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  • Oxford University Press  (200)
  • The Federation of American Societies for Experimental Biology (FASEB)  (23)
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  • 1
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    A long noncoding RNA, lincRNA-Tnfaip3, acts as a coregulator of NF-{kappa}B to modulate inflammatory gene transcription in mouse macrophages [Research] (2017)
    The Federation of American Societies for Experimental Biology (FASEB)
    Details
    Publication Date: 2017-03-01
    Description: Long intergenic noncoding RNAs (lincRNAs) are long noncoding transcripts (〉200 nt) from the intergenic regions of annotated protein-coding genes. We report here that the lincRNA gene lincRNA-Tnfaip3 , located at mouse chromosome 10 proximal to the tumor necrosis factor α-induced protein 3 ( Tnfaip3 ) gene, is an early-primary response gene controlled by nuclear factor-B (NF-B) signaling in murine macrophages. Functionally, lincRNA- Tnfaip3 appears to mediate both the activation and repression of distinct classes of inflammatory genes in macrophages. Specifically, induction of lincRNA-Tnfaip3 is required for the transactivation of NF-B-regulated inflammatory genes in response to bacterial LPSs stimulation. LincRNA-Tnfaip3 physically interacts with the high-mobility group box 1 (Hmgb1), assembling a NF-B/Hmgb1/lincRNA-Tnfaip3 complex in macrophages after LPS stimulation. This resultant NF-B/Hmgb1/lincRNA-Tnfaip3 complex can modulate Hmgb1-associated histone modifications and, ultimately, transactivation of inflammatory genes in mouse macrophages in response to microbial challenge. Therefore, our data indicate a new regulatory role of NF-B-induced lincRNA-Tnfaip3 to act as a coactivator of NF-B for the transcription of inflammatory genes in innate immune cells through modulation of epigenetic chromatin remodeling.—Ma, S., Ming, Z., Gong, A.-Y., Wang, Y., Chen, X., Hu, G., Zhou, R., Shibata, A., Swanson, P. C., Chen, X.-M. A long noncoding RNA, LincRNA-Tnfaip3, acts as a coregulator of NF-B to modulate inflammatory gene transcription in mouse macrophages.
    Print ISSN: 0892-6638
    Electronic ISSN: 1530-6860
    Topics: Biology
    Published by The Federation of American Societies for Experimental Biology (FASEB)
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  • 2
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    Imbalanced response of ATP-binding cassette transporter A1 and CD36 expression to increased oxidized low-density lipoprotein loading contributes to the development of THP-1 derived foam cells (2014)
    Oxford University Press
    Details
    Publication Date: 2014-01-07
    Description: ATP-binding cassette transporter A1 (ABCA1) and CD36, type B scavenger receptor, function as the key mediators of macrophages cholesterol efflux and intake, respectively. However, their contribution to development of foam cells still remains uncertain. We here examined the effects of increased oxidized low-density lipoprotein (oxLDL) loading on the ABCA1 and CD36 expression, and lipid accumulation in THP-1 macrophages. The cultured THP-1 macrophages were treated with different copper-oxLDL concentrations. The intracellular lipid contents and cholesterol efflux were measured, and the ABCA1 and CD36 expression were assessed. We found that expression of ABCA1 and CD36 were coordinately induced upon low to moderate doses of oxLDL loading. However, higher doses of oxLDL stimulation resulted in the imbalanced expression of ABCA1 and CD36 proteins with more preferentially suppressed ABCA1 protein, attenuated cholesterol efflux and development of THP-1 derived foam cells. The PPAR- expression was remarkably induced, and PPAR- agonist, pioglitazone, significantly promoted the ABCA1 and CD36 expression. Additionally, ABCA1 and CD36 proteins were strong colocalized in THP-1 macrophages membrane. In conclusion, the more preferentially suppressed ABCA1 expression as compared with CD36 at higher doses of oxLDL stimulation may be the initiator for the formation of macrophage-derived foam cells.
    Print ISSN: 0021-924X
    Electronic ISSN: 1756-2651
    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of The Japanese Biochemical Society (JBS).
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  • 3
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    MiR-196a exerts its oncogenic effect in glioblastoma multiforme by inhibition of I{kappa}B{alpha} both in vitro and in vivo (2014)
    Oxford University Press
    Details
    Publication Date: 2014-04-13
    Description: Background Recent studies have revealed that miR-196a is upregulated in glioblastoma multiforme (GBM) and that it correlates with the clinical outcome of patients with GBM. However, its potential regulatory mechanisms in GBM have never been reported. Methods We used quantitative real-time PCR to assess miR-196a expression levels in 132 GBM specimens in a single institution. Oncogenic capability of miR-196a was detected by apoptosis and proliferation assays in U87MG and T98G cells. Immunohistochemistry was used to determine the expression of IBα in GBM tissues, and a luciferase reporter assay was carried out to confirm whether IBα is a direct target of miR-196a. In vivo, xenograft tumors were examined for an antiglioma effect of miR-196a inhibitors. Results We present for the first time evidence that miR-196a could directly interact with IBα 3'-UTR to suppress IBα expression and subsequently promote activation of NF-B, consequently promoting proliferation of and suppressing apoptosis in GBM cells both in vitro and in vivo. Our study confirmed that miR-196a was upregulated in GBM specimens and that high levels of miR-196a were significantly correlated with poor outcome in a large cohort of GBM patients. Our data from human tumor xenografts in nude mice treated with miR-196 inhibitors demonstrated that inhibition of miR-196a could ameliorate tumor growth in vivo. Conclusions MiR-196a exerts its oncogenic effect in GBM by inhibiting IBα both in vitro and in vivo. Our findings provide new insights into the pathogenesis of GBM and indicate that miR-196a may predict clinical outcome of GBM patients and serve as a new therapeutic target for GBM.
    Print ISSN: 1522-8517
    Electronic ISSN: 1523-5866
    Topics: Medicine
    Published by Oxford University Press on behalf of The Society for Neuro-Oncology (SNO).
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  • 4
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    PRPF4 mutations cause autosomal dominant retinitis pigmentosa (2014)
    Oxford University Press
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    Publication Date: 2014-05-09
    Description: Retinitis pigmentosa (RP), a disease characterized by progressive loss of photoreceptors, exhibits significant genetic heterogeneity. Several genes associated with U4/U6–U5 triple small nuclear ribonucleoprotein (tri-snRNP) complex of the spliceosome have been implicated in autosomal dominant RP (adRP). HPrp4, encoded by PRPF4 , regulates the stability of U4/U6 di-snRNP, which is essential for continuous splicing. Here, we identified two heterozygous variants in PRPF4 , including c.-114_-97del in a simplex RP patient and c.C944T (p.Pro315Leu), which co-segregates with disease phenotype in a family with adRP. Both variants were absent in 400 unrelated controls. The c.-114_-97del, predicted to affect two transcription factor binding sites, was shown to down-regulate the promoter activity of PRPF4 by a luciferase assay, and was associated with a significant reduction of PRPF4 expression in the blood cells of the patient. In fibroblasts from an affected individual with the p.Pro315Leu variant, the expression levels of several tri-snRNP components, including PRPF4 itself, were up-regulated, with altered expression pattern of SC35, a spliceosome marker. The same alterations were also observed in cells over expressing hPrp4 Pro315Leu , suggesting that they arose as a compensatory response to a compromised splicing mechanism caused by hPrp4 dysfunction. Further, over expression of hPrp4 Pro315Leu , but not hPrp4 WT , triggered systemic deformities in wild-type zebrafish embryos with the retina primarily affected, and dramatically augmented death rates in morphant embryos, in which orthologous zebrafish prpf4 gene was silenced. We conclude that mutations of PRPF4 cause RP via haploinsufficiency and dominant-negative effects, and establish PRPF4 as a new U4/U6–U5 snRNP component associated with adRP.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 5
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    Why Are Genes Encoded on the Lagging Strand of the Bacterial Genome? (2013)
    Oxford University Press
    Details
    Publication Date: 2013-12-15
    Description: Genomic DNA is used as the template for both replication and transcription, whose machineries may collide and result in mutagenesis, among other damages. Because head-on collisions are more deleterious than codirectional collisions, genes should be preferentially encoded on the leading strand to avoid head-on collisions, as is observed in most bacterial genomes examined. However, why are there still lagging strand encoded genes? Paul et al. recently proposed that these genes take advantage of the increased mutagenesis resulting from head-on collisions and are thus adaptively encoded on the lagging strand. We show that the evidence they provided is invalid and that the existence of lagging strand encoded genes is explainable by a balance between deleterious mutations that bring genes from the leading to the lagging strand and purifying selection purging such mutants. Therefore, the adaptive hypothesis is neither theoretically needed nor empirically supported.
    Electronic ISSN: 1759-6653
    Topics: Biology
    Published by Oxford University Press
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  • 6
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    Identification of active transcription factor and miRNA regulatory pathways in Alzheimer's disease (2013)
    Oxford University Press
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    Publication Date: 2013-10-04
    Description: Motivation: Alzheimer’s disease (AD) is a severe neurodegenerative disease of the central nervous system that may be caused by perturbation of regulatory pathways rather than the dysfunction of a single gene. However, the pathology of AD has yet to be fully elucidated. Results: In this study, we systematically analyzed AD-related mRNA and miRNA expression profiles as well as curated transcription factor (TF) and miRNA regulation to identify active TF and miRNA regulatory pathways in AD. By mapping differentially expressed genes and miRNAs to the curated TF and miRNA regulatory network as active seed nodes, we obtained a potential active subnetwork in AD. Next, by using the breadth-first-search technique, potential active regulatory pathways, which are the regulatory cascade of TFs, miRNAs and their target genes, were identified. Finally, based on the known AD-related genes and miRNAs, the hypergeometric test was used to identify active pathways in AD. As a result, nine pathways were found to be significantly activated in AD. A comprehensive literature review revealed that eight out of nine genes and miRNAs in these active pathways were associated with AD. In addition, we inferred that the pathway hsa-miR-146a-〉STAT1-〉MYC, which is the source of all nine significantly active pathways, may play an important role in AD progression, which should be further validated by biological experiments. Thus, this study provides an effective approach to finding active TF and miRNA regulatory pathways in AD and can be easily applied to other complex diseases. Contact: lixia@hrbmu.edu.cn or lw2247@gmail.com . Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 7
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    Novel human lncRNA-disease association inference based on lncRNA expression profiles (2013)
    Oxford University Press
    Details
    Publication Date: 2013-10-04
    Description: Motivation: More and more evidences have indicated that long–non-coding RNAs (lncRNAs) play critical roles in many important biological processes. Therefore, mutations and dysregulations of these lncRNAs would contribute to the development of various complex diseases. Developing powerful computational models for potential disease-related lncRNAs identification would benefit biomarker identification and drug discovery for human disease diagnosis, treatment, prognosis and prevention. Results : In this article, we proposed the assumption that similar diseases tend to be associated with functionally similar lncRNAs. Then, we further developed the method of Laplacian Regularized Least Squares for LncRNA–Disease Association (LRLSLDA) in the semisupervised learning framework. Although known disease–lncRNA associations in the database are rare, LRLSLDA still obtained an AUC of 0.7760 in the leave-one-out cross validation, significantly improving the performance of previous methods. We also illustrated the performance of LRLSLDA is not sensitive (even robust) to the parameters selection and it can obtain a reliable performance in all the test classes. Plenty of potential disease–lncRNA associations were publicly released and some of them have been confirmed by recent results in biological experiments. It is anticipated that LRLSLDA could be an effective and important biological tool for biomedical research. Availability: The code of LRLSLDA is freely available at http://asdcd.amss.ac.cn/Software/Details/2 . Contact: xingchen@amss.ac.cn or yangy@amt.ac.cn Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 8
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    High Risk for Obstructive Sleep Apnea in Relation to Hypertension Among Southeast Asian Young Adults: Role of Obesity as an Effect Modifier (2013)
    Oxford University Press
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    Publication Date: 2013-12-24
    Description: BACKGROUND Obstructive sleep apnea (OSA) has been linked to hypertension among middle-aged and older adults in Western countries. Few studies have focused on young adults, especially those in Southeast Asian countries undergoing epidemiologic transitions and experiencing elevated noncommunicable disease burden. We investigated associations of high risk for OSA with hypertension among Asian young adults. METHODS A total of 2,911 college students in Thailand participated in this study. The high risk for OSA was assessed using the Berlin Questionnaire. Blood pressure (BP) and anthropometric measurements were taken by trained research staff. Elevated BP and hypertension were defined as BP ≥120/80mm Hg and ≥140/90mm Hg, respectively. Multivariable logistic regression models were fit to estimate odds ratios (ORs) and 95% confidence intervals (CIs) of elevated BP and hypertension. Stratified analyses were conducted to examine whether observed associations varied by weight status. RESULTS High risk for OSA was significantly associated with elevated BP (OR = 2.38; 95% CI = 1.68–3.39) and hypertension (OR = 2.55; 95% CI = 1.57–4.15) after adjustment for demographic and lifestyle factors. When body mass index was further controlled for, observed associations were greatly attenuated. The associations were only evident among overweight and obese students. CONCLUSIONS The high risk for OSA among overweight and obese young adults is associated with elevated BP and hypertension. Enhanced efforts directed toward screening and diagnosing OSA and weight control among young adults could be one strategy for improving cardiovascular health.
    Print ISSN: 0895-7061
    Electronic ISSN: 1879-1905
    Topics: Medicine
    Published by Oxford University Press
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  • 9
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    Observer-based event-triggered control for certain and uncertain linear systems (2013)
    Oxford University Press
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    Publication Date: 2013-12-10
    Description: This paper studies the design problem of observer-based event-triggered control for certain and uncertain linear systems. For linear systems, an event condition based on the state error of the observer is proposed. A condition in terms of a linear matrix inequality is provided to ensure the feedback control system as well as the observer error system asymptotic stability under the event-triggered control. Moreover, corresponding self-triggered control is presented where the next control task release time is predicted based on the current sampled data. Furthermore, observer-based event-triggered control for the system with norm-bounded uncertainty is investigated. Finally, simulations are shown to illustrate the feasibility and efficiency of the obtained results.
    Print ISSN: 0265-0754
    Electronic ISSN: 1471-6887
    Topics: Mathematics
    Published by Oxford University Press
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  • 10
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    Antitumor effects of naturally occurring oligomeric resveratrol derivatives [Research Communications] (2013)
    The Federation of American Societies for Experimental Biology (FASEB)
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    Publication Date: 2013-11-01
    Description: This study was designed to evaluate and characterize the molecular basis of antitumor activity of naturally occurring resveratrol (RES; 3,5,4'-trihydroxy- trans -stilbene) derivatives. The compounds were isolated from plants in previous studies and characterized spectroscopically. The antitumor activities of 31 RES derivatives, including dimers, trimers, and tetramers of RES, were evaluated using cell-based assays and validated on a murine model. Several trimeric and a tetrameric stilbenoids induced tumor cell apoptosis or growth arrest of several tumor cell lines with IC 50 values (2.8–19.7 μM), significantly lower than that of RES (IC 50 〉70 μM). Using pauciflorol B (PauB) as an example, we showed that the compound induced apoptosis p53 dependently, inducing p53 accumulation and p53-modulated gene expression in cells with wild-type p53, but not in those with nonfunctional p53. Reexpression of p53 in p53-null cells rescued cell death response. In parallel, the MAPK/p38 was activated and critical for PauB-induced killing. Interestingly, activation of p38 in p53 deficient cells was sufficient to drive cells into senescence via the p16–pRb pathway. Finally, PauB dose-dependently inhibited tumor growth on nude mice. Naturally occurring trimeric and tetrameric stilbenoids are potent antitumor agents. Those compounds exert antitumor effect through p53-dependent induction of apoptosis or senescence.—Qiao, H., Chen, X., Xu, L., Wang, J., Zhao, G., Hou, Y., Ge, H. M., Tan, R-X., Li, E. Antitumor effects of naturally occurring oligomeric resveratrol derivatives.
    Print ISSN: 0892-6638
    Electronic ISSN: 1530-6860
    Topics: Biology
    Published by The Federation of American Societies for Experimental Biology (FASEB)
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