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Rickettsial evolution in the light of comparative genomics

BIOLOGICAL REVIEWS 2011年第2期86卷 379-405页

作者： Merhej, Vicky Raoult, Didier Univ Mediterranean Fac Med CNRS IRD Unit Res Emergent & Trop Infect Dis URMITEUMR 62 Marseilles France

Rickettsia are best known as strictly intracellular vector-borne bacteria that cause mild to severe diseases in humans and other animals. Recent advances in molecular tools and biological experiments have unveiled a wide diversity of Rickettsia spp. that include species with a broad host range and some species that act as endosymbiotic associates. Molecular phylogenies of Rickettsia spp. contain some ambiguities, such as the position of R. canadensis and relationships within the spotted fever group. In the modern era of genomics, with an ever-increasing number of sequenced genomes, there is enhanced interest in the use of whole-genome sequences to understand pathogenesis and assess evolutionary relationships among rickettsial species. Rickettsia have small genomes (1.1-1.5 Mb) as a result of reductive evolution. These genomes contain split genes, gene remnants and pseudogenes that, owing to the colinearity of some rickettsial genomes, may represent different steps of the genome degradation process. Genomics reveal extreme genome reduction and massive gene loss in highly vertebrate-pathogenic Rickettsia compared to less virulent or endosymbiotic species. Information gleaned from rickettsial genomics challenges traditional concepts of pathogenesis that focused primarily on the acquisition of virulence factors. Another intriguing phenomenon about the reduced rickettsial genomes concerns the large fraction of non-coding dna and possible functionality of these "non-coding" sequences, because of the high conservation of these regions. Despite genome streamlining, Rickettsia spp. contain gene families, selfish dna, repeat palindromic elements and genes encoding eukaryotic-like motifs. These features participate in sequence and functional diversity and may play a crucial role in adaptation to the host cell and pathogenesis. Genome analyses have identified a large fraction of mobile genetic elements, including plasmids, suggesting the possibility of lateral gene transfer in

关键词： Rickettsia diversity gene loss pathogenicity non-coding dna pseudogenes dna repeats lateral gene transfer

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iDHS-EL: identifying dnase I hypersensitive sites by fusing three different modes of pseudo nucleotide composition into an ensemble learning framework

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BIOINFORMATICS 2016年第16期32卷 2411-2418页

作者： Liu, Bin Long, Ren Chou, Kuo-Chen Harbin Inst Technol Shenzhen Grad Sch Sch Comp Sci & Technol Shenzhen 518055 Guangdong Peoples R China Harbin Inst Technol Shenzhen Grad Sch Key Lab Network Oriented Intelligent Computat Shenzhen 518055 Guangdong Peoples R China Gordon Life Sci Inst Belmont MA 02478 USA King Abdulaziz Univ CEGMR Jeddah 21589 Saudi Arabia

Motivation: Regulatory dna elements are associated with dnase I hypersensitive sites (DHSs). Accordingly, identification of DHSs will provide useful insights for in-depth investigation into the function of noncoding genomic regions. Results: In this study, using the strategy of ensemble learning framework, we proposed a new predictor called iDHS-EL for identifying the location of DHS in human genome. It was formed by fusing three individual Random Forest (RF) classifiers into an ensemble predictor. The three RF operators were respectively based on the three special modes of the general pseudo nucleotide composition (PseKNC): (i) kmer, (ii) reverse complement kmer and (iii) pseudo dinucleotide composition. It has been demonstrated that the new predictor remarkably outperforms the relevant state-of-the-art methods in both accuracy and stability.

关键词： NUCLEOTIDES dna non-coding dna HUMAN genome CHROMATIN TRANSCRIPTION factors

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ChroMoS: an integrated web tool for SNP classification, prioritization and functional interpretation

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BIOINFORMATICS 2013年第17期29卷 2197-2198页

作者： Barenboim, Maxim Manke, Thomas Max Planck Inst Immunobiol & Epigenet Bioinformat & Deep Sequencing Unit D-79108 Freiburg Germany

Genome-wide association studies and re-sequencing projects are revealing an increasing number of disease-associated SNPs, a large fraction of which are non-coding. Although they could have relevance for disease susceptibility and progression, the lack of information about regulatory regions impedes the assessment of their functionality. Here we present a web server, ChroMoS (Chromatin Modified SNPs), which combines genetic and epigenetic data with the goal of facilitating SNPs' classification, prioritization and prediction of their functional consequences. ChroMoS uses a large database of SNPs and chromatin states, but allows a user to provide his/her own genetic information. Based on the SNP classification and interactive prioritization, a user can compute the functional impact of multiple SNPs using two prediction tools, one for differential analysis of transcription factor binding (sTRAP) and another for SNPs with potential impact on binding of miRNAs (MicroSNiPer).

关键词： SINGLE nucleotide polymorphisms GENOMES non-coding dna GENETIC regulation BIOINFORMATICS CHROMATIN

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Association of miR-760 with cancer: An overview

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GENE 2020年 747卷 144648-144648页

作者： Manvati, Monika Kaushik Siddharth Khan, Juveria Verma, Neeraj Dhar, Pawan K. Jawaharlal Nehru Univ Sch Biotechnol New Mehrauli Rd New Delhi 110067 India

MicroRNAs (miRNAs) are small non-coding RNA molecules of around 22 nucleotides in length. They are crucially involved in the post transcriptional regulation and thus play a significant role in the modulation of different diseases. Several studies have suggested that miRNA expression is dysregulated in various cancers through different mechanisms and the dysregulated miRNA in return affects different cancer hallmarks including cell proliferation, cell death suppression, metastasis and angiogenesis. Compilation of the available miRNA data can be a stimulator for proper understanding of the correlation between the miRNA expression and cancer progression. In this review, we have focussed on the role of miR-760 in the progression of different cancer. MicroRNA-760 (miR-760) has been found to be down regulated in various cancers, thus it can be utilized as a possible prognostic marker for cancer detection. Here, we have tried to fill a gap regarding the role of miR-760 in relation to cervical cancer also. Moreover, unravelling the role of miR-760 in different cancers will enlighten the researchers with proper understanding of biology of miR-760 in regulation of different cancers.

关键词： micro RNA Cancer miR-760 non-coding dna Regulation microRNA targets

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Repetitive elements dynamics in cell identity programming, maintenance and disease

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CURRENT OPINION IN CELL BIOLOGY 2014年 31卷 67-73页

作者： Bodega, Beatrice Orlando, Valerio Ist Nazl Genet Mol INGM Romeo & Enrica Invernizzi Genome Biol Unit I-20126 Milan Italy 4700 King Abdullah Univ Sci & Technol KAUST Environm Epigenet Res Program Biol Environm Sci & Engn Div Thuwal 239556900 Saudi Arabia

The days of 'junk dna' seem to be over. The rapid progress of genomics technologies has been unveiling unexpected mechanisms by which repetitive dna and in particular transposable elements (TEs) have evolved, becoming key issues in understanding genome structure and function. Indeed, rather than 'parasites', recent findings strongly suggest that TEs may have a positive function by contributing to tissue specific transcriptional programs, in particular as enhancer-like elements and/or modules for regulation of higher order chromatin structure. Further, it appears that during development and aging genomes experience several waves of TEs activation, and this contributes to individual genome shaping during lifetime. Interestingly, TEs activity is major target of epigenomic regulation. These findings are shedding new light on the genome-phenotype relationship and set the premises to help to explain complex disease manifestation, as consequence of TEs activity deregulation.

关键词： non-coding dna GENOMICS TRANSPOSONS PHENOTYPE GENETIC transcription CELLULAR aging

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Decoding the evolution of species

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SCIENCE 2017年第6341期356卷 904-905页

作者： Cooper, Kimberly L. Univ Calif San Diego Div Biol Sci La Jolla CA 92093 USA

In the middle of the 20th century, researchers identified dna and proteins and began to understand how they shape organisms. At first, scientists assumed that differences in protein sequence, structure, and function uniquely define any animal, including humans. Yet these building blocks are extraordinarily similar among animals, and human proteins can substitute for their counterparts in far simpler species (1-3). The modern dogma is that differences between species are largely a result of mutations in the noncoding instructions that determine when, where, and how much of a gene is expressed. On page 921 of this issue, Burga et al. (4) show that scientists may have underestimated the contribution of protein-coding mutations to evolution.

关键词： non-coding dna CIS-regulatory elements (Genetics) MUTATION (Biology) BIOSYSTEMATICS EVOLUTION (Biology) GENOMES SPECIATION (Biology)

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Two Histone/Protein Acetyltransferases, CBP and p300, Are Indispensable for Foxp3⁺ T-Regulatory Cell Development and Function

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MOLECULAR AND CELLULAR BIOLOGY 2014年第21期34卷 3993-4007页

作者： Liu, Yujie Wang, Liqing Han, Rongxiang Beier, Ulf H. Akimova, Tatiana Bhatti, Tricia Xiao, Haiyan Cole, Philip A. Brindle, Paul K. Hancock, Wayne W. Univ Penn Childrens Hosp Philadelphia Dept Pathol & Lab Med Div Transplant Immunol Philadelphia PA 19104 USA Univ Penn Childrens Hosp Philadelphia Biesecker Ctr Study Pediat Liver Dis Philadelphia PA 19104 USA Univ Penn Perelman Sch Med Philadelphia PA 19104 USA Univ Penn Childrens Hosp Philadelphia Dept Pediat Div Nephrol Philadelphia PA 19104 USA Univ Penn Childrens Hosp Philadelphia Philadelphia PA 19104 USA Perelman Sch Med Philadelphia PA USA Johns Hopkins Univ Sch Med Dept Pharmacol & Mol Sci Baltimore MD 21205 USA St Jude Childrens Res Hosp Dept Biochem Memphis TN 38105 USA

T-regulatory (Treg) cells are important to immune homeostasis, and Treg cell deficiency or dysfunction leads to autoimmune disease. A histone/protein acetyltransferase (HAT), p300, was recently found to be important for Treg function and stability, but further insights into the mechanisms by which p300 or other HATs affect Treg biology are needed. Here we show that CBP, a p300 paralog, is also important in controlling Treg function and stability. Thus, while mice with Treg-specific deletion of CBP or p300 developed minimal autoimmune disease, the combined deletion of CBP and p300 led to fatal autoimmunity by 3 to 4 weeks of age. The effects of CBP and p300 deletion on Treg development are dose dependent and involve multiple mechanisms. CBP and p300 cooperate with several key Treg transcription factors that act on the Foxp3 promoter to promote Foxp3 production. CBP and p300 also act on the Foxp3 conserved noncoding sequence 2 (CNS2) region to maintain Treg stability in inflammatory environments by regulating pCREB function and GATA3 expression, respectively. Lastly, CBP and p300 regulate the epigenetic status and function of Foxp3. Our findings provide insights into how HATs orchestrate multiple aspects of Treg development and function and identify overlapping but also discrete activities for p300 and CBP in control of Treg cells.

关键词： T cells AUTOIMMUNE diseases RESEARCH HISTONE acetyltransferase MICE as laboratory animals non-coding dna THERAPEUTIC use

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A Novel RNA In Situ Hybridization Assay for the Long noncoding RNA SChLAP1 Predicts Poor Clinical Outcome After Radical Prostatectomy in Clinically Localized Prostate Cancer

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NEOPLASIA 2014年第12期16卷 1121-1127页

作者： Mehra, Rohit Shi, Yang Udager, Aaron M. Prensner, John R. Sahu, Anirban Iyer, Matthew K. Siddiqui, Javed Cao, Xuhong Wei, John Jiang, Hui Feng, Felix Y. Chinnaiyan, Arul M. Univ Michigan Hlth Syst Dept Pathol Ann Arbor MI USA Univ Michigan Hlth Syst Ctr Comprehens Canc Ann Arbor MI USA Michigan Ctr Translat Pathol Ann Arbor MI USA Univ Michigan Sch Publ Hlth Dept Biostat Ann Arbor MI 48109 USA Univ Michigan Hlth Syst Dept Radiat Oncol Ann Arbor MI USA Univ Michigan Hlth Syst Dept Urol Ann Arbor MI USA Howard Hughes Med Inst Ann Arbor MI USA

Long noncoding RNAs (lncRNAs) are an emerging class of oncogenic molecules implicated in a diverse range of human malignancies. We recently identified SChLAP1 as a novel lncRNA that demonstrates outlier expression in a subset of prostate cancers, promotes tumor cell invasion and metastasis, and associates with lethal disease. Based on these findings, we sought to develop an RNA in situ hybridization (ISH) assay for SChLAP1 to 1) investigate the spectrum of SChLAP1 expression from benign prostatic tissue to metastatic castration-resistant prostate cancer and 2) to determine whether SChLAP1 expression by ISH is associated with outcome after radical prostatectomy in patients with clinically localized disease. The results from our current study demonstrate that SChLAP1 expression increases with prostate cancer progression, and high SChLAP1 expression by ISH is associated with poor outcome after radical prostatectomy in patients with clinically localized prostate cancer by both univariate (hazard ratio = 2.343, P = .005) and multivariate (hazard ratio = 1.99, P = .032) Cox regression analyses. This study highlights a potential clinical utility for SChLAP1 ISH as a novel tissue-based biomarker assay for outcome prognostication after radical prostatectomy.

关键词： non-coding dna RESEARCH IN situ hybridization PROSTATECTOMY PROSTATE cancer -- Genetic aspects BIOCHEMICAL markers

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High-resolution interrogation of functional elements in the noncoding genome

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SCIENCE 2016年第6307期353卷 1545-1549页

作者： Sanjana, Neville E. Wright, Jason Zheng, Kaijie Shalem, Ophir Fontanillas, Pierre Joung, Julia Cheng, Christine Regev, Aviv Zhang, Feng Broad Inst MIT & Harvard 7 Cambridge Ctr Cambridge MA 02142 USA MIT Dept Biol Engn Dept Brain & Cognit Sci McGovern Inst Brain Res Cambridge MA 02139 USA MIT Dept Biol Howard Hughes Med Inst David H Koch Inst Integrat Canc Biol 77 Massachusetts Ave Cambridge MA 02142 USA NYU New York Genome Ctr 550 1St Ave New York NY 10012 USA NYU Dept Biol 550 1St Ave New York NY 10012 USA

The noncoding genome affects gene regulation and disease, yet we lack tools for rapid identification and manipulation of noncoding elements. We developed a CRISPR screen using similar to 18,000 single guide RNAs targeting >700 kilobases surrounding the genes NF1, NF2, and CUL3, which are involved in BRAF inhibitor resistance in melanoma. We find that noncoding locations that modulate drug resistance also harbor predictive hallmarks of noncoding function. With a subset of regions at the CUL3 locus, we demonstrate that engineered mutations alter transcription factor occupancy and long-range and local epigenetic environments, implicating these sites in gene regulation and chemotherapeutic resistance. Through our expansion of the potential of pooled CRISPR screens, we provide tools for genomic discovery and for elucidating biologically relevant mechanisms of gene regulation.

关键词： non-coding dna GENETIC regulation CRISPRS (Genetics) BRAF genes MELANOMA DRUG resistance in cancer cells MUTATION (Biology)

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Rare pseudoautosomal copy-number variations involving SHOX and/or its flanking regions in individuals with and without short stature

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JOURNAL OF HUMAN GENETICS 2015年第9期60卷 553-556页

作者： Fukami, Maki Naiki, Yasuhiro Muroya, Koji Hamajima, Takashi Soneda, Shun Horikawa, Reiko Jinno, Tomoko Katsumi, Momori Nakamura, Akie Asakura, Yumi Adachi, Masanori Ogata, Tsutomu Kanzaki, Susumu Natl Res Inst Child Hlth & Dev Dept Mol Endocrinol Tokyo 1578535 Japan Natl Ctr Child Hlth & Dev Div Endocrinol & Metab Tokyo Japan Kanagawa Childrens Med Ctr Dept Endocrinol & Metab Yokohama Kanagawa Japan Aichi Childrens Hlth & Med Ctr Div Endocrinol & Metab Obu Japan St Marianna Univ Sch Med Dept Pediat Kawasaki Kanagawa Japan Hokkaido Univ Sch Med Dept Pediat Sapporo Hokkaido 060 Japan Hamamatsu Univ Sch Med Dept Pediat Hamamatsu Shizuoka 4313192 Japan Tottori Univ Fac Med Div Pediat & Perinatol Tottori 680 Japan

Pseudoautosomal region 1 (PAR1) contains SHOX, in addition to seven highly conserved non-coding dna elements (CNEs) with cis-regulatory activity. Microdeletions involving SHOX exons 1-6a and/or the CNEs result in idiopathic short stature (ISS) and Leri-Weill dyschondrosteosis (LWD). Here, we report six rare copy-number variations (CNVs) in PAR1 identified through copy-number analyzes of 245 ISS/LWD patients and 15 unaffected individuals. The six CNVs consisted of three microduplications encompassing SHOX and some of the CNEs, two microduplications in the SHOX 3'-region affecting one or four of the downstream CNEs, and a microdeletion involving SHOX exon 6b and its neighboring CNE. The amplified dna fragments of two SHOX-containing duplications were detected at chromosomal regions adjacent to the original positions. The breakpoints of a SHOX-containing duplication resided within Alu repeats. A microduplication encompassing four downstream CNEs was identified in an unaffected father-daughter pair, whereas the other five CNVs were detected in ISS patients. These results suggest that microduplications involving SHOX cause ISS by disrupting the cis-regulatory machinery of this gene and that at least some of microduplications in PAR1 arise from Alu-mediated non-allelic homologous recombination. The pathogenicity of other rare PAR1-linked CNVs, such as CNE-containing microduplications and exon 6b-flanking microdeletions, merits further investigation.

关键词： SHORT stature dna copy number variations HOMEOBOX genes CIS-regulatory elements (Genetics) non-coding dna CONSERVED sequences (Genetics) GENETIC aspects

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