Such bivalent chromatin domains also exist in embryonic stem cells and are thought to poise genes for activation while keeping them repressed. Furthermore, we found many inactive genes that were uniquely marked by H3K4me3. Despite this activating modification, these monovalent genes were neither expressed nor stably bound by RNA polymerase II. Inspection of published data sets revealed similar monovalent domains in embryonic stem cells. Moreover, H3K4me3 marks could form in the absence of both sequence-specific transcriptional activators and stable association of RNA polymerase II, as indicated by the analysis of an inducible transgene. These results indicate that bivalent and monovalent domains might poise embryonic genes for activation and that the chromatin profile associated with pluripotency is established during the maternal-zygotic transition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874748/" 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/PMC2874748/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vastenhouw, Nadine L -- Zhang, Yong -- Woods, Ian G -- Imam, Farhad -- Regev, Aviv -- Liu, X Shirley -- Rinn, John -- Schier, Alexander F -- 1R01 HG004069/HG/NHGRI NIH HHS/ -- 5R01 GM56211/GM/NIGMS NIH HHS/ -- DP1 OD003958/OD/NIH HHS/ -- R01 GM056211/GM/NIGMS NIH HHS/ -- R01 GM056211-11/GM/NIGMS NIH HHS/ -- R01 GM056211-12/GM/NIGMS NIH HHS/ -- R01 GM056211-12S1/GM/NIGMS NIH HHS/ -- R01 GM056211-13/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Apr 8;464(7290):922-6. doi: 10.1038/nature08866. Epub 2010 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20336069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/*genetics/*metabolism ; Chromatin Immunoprecipitation ; *Gene Expression Regulation, Developmental/genetics ; Gene Silencing ; Genome/*genetics ; Histones/chemistry/metabolism ; Lysine/metabolism ; Methylation ; Oligonucleotide Array Sequence Analysis ; Pluripotent Stem Cells/*metabolism ; Promoter Regions, Genetic/genetics ; RNA Polymerase II/metabolism ; Transcriptional Activation ; Transgenes ; Zebrafish/*embryology/*genetics/metabolism ; Zebrafish Proteins/genetics ; Zygote/cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2011-03-12
    Description: Disruption of the circadian clock exacerbates metabolic diseases, including obesity and diabetes. We show that histone deacetylase 3 (HDAC3) recruitment to the genome displays a circadian rhythm in mouse liver. Histone acetylation is inversely related to HDAC3 binding, and this rhythm is lost when HDAC3 is absent. Although amounts of HDAC3 are constant, its genomic recruitment in liver corresponds to the expression pattern of the circadian nuclear receptor Rev-erbalpha. Rev-erbalpha colocalizes with HDAC3 near genes regulating lipid metabolism, and deletion of HDAC3 or Rev-erbalpha in mouse liver causes hepatic steatosis. Thus, genomic recruitment of HDAC3 by Rev-erbalpha directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389392/" 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/PMC3389392/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Dan -- Liu, Tao -- Sun, Zheng -- Bugge, Anne -- Mullican, Shannon E -- Alenghat, Theresa -- Liu, X Shirley -- Lazar, Mitchell A -- DK19525/DK/NIDDK NIH HHS/ -- DK43806/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- DK49210/DK/NIDDK NIH HHS/ -- HG4069/HG/NHGRI NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- R01 DK045586/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- R37 DK043806-20/DK/NIDDK NIH HHS/ -- RC1 DK086239/DK/NIDDK NIH HHS/ -- RC1DK08623/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1315-9. doi: 10.1126/science.1198125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, 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/21393543" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Chromatin Immunoprecipitation ; Chronobiology Disorders/genetics/metabolism ; *Circadian Clocks ; *Circadian Rhythm ; DNA/metabolism ; Epigenesis, Genetic ; Fatty Liver/*metabolism ; Gene Expression Regulation ; *Genome ; Histone Deacetylases/*metabolism ; Histones/metabolism ; Homeostasis ; *Lipid Metabolism ; Lipogenesis/genetics ; Liver/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Nuclear Receptor Co-Repressor 1/metabolism ; Nuclear Receptor Subfamily 1, Group D, Member 1/genetics/metabolism ; RNA Polymerase II/metabolism ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2012-12-15
    Description: Epigenetic regulators represent a promising new class of therapeutic targets for cancer. Enhancer of zeste homolog 2 (EZH2), a subunit of Polycomb repressive complex 2 (PRC2), silences gene expression via its histone methyltransferase activity. We found that the oncogenic function of EZH2 in cells of castration-resistant prostate cancer is independent of its role as a transcriptional repressor. Instead, it involves the ability of EZH2 to act as a coactivator for critical transcription factors including the androgen receptor. This functional switch is dependent on phosphorylation of EZH2 and requires an intact methyltransferase domain. Hence, targeting the non-PRC2 function of EZH2 may have therapeutic efficacy for treating metastatic, hormone-refractory prostate cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625962/" 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/PMC3625962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Kexin -- Wu, Zhenhua Jeremy -- Groner, Anna C -- He, Housheng Hansen -- Cai, Changmeng -- Lis, Rosina T -- Wu, Xiaoqiu -- Stack, Edward C -- Loda, Massimo -- Liu, Tao -- Xu, Han -- Cato, Laura -- Thornton, James E -- Gregory, Richard I -- Morrissey, Colm -- Vessella, Robert L -- Montironi, Rodolfo -- Magi-Galluzzi, Cristina -- Kantoff, Philip W -- Balk, Steven P -- Liu, X Shirley -- Brown, Myles -- CA090381/CA/NCI NIH HHS/ -- CA097186/CA/NCI NIH HHS/ -- CA111803/CA/NCI NIH HHS/ -- CA131945/CA/NCI NIH HHS/ -- CA166507/CA/NCI NIH HHS/ -- CA85859/CA/NCI NIH HHS/ -- CA89021/CA/NCI NIH HHS/ -- CA90381/CA/NCI NIH HHS/ -- GM99409/GM/NIGMS NIH HHS/ -- K99 CA166507/CA/NCI NIH HHS/ -- P50 CA090381/CA/NCI NIH HHS/ -- R01 GM099409/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Dec 14;338(6113):1465-9. doi: 10.1126/science.1227604.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239736" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Castration ; Cell Line, Tumor ; Cohort Studies ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Humans ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Male ; Methyltransferases/chemistry/genetics/metabolism ; Mice ; Mice, Inbred ICR ; Mice, SCID ; Oncogene Proteins/genetics/*metabolism ; Polycomb Repressive Complex 2/genetics/*metabolism ; Prostatic Neoplasms/genetics/*metabolism/mortality ; Protein Structure, Tertiary ; Receptors, Androgen/metabolism ; Xenograft Model Antitumor Assays
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2014-03-29
    Description: Human neurons are functional over an entire lifetime, yet the mechanisms that preserve function and protect against neurodegeneration during ageing are unknown. Here we show that induction of the repressor element 1-silencing transcription factor (REST; also known as neuron-restrictive silencer factor, NRSF) is a universal feature of normal ageing in human cortical and hippocampal neurons. REST is lost, however, in mild cognitive impairment and Alzheimer's disease. Chromatin immunoprecipitation with deep sequencing and expression analysis show that REST represses genes that promote cell death and Alzheimer's disease pathology, and induces the expression of stress response genes. Moreover, REST potently protects neurons from oxidative stress and amyloid beta-protein toxicity, and conditional deletion of REST in the mouse brain leads to age-related neurodegeneration. A functional orthologue of REST, Caenorhabditis elegans SPR-4, also protects against oxidative stress and amyloid beta-protein toxicity. During normal ageing, REST is induced in part by cell non-autonomous Wnt signalling. However, in Alzheimer's disease, frontotemporal dementia and dementia with Lewy bodies, REST is lost from the nucleus and appears in autophagosomes together with pathological misfolded proteins. Finally, REST levels during ageing are closely correlated with cognitive preservation and longevity. Thus, the activation state of REST may distinguish neuroprotection from neurodegeneration in the ageing brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110979/" 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/PMC4110979/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Tao -- Aron, Liviu -- Zullo, Joseph -- Pan, Ying -- Kim, Haeyoung -- Chen, Yiwen -- Yang, Tun-Hsiang -- Kim, Hyun-Min -- Drake, Derek -- Liu, X Shirley -- Bennett, David A -- Colaiacovo, Monica P -- Yankner, Bruce A -- DP1 AG044161/AG/NIA NIH HHS/ -- DP1 OD006849/OD/NIH HHS/ -- DP1OD006849/OD/NIH HHS/ -- P01 AG027916/AG/NIA NIH HHS/ -- P01AG27916/AG/NIA NIH HHS/ -- P30 AG010161/AG/NIA NIH HHS/ -- P30AG10161/AG/NIA NIH HHS/ -- R01 AG015819/AG/NIA NIH HHS/ -- R01 AG017917/AG/NIA NIH HHS/ -- R01 AG026651/AG/NIA NIH HHS/ -- R01 GM105853/GM/NIGMS NIH HHS/ -- R01AG15819/AG/NIA NIH HHS/ -- R01AG17917/AG/NIA NIH HHS/ -- R01AG26651/AG/NIA NIH HHS/ -- R01GM072551/GM/NIGMS NIH HHS/ -- T32 AG000222/AG/NIA NIH HHS/ -- England -- Nature. 2014 Mar 27;507(7493):448-54. doi: 10.1038/nature13163. Epub 2014 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Biostatistics and Computational Biology, Dana-Faber Cancer Institute and Harvard School of Public Health, Boston, Massachusetts 02115, USA. ; Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, Illinois 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670762" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging/genetics/*metabolism/pathology ; Alzheimer Disease/genetics/*metabolism/pathology ; Amyloid beta-Peptides/antagonists & inhibitors/toxicity ; Animals ; Autophagy ; Brain/cytology/metabolism/pathology ; Caenorhabditis elegans Proteins/metabolism ; Cell Death/genetics ; Cell Nucleus/metabolism ; Chromatin Immunoprecipitation ; Cognition ; DNA-Binding Proteins/metabolism ; Down-Regulation ; Frontotemporal Dementia/metabolism/pathology ; Gene Expression Regulation ; Humans ; Lewy Body Disease/metabolism/pathology ; Longevity ; Mice ; Mild Cognitive Impairment/metabolism ; Neurons/cytology/metabolism/pathology ; Neuroprotective Agents/metabolism ; *Oxidative Stress/genetics/physiology ; Phagosomes ; Repressor Proteins/deficiency/genetics/*metabolism ; Transcription Factors/metabolism ; Up-Regulation ; Wnt Signaling Pathway ; Young Adult
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 7
    Publication Date: 2010-01-22
    Description: Cyclin D1 belongs to the core cell cycle machinery, and it is frequently overexpressed in human cancers. The full repertoire of cyclin D1 functions in normal development and oncogenesis is unclear at present. Here we developed Flag- and haemagglutinin-tagged cyclin D1 knock-in mouse strains that allowed a high-throughput mass spectrometry approach to search for cyclin D1-binding proteins in different mouse organs. In addition to cell cycle partners, we observed several proteins involved in transcription. Genome-wide location analyses (chromatin immunoprecipitation coupled to DNA microarray; ChIP-chip) showed that during mouse development cyclin D1 occupies promoters of abundantly expressed genes. In particular, we found that in developing mouse retinas-an organ that critically requires cyclin D1 function-cyclin D1 binds the upstream regulatory region of the Notch1 gene, where it serves to recruit CREB binding protein (CBP) histone acetyltransferase. Genetic ablation of cyclin D1 resulted in decreased CBP recruitment, decreased histone acetylation of the Notch1 promoter region, and led to decreased levels of the Notch1 transcript and protein in cyclin D1-null (Ccnd1(-/-)) retinas. Transduction of an activated allele of Notch1 into Ccnd1(-/-) retinas increased proliferation of retinal progenitor cells, indicating that upregulation of Notch1 signalling alleviates the phenotype of cyclin D1-deficiency. These studies show that in addition to its well-established cell cycle roles, cyclin D1 has an in vivo transcriptional function in mouse development. Our approach, which we term 'genetic-proteomic', can be used to study the in vivo function of essentially any protein.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943587/" 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/PMC2943587/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bienvenu, Frederic -- Jirawatnotai, Siwanon -- Elias, Joshua E -- Meyer, Clifford A -- Mizeracka, Karolina -- Marson, Alexander -- Frampton, Garrett M -- Cole, Megan F -- Odom, Duncan T -- Odajima, Junko -- Geng, Yan -- Zagozdzon, Agnieszka -- Jecrois, Marie -- Young, Richard A -- Liu, X Shirley -- Cepko, Constance L -- Gygi, Steven P -- Sicinski, Piotr -- 15603/Cancer Research UK/United Kingdom -- A15603/Cancer Research UK/United Kingdom -- HG004069/HG/NHGRI NIH HHS/ -- HG3456/HG/NHGRI NIH HHS/ -- P01 CA080111/CA/NCI NIH HHS/ -- P01 CA080111-128270/CA/NCI NIH HHS/ -- P01 CA109901/CA/NCI NIH HHS/ -- P01 CA109901-067138/CA/NCI NIH HHS/ -- P01 CA109901-067140/CA/NCI NIH HHS/ -- R01 CA108420/CA/NCI NIH HHS/ -- R01 CA108420-07/CA/NCI NIH HHS/ -- R01 EY008064/EY/NEI NIH HHS/ -- R01 EY009676/EY/NEI NIH HHS/ -- R01 EY009676-18/EY/NEI NIH HHS/ -- R01 EYO9676/PHS HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-07/HG/NHGRI NIH HHS/ -- R01 HG003456/HG/NHGRI NIH HHS/ -- R01 HG003456-06/HG/NHGRI NIH HHS/ -- R01 HG004069/HG/NHGRI NIH HHS/ -- R01 HG004069-04/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2010 Jan 21;463(7279):374-8. doi: 10.1038/nature08684.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20090754" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; CREB-Binding Protein/metabolism ; Chromatin Immunoprecipitation ; Cyclin D1/deficiency/genetics/*metabolism ; *Gene Expression Regulation, Developmental ; Genome/genetics ; High-Throughput Screening Assays ; Histone Acetyltransferases/metabolism ; Mass Spectrometry ; Mice ; Oligonucleotide Array Sequence Analysis ; Promoter Regions, Genetic/genetics ; Protein Binding ; *Proteomics/methods ; Rats ; Receptor, Notch1/genetics/metabolism ; Retina/cytology/embryology/metabolism ; Stem Cells/cytology/metabolism ; *Transcription, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 2011-05-10
    Description: 5-hydroxymethylcytosine (5hmC) is a modified base present at low levels in diverse cell types in mammals. 5hmC is generated by the TET family of Fe(II) and 2-oxoglutarate-dependent enzymes through oxidation of 5-methylcytosine (5mC). 5hmC and TET proteins have been implicated in stem cell biology and cancer, but information on the genome-wide distribution of 5hmC is limited. Here we describe two novel and specific approaches to profile the genomic localization of 5hmC. The first approach, termed GLIB (glucosylation, periodate oxidation, biotinylation) uses a combination of enzymatic and chemical steps to isolate DNA fragments containing as few as a single 5hmC. The second approach involves conversion of 5hmC to cytosine 5-methylenesulphonate (CMS) by treatment of genomic DNA with sodium bisulphite, followed by immunoprecipitation of CMS-containing DNA with a specific antiserum to CMS. High-throughput sequencing of 5hmC-containing DNA from mouse embryonic stem (ES) cells showed strong enrichment within exons and near transcriptional start sites. 5hmC was especially enriched at the start sites of genes whose promoters bear dual histone 3 lysine 27 trimethylation (H3K27me3) and histone 3 lysine 4 trimethylation (H3K4me3) marks. Our results indicate that 5hmC has a probable role in transcriptional regulation, and suggest a model in which 5hmC contributes to the 'poised' chromatin signature found at developmentally-regulated genes in ES cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3124347/" 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/PMC3124347/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pastor, William A -- Pape, Utz J -- Huang, Yun -- Henderson, Hope R -- Lister, Ryan -- Ko, Myunggon -- McLoughlin, Erin M -- Brudno, Yevgeny -- Mahapatra, Sahasransu -- Kapranov, Philipp -- Tahiliani, Mamta -- Daley, George Q -- Liu, X Shirley -- Ecker, Joseph R -- Milos, Patrice M -- Agarwal, Suneet -- Rao, Anjana -- 1 R01 HD065812-01A1/HD/NICHD NIH HHS/ -- 1 UL1 RR 025758-02/RR/NCRR NIH HHS/ -- K08 HL089150/HL/NHLBI NIH HHS/ -- K08 HL089150-01A1/HL/NHLBI NIH HHS/ -- R01 AI044432/AI/NIAID NIH HHS/ -- R01 AI044432-10/AI/NIAID NIH HHS/ -- R01 AI44432/AI/NIAID NIH HHS/ -- R01 HD065812/HD/NICHD NIH HHS/ -- R01 HD065812-01A1/HD/NICHD NIH HHS/ -- RC1 DA028422/DA/NIDA NIH HHS/ -- RC1 DA028422-02/DA/NIDA NIH HHS/ -- UL1 RR025758/RR/NCRR NIH HHS/ -- England -- Nature. 2011 May 19;473(7347):394-7. doi: 10.1038/nature10102. Epub 2011 May 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children's Hospital Boston, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21552279" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotinylation ; Cell Line ; Cytosine/*analogs & derivatives/analysis/isolation & purification/metabolism ; DNA Methylation ; Embryonic Stem Cells/*metabolism ; Exons/genetics ; Gene Expression Regulation, Developmental/genetics ; Genome/*genetics ; Glucose/metabolism ; Mice ; Periodic Acid/metabolism ; Promoter Regions, Genetic/genetics ; Sequence Analysis, DNA/*methods ; Transcription Initiation Site ; Transcription, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 9
    Publication Date: 2014-08-29
    Description: Genome function is dynamically regulated in part by chromatin, which consists of the histones, non-histone proteins and RNA molecules that package DNA. Studies in Caenorhabditis elegans and Drosophila melanogaster have contributed substantially to our understanding of molecular mechanisms of genome function in humans, and have revealed conservation of chromatin components and mechanisms. Nevertheless, the three organisms have markedly different genome sizes, chromosome architecture and gene organization. On human and fly chromosomes, for example, pericentric heterochromatin flanks single centromeres, whereas worm chromosomes have dispersed heterochromatin-like regions enriched in the distal chromosomal 'arms', and centromeres distributed along their lengths. To systematically investigate chromatin organization and associated gene regulation across species, we generated and analysed a large collection of genome-wide chromatin data sets from cell lines and developmental stages in worm, fly and human. Here we present over 800 new data sets from our ENCODE and modENCODE consortia, bringing the total to over 1,400. Comparison of combinatorial patterns of histone modifications, nuclear lamina-associated domains, organization of large-scale topological domains, chromatin environment at promoters and enhancers, nucleosome positioning, and DNA replication patterns reveals many conserved features of chromatin organization among the three organisms. We also find notable differences in the composition and locations of repressive chromatin. These data sets and analyses provide a rich resource for comparative and species-specific investigations of chromatin composition, organization and function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4227084/" 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/PMC4227084/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ho, Joshua W K -- Jung, Youngsook L -- Liu, Tao -- Alver, Burak H -- Lee, Soohyun -- Ikegami, Kohta -- Sohn, Kyung-Ah -- Minoda, Aki -- Tolstorukov, Michael Y -- Appert, Alex -- Parker, Stephen C J -- Gu, Tingting -- Kundaje, Anshul -- Riddle, Nicole C -- Bishop, Eric -- Egelhofer, Thea A -- Hu, Sheng'en Shawn -- Alekseyenko, Artyom A -- Rechtsteiner, Andreas -- Asker, Dalal -- Belsky, Jason A -- Bowman, Sarah K -- Chen, Q Brent -- Chen, Ron A-J -- Day, Daniel S -- Dong, Yan -- Dose, Andrea C -- Duan, Xikun -- Epstein, Charles B -- Ercan, Sevinc -- Feingold, Elise A -- Ferrari, Francesco -- Garrigues, Jacob M -- Gehlenborg, Nils -- Good, Peter J -- Haseley, Psalm -- He, Daniel -- Herrmann, Moritz -- Hoffman, Michael M -- Jeffers, Tess E -- Kharchenko, Peter V -- Kolasinska-Zwierz, Paulina -- Kotwaliwale, Chitra V -- Kumar, Nischay -- Langley, Sasha A -- Larschan, Erica N -- Latorre, Isabel -- Libbrecht, Maxwell W -- Lin, Xueqiu -- Park, Richard -- Pazin, Michael J -- Pham, Hoang N -- Plachetka, Annette -- Qin, Bo -- Schwartz, Yuri B -- Shoresh, Noam -- Stempor, Przemyslaw -- Vielle, Anne -- Wang, Chengyang -- Whittle, Christina M -- Xue, Huiling -- Kingston, Robert E -- Kim, Ju Han -- Bernstein, Bradley E -- Dernburg, Abby F -- Pirrotta, Vincenzo -- Kuroda, Mitzi I -- Noble, William S -- Tullius, Thomas D -- Kellis, Manolis -- MacAlpine, David M -- Strome, Susan -- Elgin, Sarah C R -- Liu, Xiaole Shirley -- Lieb, Jason D -- Ahringer, Julie -- Karpen, Gary H -- Park, Peter J -- 092096/Wellcome Trust/United Kingdom -- 101863/Wellcome Trust/United Kingdom -- 54523/Wellcome Trust/United Kingdom -- 5RL9EB008539/EB/NIBIB NIH HHS/ -- K99 HG006259/HG/NHGRI NIH HHS/ -- K99HG006259/HG/NHGRI NIH HHS/ -- R01 GM098461/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R37 GM048405/GM/NIGMS NIH HHS/ -- T32 GM071340/GM/NIGMS NIH HHS/ -- T32 HG002295/HG/NHGRI NIH HHS/ -- U01 HG004258/HG/NHGRI NIH HHS/ -- U01 HG004270/HG/NHGRI NIH HHS/ -- U01 HG004279/HG/NHGRI NIH HHS/ -- U01 HG004695/HG/NHGRI NIH HHS/ -- U01HG004258/HG/NHGRI NIH HHS/ -- U01HG004270/HG/NHGRI NIH HHS/ -- U01HG004279/HG/NHGRI NIH HHS/ -- U01HG004695/HG/NHGRI NIH HHS/ -- U54 CA121852/CA/NCI NIH HHS/ -- U54 HG004570/HG/NHGRI NIH HHS/ -- U54 HG006991/HG/NHGRI NIH HHS/ -- U54CA121852/CA/NCI NIH HHS/ -- U54HG004570/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Aug 28;512(7515):449-52. doi: 10.1038/nature13415.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA [3] [4] Victor Chang Cardiac Research Institute and The University of New South Wales, Sydney, New South Wales 2052, Australia (J.W.K.H.); Department of Biochemistry, University at Buffalo, Buffalo, New York 14203, USA (T.L.); Department of Molecular Biology and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA (K.I., T.E.J.); Department of Human Genetics, University of Chicago, Chicago, Illinois 06037, USA (J.D.L.); Division of Genomic Technologies, Center for Life Science Technologies, RIKEN, Yokohama 230-0045, Japan (A.M.); Department of Genetics, Department of Computer Science, Stanford University, Stanford, California 94305, USA (A.K.); Department of Biology, The University of Alabama at Birmingham, Birmingham, Alabama 35294, USA (N.C.R.). ; 1] Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA [3]. ; 1] Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard School of Public Health, 450 Brookline Avenue, Boston, Massachusetts 02215, USA [3] [4] Victor Chang Cardiac Research Institute and The University of New South Wales, Sydney, New South Wales 2052, Australia (J.W.K.H.); Department of Biochemistry, University at Buffalo, Buffalo, New York 14203, USA (T.L.); Department of Molecular Biology and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA (K.I., T.E.J.); Department of Human Genetics, University of Chicago, Chicago, Illinois 06037, USA (J.D.L.); Division of Genomic Technologies, Center for Life Science Technologies, RIKEN, Yokohama 230-0045, Japan (A.M.); Department of Genetics, Department of Computer Science, Stanford University, Stanford, California 94305, USA (A.K.); Department of Biology, The University of Alabama at Birmingham, Birmingham, Alabama 35294, USA (N.C.R.). ; Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Biology and Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA [2] Victor Chang Cardiac Research Institute and The University of New South Wales, Sydney, New South Wales 2052, Australia (J.W.K.H.); Department of Biochemistry, University at Buffalo, Buffalo, New York 14203, USA (T.L.); Department of Molecular Biology and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA (K.I., T.E.J.); Department of Human Genetics, University of Chicago, Chicago, Illinois 06037, USA (J.D.L.); Division of Genomic Technologies, Center for Life Science Technologies, RIKEN, Yokohama 230-0045, Japan (A.M.); Department of Genetics, Department of Computer Science, Stanford University, Stanford, California 94305, USA (A.K.); Department of Biology, The University of Alabama at Birmingham, Birmingham, Alabama 35294, USA (N.C.R.). ; 1] Department of Information and Computer Engineering, Ajou University, Suwon 443-749, Korea [2] Systems Biomedical Informatics Research Center, College of Medicine, Seoul National University, Seoul 110-799, Korea. ; 1] Department of Genome Dynamics, Life Sciences Division, Lawrence Berkeley National Lab, Berkeley, California 94720, USA [2] Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA [3] Victor Chang Cardiac Research Institute and The University of New South Wales, Sydney, New South Wales 2052, Australia (J.W.K.H.); Department of Biochemistry, University at Buffalo, Buffalo, New York 14203, USA (T.L.); Department of Molecular Biology and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA (K.I., T.E.J.); Department of Human Genetics, University of Chicago, Chicago, Illinois 06037, USA (J.D.L.); Division of Genomic Technologies, Center for Life Science Technologies, RIKEN, Yokohama 230-0045, Japan (A.M.); Department of Genetics, Department of Computer Science, Stanford University, Stanford, California 94305, USA (A.K.); Department of Biology, The University of Alabama at Birmingham, Birmingham, Alabama 35294, USA (N.C.R.). ; 1] Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Department of Molecular Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. ; The Gurdon Institute and Department of Genetics, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK. ; 1] National Institute of General Medical Sciences, National Institutes of Health, Bethesda, Maryland 20892, USA [2] National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Department of Biology, Washington University in St. Louis, St. Louis, Missouri 63130, USA. ; 1] Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA [2] Broad Institute, Cambridge, Massachusetts 02141, USA [3] Victor Chang Cardiac Research Institute and The University of New South Wales, Sydney, New South Wales 2052, Australia (J.W.K.H.); Department of Biochemistry, University at Buffalo, Buffalo, New York 14203, USA (T.L.); Department of Molecular Biology and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA (K.I., T.E.J.); Department of Human Genetics, University of Chicago, Chicago, Illinois 06037, USA (J.D.L.); Division of Genomic Technologies, Center for Life Science Technologies, RIKEN, Yokohama 230-0045, Japan (A.M.); Department of Genetics, Department of Computer Science, Stanford University, Stanford, California 94305, USA (A.K.); Department of Biology, The University of Alabama at Birmingham, Birmingham, Alabama 35294, USA (N.C.R.). ; 1] Department of Biology, Washington University in St. Louis, St. Louis, Missouri 63130, USA [2] Victor Chang Cardiac Research Institute and The University of New South Wales, Sydney, New South Wales 2052, Australia (J.W.K.H.); Department of Biochemistry, University at Buffalo, Buffalo, New York 14203, USA (T.L.); Department of Molecular Biology and Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA (K.I., T.E.J.); Department of Human Genetics, University of Chicago, Chicago, Illinois 06037, USA (J.D.L.); Division of Genomic Technologies, Center for Life Science Technologies, RIKEN, Yokohama 230-0045, Japan (A.M.); Department of Genetics, Department of Computer Science, Stanford University, Stanford, California 94305, USA (A.K.); Department of Biology, The University of Alabama at Birmingham, Birmingham, Alabama 35294, USA (N.C.R.). ; 1] Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Program in Bioinformatics, Boston University, Boston, Massachusetts 02215, USA. ; Department of Molecular, Cell and Developmental Biology, University of California Santa Cruz, Santa Cruz, California 95064, USA. ; Department of Bioinformatics, School of Life Science and Technology, Tongji University, Shanghai 200092, China. ; 1] Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854, USA [2] Food Science and Technology Department, Faculty of Agriculture, Alexandria University, 21545 El-Shatby, Alexandria, Egypt. ; Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Department of Molecular Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. ; Department of Biology and Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA. ; 1] Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Harvard/MIT Division of Health Sciences and Technology, Cambridge, Massachusetts 02139, USA. ; Department of Anatomy Physiology and Cell Biology, University of California Davis, Davis, California 95616, USA. ; Broad Institute, Cambridge, Massachusetts 02141, USA. ; 1] Department of Biology and Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA [2] Department of Biology, Center for Genomics and Systems Biology, New York University, New York, New York 10003, USA. ; National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Broad Institute, Cambridge, Massachusetts 02141, USA. ; 1] Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA. ; Princess Margaret Cancer Centre, Toronto, Ontario M6G 1L7, Canada. ; 1] Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA [2] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA. ; 1] Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA [2] Broad Institute, Cambridge, Massachusetts 02141, USA. ; 1] Department of Genome Dynamics, Life Sciences Division, Lawrence Berkeley National Lab, Berkeley, California 94720, USA [2] Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA. ; Department of Molecular Biology, Cellular Biology and Biochemistry, Brown University, Providence, Rhode Island 02912, USA. ; Department of Computer Science and Engineering, University of Washington, Seattle, Washington 98195, USA. ; 1] Department of Genome Dynamics, Life Sciences Division, Lawrence Berkeley National Lab, Berkeley, California 94720, USA [2] Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA [3] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA. ; 1] Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854, USA [2] Department of Molecular Biology, Umea University, 901 87 Umea, Sweden. ; 1] Systems Biomedical Informatics Research Center, College of Medicine, Seoul National University, Seoul 110-799, Korea [2] Seoul National University Biomedical Informatics, Division of Biomedical Informatics, College of Medicine, Seoul National University, Seoul 110-799, Korea. ; 1] Broad Institute, Cambridge, Massachusetts 02141, USA [2] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA [3] Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. ; Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey 08854, USA. ; 1] Department of Computer Science and Engineering, University of Washington, Seattle, Washington 98195, USA [2] Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; 1] Program in Bioinformatics, Boston University, Boston, Massachusetts 02215, USA [2] Department of Chemistry, Boston University, Boston, Massachusetts 02215, USA. ; 1] Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard School of Public Health, 450 Brookline Avenue, Boston, Massachusetts 02215, USA [3] Broad Institute, Cambridge, Massachusetts 02141, USA. ; 1] Center for Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Informatics Program, Children's Hospital, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25164756" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*cytology/*genetics ; Cell Line ; Centromere/genetics/metabolism ; Chromatin/chemistry/*genetics/*metabolism ; Chromatin Assembly and Disassembly/genetics ; DNA Replication/genetics ; Drosophila melanogaster/*cytology/*genetics ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic ; Heterochromatin/chemistry/genetics/metabolism ; Histones/chemistry/metabolism ; Humans ; Molecular Sequence Annotation ; Nuclear Lamina/metabolism ; Nucleosomes/chemistry/genetics/metabolism ; Promoter Regions, Genetic/genetics ; Species Specificity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 10
    Publication Date: 2014-03-29
    Description: Cancer cells induce a set of adaptive response pathways to survive in the face of stressors due to inadequate vascularization. One such adaptive pathway is the unfolded protein (UPR) or endoplasmic reticulum (ER) stress response mediated in part by the ER-localized transmembrane sensor IRE1 (ref. 2) and its substrate XBP1 (ref. 3). Previous studies report UPR activation in various human tumours, but the role of XBP1 in cancer progression in mammary epithelial cells is largely unknown. Triple-negative breast cancer (TNBC)--a form of breast cancer in which tumour cells do not express the genes for oestrogen receptor, progesterone receptor and HER2 (also called ERBB2 or NEU)--is a highly aggressive malignancy with limited treatment options. Here we report that XBP1 is activated in TNBC and has a pivotal role in the tumorigenicity and progression of this human breast cancer subtype. In breast cancer cell line models, depletion of XBP1 inhibited tumour growth and tumour relapse and reduced the CD44(high)CD24(low) population. Hypoxia-inducing factor 1alpha (HIF1alpha) is known to be hyperactivated in TNBCs. Genome-wide mapping of the XBP1 transcriptional regulatory network revealed that XBP1 drives TNBC tumorigenicity by assembling a transcriptional complex with HIF1alpha that regulates the expression of HIF1alpha targets via the recruitment of RNA polymerase II. Analysis of independent cohorts of patients with TNBC revealed a specific XBP1 gene expression signature that was highly correlated with HIF1alpha and hypoxia-driven signatures and that strongly associated with poor prognosis. Our findings reveal a key function for the XBP1 branch of the UPR in TNBC and indicate that targeting this pathway may offer alternative treatment strategies for this aggressive subtype of breast cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105133/" 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/PMC4105133/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Xi -- Iliopoulos, Dimitrios -- Zhang, Qing -- Tang, Qianzi -- Greenblatt, Matthew B -- Hatziapostolou, Maria -- Lim, Elgene -- Tam, Wai Leong -- Ni, Min -- Chen, Yiwen -- Mai, Junhua -- Shen, Haifa -- Hu, Dorothy Z -- Adoro, Stanley -- Hu, Bella -- Song, Minkyung -- Tan, Chen -- Landis, Melissa D -- Ferrari, Mauro -- Shin, Sandra J -- Brown, Myles -- Chang, Jenny C -- Liu, X Shirley -- Glimcher, Laurie H -- AI32412/AI/NIAID NIH HHS/ -- CA112663/CA/NCI NIH HHS/ -- K99 CA175290/CA/NCI NIH HHS/ -- K99CA175290/CA/NCI NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- R00 CA160351/CA/NCI NIH HHS/ -- R01 AI032412/AI/NIAID NIH HHS/ -- R01 CA112663/CA/NCI NIH HHS/ -- R01 HG004069/HG/NHGRI NIH HHS/ -- R01HG004069/HG/NHGRI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Apr 3;508(7494):103-7. doi: 10.1038/nature13119. Epub 2014 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Sandra and Edward Meyer Cancer Center of Weill Cornell Medical College, 1300 York Avenue, New York, New York 10065, USA [2] Department of Medicine, Weill Cornell Medical College, 1300 York Avenue, New York, New York 10065, USA. ; 1] Center for Systems Biomedicine, Division of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA [2] Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [3]. ; 1] Lineberger Comprehensive Cancer Center, Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA [2]. ; 1] Department of Bioinformatics, School of Life Science and Technology, Tongji University, Shanghai 200092, China [2] Institute of Animal Genetics and Breeding, College of Animal Science and Technology, Sichuan Agricultural University, Ya'an, Sichuan 625014, China [3]. ; Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. ; 1] Center for Systems Biomedicine, Division of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA [2] Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA. ; Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard School of Public Health, Boston, Massachusetts 02215, USA. ; Department of Nanomedicine, Houston Methodist Research Institute, Houston, Texas 77030, USA. ; 1] Department of Nanomedicine, Houston Methodist Research Institute, Houston, Texas 77030, USA [2] Department of Cell and Developmental Biology, Weill Cornell Medical College, 1300 York Avenue, New York, New York 10065, USA. ; Endocrine Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. ; Division of Hematology/Oncology, Children's Hospital Boston, Boston, Massachusetts 02115, USA. ; Houston Methodist Cancer Center, Houston, Texas 77030, USA. ; 1] Department of Medicine, Weill Cornell Medical College, 1300 York Avenue, New York, New York 10065, USA [2] Department of Nanomedicine, Houston Methodist Research Institute, Houston, Texas 77030, USA. ; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, 1300 York Avenue, New York, New York 10065, USA. ; 1] Department of Medicine, Weill Cornell Medical College, 1300 York Avenue, New York, New York 10065, USA [2] Houston Methodist Cancer Center, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670641" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD24/metabolism ; Antigens, CD44/metabolism ; Cell Hypoxia/genetics ; Cell Line, Tumor ; Cell Proliferation ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Gene Silencing ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism ; Mice ; Neoplasm Invasiveness ; Neoplasm Recurrence, Local ; Prognosis ; RNA Polymerase II/metabolism ; Transcription Factors/deficiency/genetics/*metabolism ; Transcription, Genetic ; Triple Negative Breast Neoplasms/blood supply/genetics/*metabolism/*pathology ; Unfolded Protein Response
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...