A+U-rich-element RNA-binding factor 1/heterogeneous nuclear ribonucleoprotein D gene expression is regulated by oestrogen in the rat uterus

2001 ◽  
Vol 361 (1) ◽  
pp. 125-132 ◽  
Author(s):  
Yukitomo ARAO ◽  
Atsumi KIKUCHI ◽  
Kazuhiro IKEDA ◽  
Satoshi NOMOTO ◽  
Hyogo HORIGUCHI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Rna Binding ◽  
Rat Uterus ◽  
Expression Levels ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
Binding Factor ◽  
Hnrnp D ◽  
Nuclear Ribonucleoprotein ◽  
Post Transcriptional Regulation

Oestrogen-mediated gene expression is regulated at both the transcriptional and post-transcriptional levels. The molecular mechanism of transcriptional regulation has been well characterized. On the other hand, there is little understanding of the mechanism of post-transcriptional regulation. To clarify the mechanism of oestrogen-mediated post-transcriptional regulation, we focused on A+U-rich-element RNA-binding factor 1/heterogeneous nuclear ribonucleoprotein D (AUF1/hnRNP D), which is known as a regulator of cytosolic mRNA degradation and nuclear pre-mRNA maturation. However, little is known about the expression levels and the regulation of AUF1/hnRNP D mRNA in tissues. We further investigated the expression levels of AUF1/hnRNP D isoform mRNAs to determine whether AUF1/hnRNP D gene expression is regulated by oestrogen in the ovariectomized adult female rat uterus. Uterine AUF1/hnRNP D mRNA was induced by a single subcutaneous injection (1μg/kg) of 17β-oestradiol (E2), reaching a peak level within 6h. Furthermore, we observed that the E2-induced AUF1/hnRNP D isoform mRNAs are p45 and p40 transcripts, and that E2-mediated induction is suppressed by the oestrogen receptor antagonist ICI 182,780. Finally, using the transcriptional inhibitor actinomycin D, we confirmed that the E2-mediated increase in AUF1/hnRNP D mRNA is caused by E2-dependent AUF1/hnRNP D mRNA stabilization.

scholarly journals A+U-rich-element RNA-binding factor 1/heterogeneous nuclear ribonucleoprotein D gene expression is regulated by oestrogen in the rat uterus

2002 ◽  
Vol 361 (1) ◽  
pp. 125 ◽  
Author(s):  
Yukitomo ARAO ◽  
Atsumi KIKUCHI ◽  
Kazuhiro IKEDA ◽  
Satoshi NOMOTO ◽  
Hyogo HORIGUCHI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Binding ◽  
Rat Uterus ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
Binding Factor ◽  
Nuclear Ribonucleoprotein

scholarly journals PSDX: A Comprehensive Multi-Omics Association Database of Populus trichocarpa With a Focus on the Secondary Growth in Response to Stresses

2021 ◽  
Vol 12 ◽  
Author(s):  
Huiyuan Wang ◽  
Sheng Liu ◽  
Xiufang Dai ◽  
Yongkang Yang ◽  
Yunjun Luo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Transcription Initiation ◽  
High Throughput Sequencing ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Populus Trichocarpa ◽  
Secondary Growth ◽  
A Genome ◽  
Post Transcriptional Regulation

Populus trichocarpa (P. trichocarpa) is a model tree for the investigation of wood formation. In recent years, researchers have generated a large number of high-throughput sequencing data in P. trichocarpa. However, no comprehensive database that provides multi-omics associations for the investigation of secondary growth in response to diverse stresses has been reported. Therefore, we developed a public repository that presents comprehensive measurements of gene expression and post-transcriptional regulation by integrating 144 RNA-Seq, 33 ChIP-seq, and six single-molecule real-time (SMRT) isoform sequencing (Iso-seq) libraries prepared from tissues subjected to different stresses. All the samples from different studies were analyzed to obtain gene expression, co-expression network, and differentially expressed genes (DEG) using unified parameters, which allowed comparison of results from different studies and treatments. In addition to gene expression, we also identified and deposited pre-processed data about alternative splicing (AS), alternative polyadenylation (APA) and alternative transcription initiation (ATI). The post-transcriptional regulation, differential expression, and co-expression network datasets were integrated into a new P. trichocarpa Stem Differentiating Xylem (PSDX) database, which further highlights gene families of RNA-binding proteins and stress-related genes. The PSDX also provides tools for data query, visualization, a genome browser, and the BLAST option for sequence-based query. Much of the data is also available for bulk download. The availability of PSDX contributes to the research related to the secondary growth in response to stresses in P. trichocarpa, which will provide new insights that can be useful for the improvement of stress tolerance in woody plants.

scholarly journals The Tristetraprolin Family of RNA-Binding Proteins in Cancer: Progress and Future Prospects

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1539 ◽  
Author(s):  
Yogesh Saini ◽  
Jian Chen ◽  
Sonika Patial
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Zinc Finger ◽  
Binding Proteins ◽  
Rna Binding ◽  
Zinc Finger Protein ◽  
Rna Binding Proteins ◽  
Regulation Of Gene Expression ◽  
Finger Protein ◽  
Post Transcriptional Regulation

Post-transcriptional regulation of gene expression plays a key role in cellular proliferation, differentiation, migration, and apoptosis. Increasing evidence suggests dysregulated post-transcriptional gene expression as an important mechanism in the pathogenesis of cancer. The tristetraprolin family of RNA-binding proteins (RBPs), which include Zinc Finger Protein 36 (ZFP36; commonly referred to as tristetraprolin (TTP)), Zinc Finger Protein 36 like 1 (ZFP36L1), and Zinc Finger Protein 36 like 2 (ZFP36L2), play key roles in the post-transcriptional regulation of gene expression. Mechanistically, these proteins function by binding to the AU-rich elements within the 3′-untranslated regions of their target mRNAs and, in turn, increasing mRNA turnover. The TTP family RBPs are emerging as key regulators of multiple biological processes relevant to cancer and are aberrantly expressed in numerous human cancers. The TTP family RBPs have tumor-suppressive properties and are also associated with cancer prognosis, metastasis, and resistance to chemotherapy. Herein, we summarize the various hallmark molecular traits of cancers that are reported to be regulated by the TTP family RBPs. We emphasize the role of the TTP family RBPs in the regulation of trait-associated mRNA targets in relevant cancer types/cell lines. Finally, we highlight the potential of the TTP family RBPs as prognostic indicators and discuss the possibility of targeting these TTP family RBPs for therapeutic benefits.

Post-transcriptional regulation of gene expression by Unr

2015 ◽  
Vol 43 (3) ◽  
pp. 323-327 ◽  
Author(s):  
Swagat Ray ◽  
Pól Ó Catnaigh ◽  
Emma C. Anderson
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Protein Interactions ◽  
Rna Binding ◽  
Regulation Of Gene Expression ◽  
Negative Regulator ◽  
Cellular Translation ◽  
Cellular Mrnas ◽  
Internal Initiation ◽  
Post Transcriptional Regulation

Unr (upstream of N-ras) is a eukaryotic RNA-binding protein that has a number of roles in the post-transcriptional regulation of gene expression. Originally identified as an activator of internal initiation of picornavirus translation, it has since been shown to act as an activator and inhibitor of cellular translation and as a positive and negative regulator of mRNA stability, regulating cellular processes such as mitosis and apoptosis. The different post-transcriptional functions of Unr depend on the identity of its mRNA and protein partners and can vary with cell type and changing cellular conditions. Recent high-throughput analyses of RNA–protein interactions indicate that Unr binds to a large subset of cellular mRNAs, suggesting that Unr may play a wider role in translational responses to cellular signals than previously thought.

scholarly journals Novel Pathological Role of hnRNPA1 (Heterogeneous Nuclear Ribonucleoprotein A1) in Vascular Smooth Muscle Cell Function and Neointima Hyperplasia

2017 ◽  
Vol 37 (11) ◽  
pp. 2182-2194 ◽  
Author(s):  
Li Zhang ◽  
Qishan Chen ◽  
Weiwei An ◽  
Feng Yang ◽  
Eithne Margaret Maguire ◽  
...  
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Expression Levels ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
Atherosclerotic Lesions ◽  
Nuclear Ribonucleoprotein

Objective— hnRNPA1 (heterogeneous nuclear ribonucleoprotein A1) plays a variety of roles in gene expression. However, little is known about the functional involvement of hnRNPA1 in vascular smooth muscle cell (VSMC) function and neointima hyperplasia. In this study, we have attempted to investigate the functional roles of hnRNPA1 in the contexts of VSMC function, injury-induced vessel remodeling, and human atherosclerotic lesions, as well as discern the molecular mechanisms involved. Approach and Results— hnRNPA1 expression levels were consistently modulated during VSMC phenotype switching and neointimal lesion formation induced by wire injury. Functional studies showed that VSMC-specific gene expression, proliferation, and migration were regulated by hnRNPA1. Our data show that hnRNPA1 exerts its effects on VSMC functions through modulation of IQGAP1 (IQ motif containing GTPase activating protein 1). Mechanistically, hnRNPA1 regulates IQGAP1 mRNA degradation through 2 mechanisms: upregulating microRNA-124 (miR-124) and binding to AU-rich element of IQGAP1 gene. Further evidence suggests that hnRNPA1 upregulates miR-124 by modulating miR-124 biogenesis and that IQGAP1 is the authentic target gene of miR-124. Importantly, ectopic overexpression of hnRNPA1 greatly reduced VSMC proliferation and inhibited neointima formation in wire-injured carotid arteries. Finally, lower expression levels of hnRNPA1 and miR-124, while higher expression levels of IQGAP1, were observed in human atherosclerotic lesions. Conclusions— Our data show that hnRNPA1 is a critical regulator of VSMC function and behavior in the context of neointima hyperplasia, and the hnRNPA1/miR-124/IQGAP1 regulatory axis represents a novel therapeutic target for the prevention of cardiovascular diseases.

MicroRNAs Act as Decoy Molecules To Restore Granulocytic Maturation of Differentiation-Arrested BCR/ABL+ Myeloid Precursors.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 31-31 ◽  
Author(s):  
Anna M. Eiring ◽  
Paolo Neviani ◽  
George A. Calin ◽  
Denis C. Roy ◽  
Carlo M. Croce ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Rna Binding ◽  
Regulation Of Gene Expression ◽  
Ectopic Expression ◽  
Negative Regulator ◽  
Myelogenous Leukemia ◽  
Imatinib Treatment ◽  
E2 Protein ◽  
Post Transcriptional Regulation

Abstract Altered microRNA (miR) expression contributes to aberrant post-transcriptional regulation of gene expression in different type of cancers; however, their role in the pathogenesis and progression of chronic myelogenous leukemia (CML) from chronic phase (CML-CP) to blast crisis (CML-BC) is still largely unknown. Microarray analysis of miR expression reveals that a discrete number of miRs are significantly upregulated (∼ 6.7% of the total 505 miRs present on the chip; 34 miRs) or downregulated (∼2.8% of the miRs present on the chip; 14 miRs) in an imatinib-sensitive manner in CML-BCCD34+ compared to CML-CPCD34+ progenitors and in BCR/ABL-expressing hematopoietic cell lines compared to untransformed parental cells. Among them, we focused our attention on miR-223, miR-15a/16-1 and miR-328, a microRNA with no currently known function, because of their importance in myelopoiesis, potential role as tumor suppressors and sequence homology with the 5’UTR of CEBPA mRNA, respectively. In 32D-BCR/ABL and K562 cells, Northern blot and TaqMan RT-PCR analyses revealed that expression of miR-223, miR-328, miR-15a and miR-16-1 was markedly suppressed (50–75% inhibition) by p210-BCR/ABL kinase activity and that imatinib treatment (1mM; 24h) restored the expression of these miRs to levels similar to those detected in non-transformed 32Dcl3 cells. Interestingly, sequence analysis of both miR-223 and miR-328 revealed homology with the hnRNP E2-binding site contained in the CEBPA uORF/spacer mRNA, a known target of the negative regulator of myeloid differentiation hnRNP E2. Accordingly, REMSA and UV-crosslinking experiments showed that synthetic miR-223 and to a greater extent miR-328 bind efficiently to recombinant hnRNP E2 protein and compete for its binding to an oligoribonucleotide containing the CEBPA uORF/spacer region, which is required for hnRNP E2-mediated translational inhibition of CEBPA in CML-BCCD34+ progenitors. Furthermore, both miR-223 and miR-328 bind endogenous hnRNP E2 from lysates of BCR/ABL-expressing but not parental cells, and from lysates of parental 32Dcl3 myeloid precursors ectopically expressing a Flag-tagged hnRNP E2 protein, suggesting that miR-223 and miR-328 may act as decoy molecules that interfere with the translation-inhibitory activity of hnRNP E2. Indeed, ectopic expression of miR-223 restored G-CSF-driven granulocytic maturation of differentiation-arrested 32D-BCR/ABL cells and restored C/EBPα expression, whereas it did not have any effect on cytokine-independent growth and clonogenic potential. Consistent with its ability to bind hnRNP E2, miR-328 also rescued C/EBPα expression and differentiation of cytokine-independent BCR/ABL-expressing myeloid precursor 32Dcl3 cells. By contrast, BCR/ABL-dependent colony formation was markedly reduced by overexpression of miR-15a and miR-16-1 (65–75% inhibition, P<0.001) and slightly decreased (40–50% inhibition, P<0.01) by ectopic miR-328 expression. Altogether, these data not only reinforce the importance of BCR/ABL-dependent post-transcriptional regulation of gene expression during CML disease progression but also suggest a new function for microRNAs as functional regulators of RNA binding proteins involved in the control of malignant cell growth, survival and differentiation.

scholarly journals Identification of S1 proteins B2, C1 and D1 as AUF1 isoforms and their major role as heterogeneous nuclear ribonucleoprotein proteins

2003 ◽  
Vol 372 (3) ◽  
pp. 775-785 ◽  
Author(s):  
Akira INOUE ◽  
Yukitomo ARAO ◽  
Akira OMORI ◽  
Sachiyo ICHINOSE ◽  
Koji NISHIO ◽  
...  
Keyword(s):  
Rna Binding ◽  
Rnase A ◽  
Product Analysis ◽  
Heterogeneous Nuclear Ribonucleoprotein ◽  
Hnrnp Proteins ◽  
Binding Factor ◽  
Hypersensitive Sites ◽  
Hnrnp Protein ◽  
Nuclear Ribonucleoprotein ◽  
Relationship Of

AUF1 (A+U-rich RNA binding factor) participates in the rapid decay of mRNAs in the cytoplasm. It is sometimes called heterogeneous nuclear ribonucleoprotein (hnRNP) D0; however, evidence for its characterization as an hnRNP protein has been scarce. S1 proteins A–D are those selectively extracted at pH 4.9 from isolated nuclei pretreated with either RNase A or DNase I. In the present study we identified S1 (‘first supernatant’) proteins B2, C1 and D1 with p45, p40 and p37 AUF1s respectively, by microsequencing and product analysis of transfected cDNAs. We found, further, that more than 96% of the S1 proteins occurred in the nucleus, and localized largely in RNase-sensitive structures. B2 was confined in the nucleus and C1 directly bound to heterogeneous nuclear RNAs (hnRNAs). These B2 and C1 proteins formed hnRNP structures responsible for the 33 S, and, to lesser extent, the 40 S particles, which were liberated upon mild nucleolytic cleavage. On the other hand, D1 and the remainder of C1 were associated with nuclease-hypersensitive sites of hnRNAs, and comprised the major cytoplasmic AUF1s that may be involved in mRNA decay. Two-dimensional immunoblotting resolved each S1 isoform into up to six spots or more, and suggested that the previous uncertain relationship of hnRNP D0 and hnRNP D is resolved in terms of charge differences and differential splicing arising from one gene. The present results thus indicate that S1 proteins B2, C1 and D1 are identical with AUF1 proteins, but largely occur as hnRNP proteins in the nucleus. That hnRNP D0 is indeed an hnRNP protein was verified.

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