Browse
Submit Data
Databases
API
Help

Dataset Information

27 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Alternative Splicing of FOXP3-Virtue and Vice.

ABSTRACT: FOXP3 is the lineage-defining transcription factor of CD4+ CD25+ regulatory T cells. While many aspects of its regulation, interaction, and function are conserved among species, alternatively spliced FOXP3 isoforms are expressed only in human cells. This review summarizes current knowledge about alternative splicing of FOXP3 and the specific functions of FOXP3 isoforms in health and disease. Future perspectives in research and the therapeutic potential of manipulating alternative splicing of FOXP3 are discussed.

SUBMITTER: Mailer RKW

PROVIDER: S-EPMC5859138 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Alternative Splicing of FOXP3-Virtue and Vice.

Mailer Reiner K W RKW

Frontiers in immunology 20180313

FOXP3 is the lineage-defining transcription factor of CD4+ CD25+ regulatory T cells. While many aspects of its regulation, interaction, and function are conserved among species, alternatively spliced FOXP3 isoforms are expressed only in human cells. This review summarizes current knowledge about alternative splicing of FOXP3 and the specific functions of FOXP3 isoforms in health and disease. Future perspectives in research and the therapeutic potential of manipulating alternative splicing of FOX ...[more]

PMID: 29593749

Similar Datasets

FOXP3 interacts with hnRNPF to modulate pre-mRNA alternative splicing.

Project description:FOXP3 promotes the development and function of regulatory T cells mainly through regulating the transcription of target genes. RNA alternative splicing has been implicated in a wide range of physiological and pathophysiological processes. We report here that FOXP3 associates with heterogeneous nuclear ribonucleoprotein (hnRNP) F through the exon 2-encoded region of FOXP3 and the second quasi-RNA recognition motif (qRRM) of hnRNPF. FOXP3 represses the ability of hnRNPF to bind to its target pre-mRNA and thus modulates RNA alternative splicing. Furthermore, overexpression of mouse hnRNPF in in vitro-differentiated regulatory T cells (Tregs) reduced their suppressive function. Thus, our studies identify a novel mechanism by which FOXP3 regulates mRNA alternative splicing to modulate the function of regulatory T cells.

| S-EPMC6028976 | biostudies-literature

IL-1β promotes Th17 differentiation by inducing alternative splicing of FOXP3.

Project description:CD4(+)FOXP3(+) regulatory T (Treg) cells are essential for maintaining immunological self-tolerance. Treg cell development and function depend on the transcription factor FOXP3, which is present in several distinct isoforms due to alternative splicing. Despite the importance of FOXP3 in the proper maintenance of Treg cells, the regulation and functional consequences of FOXP3 isoform expression remains poorly understood. Here, we show that in human Treg cells IL-1β promotes excision of FOXP3 exon 7. FOXP3 is not only expressed by Treg cells but is also transiently expressed when naïve T cells differentiate into Th17 cells. Forced splicing of FOXP3 into FOXP3Δ2Δ7 strongly favored Th17 differentiation in vitro. We also found that patients with Crohn's disease express increased levels of FOXP3 transcripts lacking exon 7, which correlate with disease severity and IL-17 production. Our results demonstrate that alternative splicing of FOXP3 modulates T cell differentiation. These results highlight the importance of characterizing FOXP3 expression on an isoform basis and suggest that immune responses may be manipulated by modulating the expression of FOXP3 isoforms, which has broad implications for the treatment of autoimmune diseases.

| S-EPMC4593960 | biostudies-literature

Turning Vice into Virtue: Using Batch-Effects to Detect Errors in Large Genomic Data Sets.

Project description:It is often unavoidable to combine data from different sequencing centers or sequencing platforms when compiling data sets with a large number of individuals. However, the different data are likely to contain specific systematic errors that will appear as SNPs. Here, we devise a method to detect systematic errors in combined data sets. To measure quality differences between individual genomes, we study pairs of variants that reside on different chromosomes and co-occur in individuals. The abundance of these pairs of variants in different genomes is then used to detect systematic errors due to batch effects. Applying our method to the 1000 Genomes data set, we find that coding regions are enriched for errors, where ?1% of the higher frequency variants are predicted to be erroneous, whereas errors outside of coding regions are much rarer (<0.001%). As expected, predicted errors are found less often than other variants in a data set that was generated with a different sequencing technology, indicating that many of the candidates are indeed errors. However, predicted 1000 Genomes errors are also found in other large data sets; our observation is thus not specific to the 1000 Genomes data set. Our results show that batch effects can be turned into a virtue by using the resulting variation in large scale data sets to detect systematic errors.

| S-EPMC6185451 | biostudies-literature

Personal and Psychological Traits Influencing the Willingness to Pay for Food with Nutritional Claims: A Comparison between Vice and Virtue Food Products.

Project description:Several studies have demonstrated the usefulness of nutritional claims (NCs) to help consumers make more informed food decisions. However, fewer studies have investigated the effect of personal and psychological consumer characteristics on their food purchase decision. Hence, the main aim of this study is to examine the impact of body image, emotional eating style, anxiety traits, and body mass index on consumer preferences for multiple NCs on the front of the package (FOP) of hedonic (potato chips) and utilitarian (toasted bread) products carrying the same NCs. Therefore, a real choice experiment (RCE) has been used and the willingness-to-pay-space model was estimated to analyse the interaction between personal and psychological characteristics and consumer preferences. The main finding suggests differences in purchase behaviour between potato chips and toasted bread. In particular, consumers are willing to pay more for toasted bread with one NC than potato chips with one NC. Moreover, personal and psychological consumer characteristics influence the purchase behaviour regarding food products with nutritional claims. However, only the anxiety trait appears to explain the differences between the selection of both types of food products. In line with this new evidence, we proposed some behavioural, political, and managerial implications.

| S-EPMC7353545 | biostudies-literature

Virtue Discounting: Observability Reduces Moral Actors' Perceived Virtue.

Project description:Performing prosociality in public presents a paradox: only by doing so can people demonstrate their virtue and also influence others through their example, yet observers may derogate actors' behavior as mere "virtue signaling." Here we investigate the role of observability of actors' behavior as one reason that people engage in such "virtue discounting." Further, we investigate observers' motivational inferences as a mechanism of this effect, using the comparison of generosity and fairness as a case study among virtues. Across 14 studies (7 preregistered, total N = 9,360), we show that public actors are perceived as less virtuous than private actors, and that this effect is stronger for generosity compared to fairness (i.e., differential virtue discounting). Exploratory factor analysis suggests that three types of motives-principled, reputation-signaling, and norm-signaling-affect virtue discounting. Using structural equation modeling, we show that observability's effect on actors' trait virtue ratings is largely explained by inferences that actors have less principled motivations. Further, we leverage experimental evidence to provide stronger causal evidence of these effects. We discuss theoretical and practical implications of our findings, as well as future directions for research on the social perception of virtue.

| S-EPMC10449397 | biostudies-literature

Diverse alternative back-splicing and alternative splicing landscape of circular RNAs.

Project description:Circular RNAs (circRNAs) derived from back-spliced exons have been widely identified as being co-expressed with their linear counterparts. A single gene locus can produce multiple circRNAs through alternative back-splice site selection and/or alternative splice site selection; however, a detailed map of alternative back-splicing/splicing in circRNAs is lacking. Here, with the upgraded CIRCexplorer2 pipeline, we systematically annotated different types of alternative back-splicing and alternative splicing events in circRNAs from various cell lines. Compared with their linear cognate RNAs, circRNAs exhibited distinct patterns of alternative back-splicing and alternative splicing. Alternative back-splice site selection was correlated with the competition of putative RNA pairs across introns that bracket alternative back-splice sites. In addition, all four basic types of alternative splicing that have been identified in the (linear) mRNA process were found within circRNAs, and many exons were predominantly spliced in circRNAs. Unexpectedly, thousands of previously unannotated exons were detected in circRNAs from the examined cell lines. Although these novel exons had similar splice site strength, they were much less conserved than known exons in sequences. Finally, both alternative back-splicing and circRNA-predominant alternative splicing were highly diverse among the examined cell lines. All of the identified alternative back-splicing and alternative splicing in circRNAs are available in the CIRCpedia database (http://www.picb.ac.cn/rnomics/circpedia). Collectively, the annotation of alternative back-splicing and alternative splicing in circRNAs provides a valuable resource for depicting the complexity of circRNA biogenesis and for studying the potential functions of circRNAs in different cells.

| S-EPMC5052039 | biostudies-literature

EtEC81 reprograms alternative splicing

Project description:The fungus Exserohilum turcicum is the causal agent of northern corn leaf blight, a damaging maize (Zea mays) disease worldwide. Here, using an alternative splicing (AS) reporter system, we identified the secreted protein EtEC81 (Exserohilum turcicum effector 81), which modulates the AS of maize pre-mRNAs and negatively regulates the pathogenicity of E. turcicum. EtEC81 physically interacts with EtEC81-interactiNG protein 1 (ZmEIP1), which associates with maize spliceosome components, regulating AS and positively regulating the defense response against E. turcicum. EtEC81 binding further enhanced the effect of ZmEIP1 on AS.

2024-08-30 | PXD055437 |

Function of alternative splicing.

Project description:Almost all polymerase II transcripts undergo alternative pre-mRNA splicing. Here, we review the functions of alternative splicing events that have been experimentally determined. The overall function of alternative splicing is to increase the diversity of mRNAs expressed from the genome. Alternative splicing changes proteins encoded by mRNAs, which has profound functional effects. Experimental analysis of these protein isoforms showed that alternative splicing regulates binding between proteins, between proteins and nucleic acids as well as between proteins and membranes. Alternative splicing regulates the localization of proteins, their enzymatic properties and their interaction with ligands. In most cases, changes caused by individual splicing isoforms are small. However, cells typically coordinate numerous changes in 'splicing programs', which can have strong effects on cell proliferation, cell survival and properties of the nervous system. Due to its widespread usage and molecular versatility, alternative splicing emerges as a central element in gene regulation that interferes with almost every biological function analyzed.

| S-EPMC5632952 | biostudies-literature

Alternative splicing and disease.

Project description:Almost all protein-coding genes are spliced and their majority is alternatively spliced. Alternative splicing is a key element in eukaryotic gene expression that increases the coding capacity of the human genome and an increasing number of examples illustrates that the selection of wrong splice sites causes human disease. A fine-tuned balance of factors regulates splice site selection. Here, we discuss well-studied examples that show how a disturbance of this balance can cause human disease. The rapidly emerging knowledge of splicing regulation now allows the development of treatment options.

| S-EPMC5632948 | biostudies-literature

Cohesin regulates alternative splicing.

Project description:Cohesin, a trimeric complex that establishes sister chromatid cohesion, has additional roles in chromatin organization and transcription. We report that among those roles is the regulation of alternative splicing through direct interactions and in situ colocalization with splicing factors. Degradation of cohesin results in marked changes in splicing, independent of its effects on transcription. Introduction of a single cohesin point mutation in embryonic stem cells alters splicing patterns, demonstrating causality. In primary human acute myeloid leukemia, mutations in cohesin are highly correlated with distinct patterns of alternative splicing. Cohesin also directly interacts with BRD4, another splicing regulator, to generate a pattern of splicing that is distinct from either factor alone, documenting their functional interaction. These findings identify a role for cohesin in regulating alternative splicing in both normal and leukemic cells and provide insights into the role of cohesin mutations in human disease.

| S-EPMC9977177 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data