Posttranscriptional Regulation

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Jianying Wang - One of the best experts on this subject based on the ideXlab platform.

  • Posttranscriptional Regulation of intestinal epithelial integrity by noncoding rnas
    Wiley Interdisciplinary Reviews - Rna, 2017
    Co-Authors: Junyao Wang, Lan Xiao, Jianying Wang
    Abstract:

    Maintenance of the gut epithelial integrity under stressful environments requires epithelial cells to rapidly elicit changes in gene expression patterns to regulate their survival, adapt to stress, and keep epithelial homeostasis. Disruption of the intestinal epithelial integrity occurs commonly in patients with various critical illnesses, leading to the translocation of luminal toxic substances and bacteria to the blood stream. Recently, noncoding RNAs (ncRNAs) have emerged as a novel class of master regulators of gene expression and are fundamentally involved in many aspects of gut mucosal regeneration, protection, and epithelial barrier function. Here, we highlight the roles of several intestinal epithelial tissue-specific microRNAs, including miR-222, miR-29b, miR-503, and miR-195, and long ncRNAs such as H19 and SPRY4-IT1 in the Regulation of cell proliferation, apoptosis, migration, and cell-to-cell interactions and also further analyze the mechanisms through which ncRNAs and their interactions with RNA-binding proteins modulate the stability and translation of target mRNAs. WIREs RNA 2017, 8:e1399. doi: 10.1002/wrna.1399 For further resources related to this article, please visit the WIREs website.

Kounosuke Watabe - One of the best experts on this subject based on the ideXlab platform.

  • p53 represses c myc through induction of the tumor suppressor mir 145
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Mohit Sachdeva, Fangting Wu, Hailong Wu, Vijay Walia, Sumit Kumar, Randolph C Elble, Kounosuke Watabe, Yinyuan Mo
    Abstract:

    The tumor suppressor p53 negatively regulates a number of genes, including the proto-oncogene c-Myc, in addition to activating many other genes. One mechanism of the p53-mediated c-Myc repression may involve transcriptional Regulation. However, it is not clear whether microRNAs (miRNAs) play a role in the p53-mediated Posttranscriptional Regulation of c-Myc. In this study, we show that a putative tumor suppressor, miR-145, is expressed through the phosphoinositide-3 kinase (PI-3K)/Akt and p53 pathways. Importantly, p53 transcriptionally induces the expression of miR-145 by interacting with a potential p53 response element (p53RE) in the miR-145 promoter. We further show that c-Myc is a direct target for miR-145. Although miR-145 silences the expression of c-Myc, anti-miR-145 enhances its expression. This specific silencing of c-Myc by miR-145 accounts at least in part for the miR-145-mediated inhibition of tumor cell growth both in vitro and in vivo. Finally, the blockade of miR-145 by anti-miR-145 is able to reverse the p53-mediated c-Myc repression. Together, these results define the role of miR-145 in the Posttranscriptional Regulation of c-Myc by p53 and suggest that, as a new member of the p53 regulatory network, miR-145 provides a direct link between p53 and c-Myc in this gene regulatory network.

  • p53 represses c myc through induction of the tumor suppressor mir 145
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Mohit Sachdeva, Vijay Walia, Sumit Kumar, Randolph C Elble, Shoumin Zhu, Kounosuke Watabe
    Abstract:

    The tumor suppressor p53 negatively regulates a number of genes, including the proto-oncogene c-Myc, in addition to activating many other genes. One mechanism of the p53-mediated c-Myc repression may involve transcriptional Regulation. However, it is not clear whether microRNAs (miRNAs) play a role in the p53-mediated Posttranscriptional Regulation of c-Myc. In this study, we show that a putative tumor suppressor, miR-145, is expressed through the phosphoinositide-3 kinase (PI-3K)/Akt and p53 pathways. Importantly, p53 transcriptionally induces the expression of miR-145 by interacting with a potential p53 response element (p53RE) in the miR-145 promoter. We further show that c-Myc is a direct target for miR-145. Although miR-145 silences the expression of c-Myc, anti-miR-145 enhances its expression. This specific silencing of c-Myc by miR-145 accounts at least in part for the miR-145-mediated inhibition of tumor cell growth both in vitro and in vivo. Finally, the blockade of miR-145 by anti-miR-145 is able to reverse the p53-mediated c-Myc repression. Together, these results define the role of miR-145 in the Posttranscriptional Regulation of c-Myc by p53 and suggest that, as a new member of the p53 regulatory network, miR-145 provides a direct link between p53 and c-Myc in this gene regulatory network.

Mohit Sachdeva - One of the best experts on this subject based on the ideXlab platform.

  • p53 represses c myc through induction of the tumor suppressor mir 145
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Mohit Sachdeva, Fangting Wu, Hailong Wu, Vijay Walia, Sumit Kumar, Randolph C Elble, Kounosuke Watabe, Yinyuan Mo
    Abstract:

    The tumor suppressor p53 negatively regulates a number of genes, including the proto-oncogene c-Myc, in addition to activating many other genes. One mechanism of the p53-mediated c-Myc repression may involve transcriptional Regulation. However, it is not clear whether microRNAs (miRNAs) play a role in the p53-mediated Posttranscriptional Regulation of c-Myc. In this study, we show that a putative tumor suppressor, miR-145, is expressed through the phosphoinositide-3 kinase (PI-3K)/Akt and p53 pathways. Importantly, p53 transcriptionally induces the expression of miR-145 by interacting with a potential p53 response element (p53RE) in the miR-145 promoter. We further show that c-Myc is a direct target for miR-145. Although miR-145 silences the expression of c-Myc, anti-miR-145 enhances its expression. This specific silencing of c-Myc by miR-145 accounts at least in part for the miR-145-mediated inhibition of tumor cell growth both in vitro and in vivo. Finally, the blockade of miR-145 by anti-miR-145 is able to reverse the p53-mediated c-Myc repression. Together, these results define the role of miR-145 in the Posttranscriptional Regulation of c-Myc by p53 and suggest that, as a new member of the p53 regulatory network, miR-145 provides a direct link between p53 and c-Myc in this gene regulatory network.

  • p53 represses c myc through induction of the tumor suppressor mir 145
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Mohit Sachdeva, Vijay Walia, Sumit Kumar, Randolph C Elble, Shoumin Zhu, Kounosuke Watabe
    Abstract:

    The tumor suppressor p53 negatively regulates a number of genes, including the proto-oncogene c-Myc, in addition to activating many other genes. One mechanism of the p53-mediated c-Myc repression may involve transcriptional Regulation. However, it is not clear whether microRNAs (miRNAs) play a role in the p53-mediated Posttranscriptional Regulation of c-Myc. In this study, we show that a putative tumor suppressor, miR-145, is expressed through the phosphoinositide-3 kinase (PI-3K)/Akt and p53 pathways. Importantly, p53 transcriptionally induces the expression of miR-145 by interacting with a potential p53 response element (p53RE) in the miR-145 promoter. We further show that c-Myc is a direct target for miR-145. Although miR-145 silences the expression of c-Myc, anti-miR-145 enhances its expression. This specific silencing of c-Myc by miR-145 accounts at least in part for the miR-145-mediated inhibition of tumor cell growth both in vitro and in vivo. Finally, the blockade of miR-145 by anti-miR-145 is able to reverse the p53-mediated c-Myc repression. Together, these results define the role of miR-145 in the Posttranscriptional Regulation of c-Myc by p53 and suggest that, as a new member of the p53 regulatory network, miR-145 provides a direct link between p53 and c-Myc in this gene regulatory network.

Myriam Gorospe - One of the best experts on this subject based on the ideXlab platform.

  • Posttranscriptional Regulation of cancer traits by hur
    Wiley Interdisciplinary Reviews - Rna, 2010
    Co-Authors: Kotb Abdelmohsen, Myriam Gorospe
    Abstract:

    Cancer-related gene expression programs are strongly influenced by Posttranscriptional mechanisms. The RNA-binding protein HuR is highly abundant in many cancers. Numerous HuR-regulated mRNAs encode proteins implicated in carcinogenesis. Here, we review the collections of HuR target mRNAs that encode proteins responsible for implementing five major cancer traits. By interacting with specific mRNA subsets, HuR enhances the levels of proteins that (1) promote cell proliferation, (2) increase cell survival, (3) elevate local angiogenesis, (4) help the cancer cell evade immune recognition, and (5) facilitate cancer cell invasion and metastasis. We propose that HuR exerts a tumorigenic function by enabling these cancer phenotypes. We discuss evidence that links HuR to several specific cancers and suggests its potential usefulness in cancer diagnosis, prognosis, and therapy.

  • minireview Posttranscriptional Regulation of the insulin and insulin like growth factor systems
    Endocrinology, 2010
    Co-Authors: Eun Kyung Lee, Myriam Gorospe
    Abstract:

    Insulin and IGFs share structural similarities and regulate metabolic processes including glucose homeostasis. Acute alterations in glucose levels trigger rapid changes in insulin concentration and insulin signaling. These processes are tightly regulated by Posttranscriptional mechanisms that alter the stability and translation of mRNAs encoding insulin and the insulin receptor. Long-term glucose homeostasis is also modulated by IGFs and IGF receptors, whose expression is likewise subject to changes in the stability and translation of the encoding mRNAs. The control of mRNA half-life and translation is governed by RNA-binding proteins and microRNAs that interact with target transcripts at the 3′ and 5′ untranslated regions. In this review, we describe the RNA-binding proteins and microRNAs that target the mRNAs encoding insulin, IGFs, and their receptors. We discuss how these mRNA-binding factors help to elicit timely, versatile, and tissue-specific changes in insulin and IGF function, thereby effecting c...

  • Posttranscriptional Regulation of il 13 in t cells role of the rna binding protein hur
    The Journal of Allergy and Clinical Immunology, 2008
    Co-Authors: Vincenzo Casolaro, Xi Fang, B Tancowny, Jinshui Fan, Subramanya Srikantan, Yukiko S Asaki, Umberto De Fanis, Shau Ku Huang, Myriam Gorospe, Ulus Atasoy
    Abstract:

    Background IL-13, a critical cytokine in allergy, is regulated by as-yet-elusive mechanisms. Objective We investigated IL-13 Posttranscriptional Regulation by HuR, a protein associating with adenylate-uridylate-rich elements in the 3′ untranslated regions (UTRs) of mRNA, promoting mRNA stability and translation. Methods IL-13 mRNA decay was monitored in human T H 2-skewed cells by using the transcriptional inhibitor actinomycin D. The IL-13 3′UTR was subcloned into an inducible β-globin reporter transiently expressed in H2 cells in the absence or presence of overexpressed HuR. Association of HuR with IL-13 mRNA was detected by means of immunoprecipitation of ribonucleoprotein complexes and a biotin pull-down assay. The effects of HuR transient overexpression and silencing on IL-13 expression were investigated. Results IL-13 mRNA half-life increased significantly in restimulated T H 2-skewed cells compared with baseline values. Decay of β-globin mRNA was significantly faster in H2 cells transfected with the IL-13 3′UTR-containing plasmid than in those carrying a control vector. HuR overexpression increased the β-globin IL-13 3′UTR reporter half-life. Significant enrichment of IL-13 mRNA was produced by means of immunoprecipitation of Jurkat cell ribonucleoprotein complexes with anti-HuR. HuR binding to the IL-13 3′UTR was confirmed by means of pull-down assay of biotin-labeled RNA probes spanning the IL-13 3′UTR. Two-dimensional Western blot analysis showed stimulus-induced posttranslational modification of HuR. In Jurkat cells mitogen-induced IL-13 mRNA was significantly affected by HuR overexpression and silencing. Conclusions Mitogen-induced IL-13 expression involves changes in transcript turnover and a change in phosphorylation of HuR and its association with the mRNA 3′UTR.

Yinyuan Mo - One of the best experts on this subject based on the ideXlab platform.

  • p53 represses c myc through induction of the tumor suppressor mir 145
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Mohit Sachdeva, Fangting Wu, Hailong Wu, Vijay Walia, Sumit Kumar, Randolph C Elble, Kounosuke Watabe, Yinyuan Mo
    Abstract:

    The tumor suppressor p53 negatively regulates a number of genes, including the proto-oncogene c-Myc, in addition to activating many other genes. One mechanism of the p53-mediated c-Myc repression may involve transcriptional Regulation. However, it is not clear whether microRNAs (miRNAs) play a role in the p53-mediated Posttranscriptional Regulation of c-Myc. In this study, we show that a putative tumor suppressor, miR-145, is expressed through the phosphoinositide-3 kinase (PI-3K)/Akt and p53 pathways. Importantly, p53 transcriptionally induces the expression of miR-145 by interacting with a potential p53 response element (p53RE) in the miR-145 promoter. We further show that c-Myc is a direct target for miR-145. Although miR-145 silences the expression of c-Myc, anti-miR-145 enhances its expression. This specific silencing of c-Myc by miR-145 accounts at least in part for the miR-145-mediated inhibition of tumor cell growth both in vitro and in vivo. Finally, the blockade of miR-145 by anti-miR-145 is able to reverse the p53-mediated c-Myc repression. Together, these results define the role of miR-145 in the Posttranscriptional Regulation of c-Myc by p53 and suggest that, as a new member of the p53 regulatory network, miR-145 provides a direct link between p53 and c-Myc in this gene regulatory network.