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Homo sapiens

ABSTRACT: Dual role of Act1 in keratinocyte differentiation and host defense: TRAF3IP2 silencing alters keratinocyte differentiation while inhibiting IL-17 responses

PROVIDER: PRJNA341946 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4174900.fastq.gz	Fastqsanger.gz
	SRR4174910.fastq.gz	Fastqsanger.gz
	SRR4174920.fastq.gz	Fastqsanger.gz
	SRR4174930.fastq.gz	Fastqsanger.gz
	SRR4174901.fastq.gz	Fastqsanger.gz

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Similar Datasets

Dual role of Act1 in keratinocyte differentiation and host defense: TRAF3IP2 silencing alters keratinocyte differentiation while inhibiting IL-17 responses

Project description:TRAF3IP2 is a candidate psoriasis susceptibility gene encoding Act1, a ubiquitin ligase that couples the IL-17 receptor to downstream signaling pathways. We investigated the role of Act1 in keratinocyte responses to IL-17 using a tetracycline inducible shRNA targeting TRAF3IP2. Tet exposure for seven days effectively silenced TRAF3IP2 mRNA and Act1 protein, resulting in 761 genes with significant changes in expression (495 down, 266 up, >1.5-fold, p<0.05). Gene Ontology analysis revealed that genes affected by TRAF3IP2 silencing are involved in epidermal differentiation, with early differentiation genes (KRT1, KRT10, DSC1, DSG1) being downregulated and late differentiation genes (SPRR2, SPRR3, LCE3) being upregulated. AP1 binding sites were enriched upstream of genes up-regulated by TRAF3IP2 silencing. Correspondingly, nuclear expression of FosB and Fra1 was increased in TRAF3IP2-silenced cells. Many genes involved in host defense were induced by IL-17 in a TRAF3IP2-dependent fashion. Inflammatory differentiation conditions (serum addition for 4 days postconfluence) markedly amplified these IL-17 responses, while increasing basal levels and TRAF3IP2 silencing-dependent upregulation of late differentiation genes. These findings suggest that TRAF3IP2 may alter both epidermal homeostasis and keratinocyte defense responses to influence psoriasis risk.

2017-08-21 | GSE86451 | GEO

Identification of LncRNA TRAF3IP2-AS1 as a key regulator of IL-17 signaling through the SRSF10-IRF1-Act1 axis in autoimmune diseases

Project description:Our study indicates that lncRNA TRAF3IP2-AS1 serving as a negative regulator of Act1 transcriptional expression and IL-17 signaling pathway activity,recruits SRSF10 to downregulate the transcription of IRF1, which is itself a transcriptional factor for Act1. And the psoriasis-susceptible variant A4165G of TRAF3IP2-AS1 is a gain-of-function mutant that binds more strongly than the wild-type form to SRSF10. It means that TRAF3IP2-AS1 or SRSF10 may be a good target for the treatment of human IL-17-related autoimmune diseases.

2021-01-30 | GSE165781 | GEO

Act1 modulates mRNA metabolism upon IL-17 stimulation

Project description:The IL-17 receptor adaptor molecule Act1, an RNA binding protein, plays a critical role in IL-17-mediated cancer progression. Here we report a novel mechanism for how IL-17/Act1 induces chemoresistance by modulating redox homeostasis through epitranscriptomic regulation of antioxidant RNA metabolism. Transcriptome-wide mapping of direct Act1-RNA interactions revealed that Act1 binds to the 5'UTR of antioxidant mRNAs and Wilms' tumor 1-associating protein (WTAP), a key regulator in m6A methyltransferase complex. Strikingly, Act1's binding sites are located in proximity to m6A modification sites, which allows Act1 to promote the recruitment of elF3G for cap-independent translation. Loss of Act1’s RNA binding activity or Wtap knockdown abolished IL-17-induced m6A modification and translation of Wtap and antioxidant mRNAs, indicating a feedforward mechanism of Act1-WTAP loop. We then developed antisense oligonucleotides (Wtap ASO) that specifically disrupts Act1’s binding to Wtap mRNA, abolishing IL-17/Act1-WTAP-mediated antioxidant protein production during chemotherapy. Wtap ASO substantially increased the antitumor efficacy of cisplatin, demonstrating a potential therapeutic strategy for chemoresistance.

2024-06-06 | GSE263835 | GEO

RNAseq of Mouse Embryonic Fibroblasts(MEFs) stimulated by IL-17

2024-06-06 | GSE263596 | GEO

RNA Seq analysis of the response of fisetin and rapamycin treatment on TNFα plus IL17A-stimulated primary human keratinocytes

Project description:Chronic autoimmune skin disease characterized by epidermal proliferation with hyper- and para-keratosis. The aberrant background immune response involves helper T-lymphocyte types 1 and 17 and their respective secreted cytokines tumor necrosis factor alpha (TNF) and interleukin 17 (IL-17). These pro-inflammatory cytokines stimulate the activation of keratinocytes, resulting in the release of acute phase cytokines, followed by chronic phase cytokines thus promotes induced hyperplasia of keratinocyte. The pro-differentiative action of fisetin on dual cytokine-induced abnormally proliferating keratinocyte revealed downregulation of psoriasis-associated genes and activation of autophagic genes, as well as normalization of genes involved in keratinocyte terminal differentiation. These result supports the effect of fisetin on improving psoriasis like inflammatory flareups in cultured keratinocyte in vitro.

2023-01-10 | GSE217552 | GEO

Oleic acid-dependent modulation of Nitric Oxide Associated 1 protein levels regulate nitric oxide mediate signaling in plant defense.

Project description:Oleic acid-dependent modulation of Nitric Oxide Associated 1 protein levels regulate nitric oxide- mediate signaling in plant defense. Nitric Oxide, Oleic acid, Salicylic acid, Arabidopsis, Defense Wild-type Col-0, mutant genotypes ssi2, ssi2 act1 and ssi2 sid2 with three biological replicates were analyzed (one array each)

2012-07-31 | E-GEOD-36797 | biostudies-arrayexpress

Identification of LncRNA TRAF3IP2-AS1 as a key regulator of IL-17 signaling through the SRSF10-IRF1-Act1 axis in autoimmune diseases

Project description:Identification of LncRNA TRAF3IP2-AS1 as a key regulator of IL-17 signaling through the SRSF10-IRF1-Act1 axis in autoimmune diseases

| PRJNA697878 | ENA

IL-17-induced NF-kB activation via CIKS/Act1: Physiologic significance and signaling mechanisms

Project description:Interleukin-17 (IL-17) is essential in host defense against extracellular bacteria and fungi, especially at mucosal sites, but it also contributes significantly to inflammatory and autoimmune disease pathologies. Binding of IL-17 to its receptor leads to recruitment of the adaptor protein CIKS/Act1 via heterotypic association of their respective SEFIR domains and to activation of the transcription factor NF-kB; it is not known whether CIKS and/or NF-kB are required for all gene induction events. Here we report that CIKS is essential for all IL-17 induced immediate-early genes in primary mouse embryo fibroblasts, while NF-kB is profoundly involved. We also identify a novel sub-domain in the N-terminus of CIKS that is essential for IL-17-mediated NF-kB activation. This domain is both necessary and sufficient for the interaction between CIKS and TRAF6, an adaptor required for NF-kB activation. The ability of decoy peptides to block this interaction may provide a new therapeutic strategy for intervention in IL-17-driven autoimmune and inflammatory diseases. Keywords: strain comparisons strain comparisons

2011-10-18 | E-GEOD-24873 | biostudies-arrayexpress

Act1 modulates mRNA metabolism upon IL-17 stimulation

Project description:Act1 modulates mRNA metabolism upon IL-17 stimulation

| PRJNA1099569 | ENA

Specific decorations of 17-hydroxygeranyllinalool diterpene glycosides solve the autotoxicity problem of chemical defense in Nicotiana attenuata

Project description:The native diploid tobacco Nicotiana attenuata produces abundant, potent anti-herbivore defense metabolites known as 17-hydroxygeranyllinalool diterpene glycosides (HGL-DTGs) whose glycosylation and malonylation biosynthetic steps are regulated by jasmonate signaling. To characterize the biosynthetic pathway of HGL-DTGs, we conducted a genome-wide analysis of uridine diphosphate glycosyltransferases (UGTs) and identified 107 family-1 UGT members. The transcript levels of three UGTs were highly correlated with the transcript levels two key HGL-DTG biosynthetic genes: geranylgeranyl diphosphate synthase (NaGGPPS) and geranyllinalool synthase (NaGLS). NaGLS's role in HGL-DTG biosynthesis was confirmed by virus-induced gene silencing. Silencing the Uridine diphosphate (UDP)-rhamnosyltransferase gene UGT91T1 demonstrated its role in the rhamnosylation of HGL-DTGs. In vitro enzyme assays revealed that UGT74P3 and UGT74P4 use UDP-glucose for the glucosylation of 17-hydroxygeranyllinalool (17-HGL) to lyciumoside I. Plants with stable silencing of UGT74P3 and UGT74P5 were severely developmentally deformed, pointing to a phytotoxic effect of the aglycone. The application of synthetic 17-HGL and silencing of the UGTs in HGL-DTG-free plants confirmed this phytotoxic effect. Feeding assays with tobacco hornworm (Manduca sexta) larvae revealed the defensive functions of the glucosylation and rhamnosylation steps in HGL-DTG biosynthesis. Glucosylation of 17-HGL is therefore a critical step that contributes to the resulting metabolites' defensive function and solves the autotoxicity problem of this potent chemical defense.

2021-10-06 | MTBLS1819 | MetaboLights

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