scholarly journals Cellular RNA Binding Proteins NS1-BP and hnRNP K Regulate Influenza A Virus RNA Splicing

2013 ◽  
Vol 9 (6) ◽  
pp. e1003460 ◽  
Author(s):  
Pei-Ling Tsai ◽  
Ni-Ting Chiou ◽  
Sharon Kuss ◽  
Adolfo García-Sastre ◽  
Kristen W. Lynch ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Rna Splicing ◽  
Influenza A ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Hnrnp K ◽  
Virus Rna

scholarly journals Aberrant RNA Splicing Events Driven by Mutations of RNA-Binding Proteins as Indicators for Skin Cutaneous Melanoma Prognosis

2020 ◽  
Vol 10 ◽  
Author(s):  
Chao Mei ◽  
Pei-Yuan Song ◽  
Wei Zhang ◽  
Hong-Hao Zhou ◽  
Xi Li ◽  
...  
Keyword(s):  
Cutaneous Melanoma ◽  
Rna Splicing ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Melanoma Prognosis ◽  
Aberrant Rna

scholarly journals P2-218: DEEP PROTEOMIC NETWORK ANALYSIS OF ALZHEIMER'S DISEASE BRAIN REVEALS ALTERATIONS IN RNA BINDING PROTEINS AND RNA SPLICING ASSOCIATED WITH DISEASE

2019 ◽  
Vol 15 ◽  
pp. P660-P661
Author(s):  
Erik C.B. Johnson ◽  
Eric B. Dammer ◽  
Duc Duong ◽  
Luming Yin ◽  
Madhav Thambisetty ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Network Analysis ◽  
Rna Splicing ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins

scholarly journals Identification of RNA Binding Proteins Associated with Dengue Virus RNA in Infected Cells Reveals Temporally Distinct Host Factor Requirements

2016 ◽  
Vol 10 (8) ◽  
pp. e0004921 ◽  
Author(s):  
Olga V. Viktorovskaya ◽  
Todd M. Greco ◽  
Ileana M. Cristea ◽  
Sunnie R. Thompson
Keyword(s):  
Dengue Virus ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Host Factor ◽  
Virus Rna ◽  
Infected Cells

scholarly journals Increased hnRNP K Expression Impacts Myelopoiesis By Altering RUNX1 Splicing

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 3317-3317
Author(s):  
Sean M Post ◽  
Marisa J Aitken ◽  
Prerna Malaney ◽  
Xiaorui Zhang ◽  
Todd Link ◽  
...  
Keyword(s):  
Binding Proteins ◽  
Rna Binding ◽  
Conflicts Of Interest ◽  
Rna Binding Proteins ◽  
Fetal Liver ◽  
Full Length ◽  
Clinical Samples ◽  
Differentiation Potential ◽  
Hnrnp K ◽  
Mutational Status

Abstract Mutations in RNA binding proteins have been identified as pathogenic drivers in many hematological malignancies. However, in addition to mutational status, expression changes in RNA binding proteins likely impact disease processes. Through our studies, we identified that overexpression of hnRNP K (heterogeneous ribonucleoprotein K) -a poly(C)-RNA binding protein that governs the expression of numerous genes and transcripts- plays a pivotal role in myeloid malignancies. Using clinical samples, we determined that hnRNP K overexpression is a recurrent abnormality, occurring in nearly 30% of AML cases. Importantly, elevated hnRNP K levels associate with decreased overall survival (24.3 months versus 48.7 months; HR 1.9; 95% CI 1.3-2.7). However, the role of hnRNP K overexpression in AML remains unclear. To evaluate its putative oncogenic potential, we overexpressed hnRNP K in murine fetal liver cells (FLCs). Using colony formation assays (CFAs), we demonstrated that hnRNP K-overexpressing FLCs have an altered differentiation potential (increased number of immature (c-kit +Sca-1 +) and decreased number of mature myeloid (Gr1 +CD11b +) cells) and an increase in self-renewal capacity (increased number of colonies) (p=0.008). Mice transplanted with hnRNP K overexpressing FLCs had markedly shortened survival compared to empty vector controls, despite similar engraftment (median survival 8.1 weeks versus median not reached (HR 3.0, 95% CI 1.2 - 7.3, p=0.02). Significantly, extramedullary hematopoiesis was observed in the spleens and the hepatic parenchyma of mice transplanted with FLCs that overexpress hnRNP K. This resulted in disrupted splenic architecture and the presence of immature hematopoietic cells and cells of myeloid origin (CD117, CD14, and myeloperoxidase). Furthermore, analyses of the bone marrow revealed an increase in myeloid cells in hnRNP K transplanted mice. We next used unbiased and biochemical approaches to discover a direct interaction between hnRNP K and the RUNX1 transcript-a critical transcriptional factor often dysregulated in leukemia. Molecular analyses revealed hnRNP K-dependent alternative splicing of RUNX1 (delExon6) , resulting in the generation of a functionally distinct isoform that is more stable than full-length RUNX1. RNA-Seq and reporter assays demonstrated that delExon6 has a unique transcriptional profile compared to full-length RUNX1, suggesting this spliced transcript may have a pathogenic role. To examine the functionality of delExon6, we performed CFAs. Here, we observed that delExon6 expression results in an increased proliferation potential that is mediated by hnRNP K's RNA binding activity. Together, these data establish hnRNP K as an oncogene in myeloid leukemia through its ability to directly bind the RUNX1 transcript, modify RUNX1 splicing, and subsequently alter its transcriptional activity. Disclosures No relevant conflicts of interest to declare.

scholarly journals Binding patterns of RNA-binding proteins to repeat-derived RNA sequences reveal putative functional RNA elements

2021 ◽  
Vol 3 (3) ◽  
Author(s):  
Masahiro Onoguchi ◽  
Chao Zeng ◽  
Ayako Matsumaru ◽  
Michiaki Hamada
Keyword(s):  
Rna Splicing ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Noncoding Rnas ◽  
Biological Processes ◽  
Rna Sequences ◽  
Rna Elements ◽  
Long Interspersed Element ◽  
Functional Rna

Abstract Recent reports have revealed that repeat-derived sequences embedded in introns or long noncoding RNAs (lncRNAs) are targets of RNA-binding proteins (RBPs) and contribute to biological processes such as RNA splicing or transcriptional regulation. These findings suggest that repeat-derived RNAs are important as scaffolds of RBPs and functional elements. However, the overall functional sequences of the repeat-derived RNAs are not fully understood. Here, we show the putative functional repeat-derived RNAs by analyzing the binding patterns of RBPs based on ENCODE eCLIP data. We mapped all eCLIP reads to repeat sequences and observed that 10.75 % and 7.04 % of reads on average were enriched (at least 2-fold over control) in the repeats in K562 and HepG2 cells, respectively. Using these data, we predicted functional RNA elements on the sense and antisense strands of long interspersed element 1 (LINE1) sequences. Furthermore, we found several new sets of RBPs on fragments derived from other transposable element (TE) families. Some of these fragments show specific and stable secondary structures and are found to be inserted into the introns of genes or lncRNAs. These results suggest that the repeat-derived RNA sequences are strong candidates for the functional RNA elements of endogenous noncoding RNAs.

scholarly journals RNA-Binding Proteins as Targets to Improve Salt Stress Tolerance in Crops

Agronomy ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 250 ◽  
Author(s):  
Sara Rosa Téllez ◽  
Rodoldphe Kanhonou ◽  
Carlos Castellote Bellés ◽  
Ramón Serrano ◽  
Paula Alepuz ◽  
...  
Keyword(s):  
Salt Stress ◽  
Salt Tolerance ◽  
Sugar Beet ◽  
Rna Splicing ◽  
Yeast Strain ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Crop Improvement ◽  
Salt Toxicity

Salt stress drastically reduce crop productivity. In order to identify genes that could improve crop salt tolerance, we randomly expressed a cDNA library of the halotolerant sugar beet in a sodium-sensitive yeast strain. We identified six sugar beet genes coding for RNA binding proteins (RBP) able to increase the yeast Na+-tolerance. Two of these genes, named Beta vulgaris Salt Tolerant 3 (BvSATO3) and BvU2AF35b, participate in RNA splicing. The other four BvSATO genes (BvSATO1, BvSATO2, BvSATO4 and BvSATO6) are putatively involved in other processes of RNA metabolism. BvU2AF35b improved the growth of a wild type yeast strain under salt stress, and also in mutant backgrounds with impaired splicing, thus confirming that splicing is a target of salt toxicity. To validate the yeast approach, we characterized BvSATO1 in sugar beet and Arabidopsis. BvSATO1 expression was repressed by salt treatment in sugar beet, suggesting that this gene could be a target of salt toxicity. Expression of BvSATO1 in Arabidopsis increased the plant salt tolerance. Our results suggest that not only RNA splicing, but RNA metabolic processes such as such as RNA stability or nonsense-mediated mRNA decay may also be affected by salt stress and could be biotechnological targets for crop improvement.

Comprehensive analysis of differences of N6-methyladenosine RNA methylomes between high-fat-fed and normal mouse livers

Epigenomics ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 1267-1282 ◽  
Author(s):  
Zupeng Luo ◽  
Zhiwang Zhang ◽  
Lina Tai ◽  
Lifang Zhang ◽  
Zheng Sun ◽  
...  
Keyword(s):  
Fatty Liver ◽  
High Fat Diet ◽  
Rna Splicing ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Normal Liver ◽  
Comprehensive Analysis ◽  
Control Group ◽  
High Fat

Aim: To assess the m6A methylome in mouse fatty liver induced by a high-fat diet (HFD). Materials & methods: MeRIP-seq was performed to identify differences in the m6A methylomes between the normal liver and fatty liver induced by an HFD. Results: As compared with the control group, the upmethylated coding genes upon feeding an HFD were primarily enriched in processes associated with lipid metabolism, while genes with downmethylation were enriched in processes associated with metabolism and translation. Furthermore, many RNA-binding proteins that potentially bind to differentially methylated m6A sites were mainly annotated in processes of RNA splicing. Conclusion: These findings suggest that differential m6A methylation may act on functional genes through RNA-binding proteins to regulate the metabolism of lipids in fatty liver disease.

scholarly journals Structural Basis of the Influenza A Virus RNA Polymerase PB2 RNA-binding Domain Containing the Pathogenicity-determinant Lysine 627 Residue

2009 ◽  
Vol 284 (11) ◽  
pp. 6855-6860 ◽  
Author(s):  
Takashi Kuzuhara ◽  
Daisuke Kise ◽  
Hiroko Yoshida ◽  
Takahiro Horita ◽  
Yoshimi Murazaki ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Influenza A Virus ◽  
Influenza A ◽  
Rna Binding ◽  
Binding Domain ◽  
Structural Basis ◽  
Virus Rna ◽  
Pathogenicity Determinant ◽  
Rna Binding Domain

scholarly journals The QKI-5 and QKI-6 RNA Binding Proteins Regulate the Expression of MicroRNA 7 in Glial Cells

2013 ◽  
Vol 33 (6) ◽  
pp. 1233-1243 ◽  
Author(s):  
Yunling Wang ◽  
Gillian Vogel ◽  
Zhenbao Yu ◽  
Stéphane Richard
Keyword(s):  
Glial Cells ◽  
Rna Splicing ◽  
Cellular Localization ◽  
Binding Proteins ◽  
Rna Binding ◽  
Egf Receptor ◽  
Cell Function ◽  
Rna Binding Proteins ◽  
Glioblastoma Cells ◽  
Egfr Expression

Thequaking(qkI) gene encodes 3 major alternatively spliced isoforms that contain unique sequences at their C termini dictating their cellular localization. QKI-5 is predominantly nuclear, whereas QKI-6 is distributed throughout the cell and QKI-7 is cytoplasmic. The QKI isoforms are sequence-specific RNA binding proteins expressed mainly in glial cells modulating RNA splicing, export, and stability. Herein, we identify a new role for the QKI proteins in the regulation of microRNA (miRNA) processing. We observed that small interfering RNA (siRNA)-mediated QKI depletion of U343 glioblastoma cells leads to a robust increase in miR-7 expression. The processing from primary to mature miR-7 was inhibited in the presence QKI-5 and QKI-6 but not QKI-7, suggesting that the nuclear localization plays an important role in the regulation of miR-7 expression. The primary miR-7-1 was bound by the QKI isoforms in a QKI response element (QRE)-specific manner. We observed that the pri-miR-7-1 RNA was tightly bound to Drosha in the presence of the QKI isoforms, and this association was not observed in siRNA-mediated QKI or Drosha-depleted U343 glioblastoma cells. Moreover, the presence of the QKI isoforms led to an increase presence of pri-miR-7 in nuclear foci, suggesting that pri-miR-7-1 is retained in the nucleus by the QKI isoforms. miR-7 is known to target the epidermal growth factor (EGF) receptor (EGFR) 3′ untranslated region (3′-UTR), and indeed, QKI-deficient U343 cells had reduced EGFR expression and decreased ERK activation in response to EGF. Elevated levels of miR-7 are associated with cell cycle arrest, and it was observed that QKI-deficient U343 that harbor elevated levels of miR-7 exhibited defects in cell proliferation that were partially rescued by the addition of a miR-7 inhibitor. These findings suggest that the QKI isoforms regulate glial cell function and proliferation by regulating the processing of certain miRNAs.

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