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Keratinocyte DDX5 in response to IL-36γ

ABSTRACT: Keratinocyte DDX5 in response to IL-36γ

PROVIDER: PRJNA860581 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20329986_1.fastq.gz	Fastqsanger.gz
	SRR20329986_2.fastq.gz	Fastqsanger.gz
	SRR20329987_1.fastq.gz	Fastqsanger.gz
	SRR20329987_2.fastq.gz	Fastqsanger.gz
	SRR20329988_1.fastq.gz	Fastqsanger.gz

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Keratinocyte DDX5 in response to IL-36γ

Project description:To compare how WT and DDX5-/- keratinocyte in response toIL-36γ, we performed gene expression profiling analysis using data obtained from RNA-seq of WT and DDX5-/- keratinocyte stimulated by IL-36γ

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DDX5-sIL-36R in keratinocytes controls skin inflammation

Project description:The DEAD-box (DDX) proteins function in diverse cellular processes including RNA alternative splicing, and are linked to immune-mediated diseases. However, little is known about the roles of DDXs in skin inflammatory diseases. Here, we show that DDX5, one of the founding members of the DDX RNA helicase family, controls skin inflammation and participates in the pathogenesis of psoriasis via regulating IL-36R pre-mRNA splicing. We found that both mRNA and protein of DDX5 are decreased in lesional skin from patients with psoriasis and psoriasis-like mice, and that mice with keratinocyte-specific ablation of DDX5 spontaneously develop psoriasis-like phenotypes. Mechanistically, DDX5 complexes with serine/arginine-rich splicing factor 1(SRSF1) to typically regulate IL-36R pre-mRNA splicing in keratinocytes, which generates mRNAs encoding full-length IL-36R and a previously unknown soluble form of IL-36R (sIL-36R). sIL-36R controls IL-36/IL-36R signaling by competing with IL-36R for IL-36γ ligation. The reduction or deficiency of DDX5 leads to IL-36R pre-mRNA splicing preferring to the generation of IL-36R but not sIL-36R, thereby selectively amplifying inflammatory responses of keratinocytes to IL-36γ and then aggravating cutaneous inflammation in psoriasis. Genetic restoration or intradermal administration of sIL-36R in psoriasis-like mice suppresses IL-36R signaling and alleviates the disease phenotype of psoriasis. Altogether, these data reveal a pathogenic role of DDX5 during psoriasis, and provide mechanistic insights into the regulation of IL-36R splicing and its impact on psoriasis development.

2020-09-09 | PXD021379 |

The role of keratinocyte DDX5 in IMQ-induced psoriatic mice

Project description:The role of keratinocyte DDX5 in IMQ-induced psoriatic mice

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Keratinocyte response to SNHG26 silencing

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Human Keratinocyte Response to Superantigens

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The role of keratinocyte DDX5 in MC903-induced atopic dermatitis (AD) mice

Project description:The role of keratinocyte DDX5 in MC903-induced atopic dermatitis (AD) mice

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DDX5 RNA interactome in cultured T cells

Project description:RAR-related orphan receptor gamma (ROR t)-expressing regulatory T (ROR t+ Treg) cells play pivotal roles in preventing T cell hyperactivation and maintaining tissue homeostasis, in part, by secreting the anti-inflammation cytokine interleukin 10 (IL-10). Here, we report that Hypoxia Induced Factor 1a (HIF1alpha) is the master transcription factor for *Il10* in ROR t+ Tregs. Interestingly, this critical anti-inflammatory pathway is negatively regulated by an RNA-binding protein DEAD box helicase 5 (DDX5). As a transcriptional corepressor, DDX5 restricts the expression of HIF1 and its downstream target gene *Il10* in ROR t+ Tregs. T cell specific *Ddx5* knockout (DDX5 T) mice have augmented ROR t+ Treg suppressor activities and are better protected from intestinal inflammation. Genetic ablation or pharmacologic inhibition of HIF1a restores enteropathy susceptibility in DDX5 T mice. The DDX5-HIF1 -IL-10 pathway is conserved in mice and humans. These findings reveal potential therapeutic targets for intestinal inflammatory diseases.

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The role of keratinocyte DDX5 in IMQ-induced psoriatic mice

Project description:To investigate whether DDX5 is involved in the development of psoriasis,we performed gene expression profiling analysis using data obtained from RNA-seq of ear skins from Ddx5f/f and K14Ddx5f/f psoriatic mice

2022-10-24 | GSE208671 | GEO

The role of keratinocyte DDX5 in MC903-induced atopic dermatitis (AD) mice

Project description:To investigate whether DDX5 is involved in the development of atopic dermatitis, we performed gene expression profiling analysis using data obtained from RNA-seq of ear skins from Ddx5f/f and K14Ddx5f/f atopic dermatitis mice

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DDX5 promotes prostate cancer progression and activates DNA repair pathway

Project description:The small heat shock protein Hsp27 has been long demonstrated as a major driver of Castration Resistant Prostate Cancer (CRPC) progression via an androgen receptor-independent pathway. In the light of identification of its molecular mechanisms, we found that the RNA helicase protein DDX5 was an interactor of Hsp27 and DDX5 expression was regulated by Hsp27 through its cytoprotective function. We showed that DDX5 was overexpressed in a large collection of human samples in aggressive PCs, especially CRPC. Here, we described the protein-protein interaction network of DDX5 which were identified in four human prostate cell lines (PNT1A, LNCaP, DU-145 and PC-3) representing different disease stages using immunoaffinity purification and quantitative mass spectrometry. The DDX5 interactome in CRPC cells was enriched in several functions (DNA damage response, translation, transcription, RNA stability, and DNA conformation changes) involved in disease progression. Furthermore, we found a new critical function of DDX5 in DNA damage repair in CRPC and validated the interaction of DDX5 with the DNA repair complex Ku70/Ku86 which plays a pivotal role in the NHEJ process. We also showed that DDX5 overexpression conferred resistance to DNA damage poisoners (such as irradiation and cisplatin) in CRPC, a feature that could lead to genome maintenance, tumor progression and treatment resistance.

2022-08-21 | PXD023252 | Pride

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