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OASL Regulates Endothelial Function via USP39-Mediated Deubiquitination of CDK1 to Promote Large Full-Thickness Skin Defect Healing

ABSTRACT: Large full-thickness skin defects (LFSDs) remain a major clinical challenge due to insufficient vascular regeneration and impaired tissue repair. Emerging evidence suggests that oligoadenylate synthase-like protein (OASL), an interferon-stimulated protein, contributes to endothelial homeostasis and vascular function; however, its role in endothelial regeneration and wound healing has not been elucidated. Here, we investigated the molecular mechanism by which OASL regulates endothelial regeneration and explored its therapeutic potential for LFSD repair.

ORGANISM(S): Homo sapiens

PROVIDER: GSE337629 | GEO | 2026/07/09

REPOSITORIES: GEO

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	GSE337629_gene_count.txt.gz	Txt
	GSE337629_gene_fpkm.txt.gz	Txt

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Investigation of cytoplasmic cGAS interactions reveals association with OASL during HSV-1 infection

Project description:Viral DNA sensing is an essential component of mammalian innate immune response. Upon binding viral DNA, the cyclic-GMP-AMP synthase (cGAS) catalyzes the production of cyclic dinucleotides to induce type I interferons. However, little is known about how cGAS is homeostatically maintained or regulated upon infection. Here, we define cytoplasmic cGAS interactions with cellular and viral proteins upon herpes simplex virus (HSV-1) infection in primary human fibroblasts. We compare several HSV-1 strains (wild-type, d109, d106) that induce cytokine responses and apoptosis, and place cGAS interactions in the context of temporal proteome alterations using isobaric-labeling mass spectrometry. Follow-up analyses establish a functional interaction between cGAS and 2’-5’-oligoadenylate synthase-like protein OASL. The OAS-like domain interacts with the cGAS Mab21 domain, while the OASL ubiquitin-like domain further inhibits cGAS-mediated interferon response. Our findings explain how cGAS may be inactively maintained in cellular homeostasis, with OASL functioning as a negative feedback loop for cytokine induction.

2018-11-21 | PXD010162 | Pride

Transcriptomic profiles of OASL knockdown HUVECs under basal or activated condition

Project description:Purpose: The goal of this study is to compare endothelial transcriptome affected by OASL knockdown under basal or stimulated conditions by utilizing RNA-seq. Methods: Endothelial mRNA profilies of siCTL or siOASL transfected HUVECs were generated by illumina sequencing method, in duplicate. Following an optimized data analysis workflow, RNA sequence reads were counted using StringTie-2.1.3b and used to identify genes differentially expressed between siCTL- and siOASL-transfected HUVECs treated with or without TNFα and IFNγ. Results: DESeq2 was used to identify genes differentially expressed between siCTL- and siOASL-transfected HUVECs under basal or stimulated conditions. Genes showing <10 read counts total were pre-filtered. Conclusions: Our study represents the first analysis of endothelial mRNA affected by OASL knockdown with biologic replicates, generated by RNA-seq.

2022-09-06 | GSE186352 | GEO

The role of OASL in Helicobacter pylori infection and Gastric Cancer

Project description:Our previous studies have shown thatHelicobacter pylori can induce the expression of OASL, which plays a crucial role in gastritis-cancer progression. In order to further investigate the detailed mechanism of OASL, we constructed an OASL overexpression model in HGC27 cells.

2025-03-19 | GSE291766 | GEO

Oligoadenylate synthetase-like (OASL) aggravated newcastle disease virus (NDV)-induced necroptosis in glioma cells

Project description:Oligoadenylate synthetase-like (OASL) aggravated newcastle disease virus (NDV)-induced necroptosis in glioma cells

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Investigation of cytoplasmic cGAS interactions reveals association with OASL during HSV-1 infection

Project description:Viral DNA sensing is an essential component of mammalian innate immune response. Upon binding viral DNA, the cyclic-GMP-AMP synthase (cGAS) catalyzes the production of cyclic dinucleotides to induce type I interferons. However, little is known about how cGAS is homeostatically maintained or regulated upon infection. Here, we define cytoplasmic cGAS interactions with cellular and viral proteins upon herpes simplex virus (HSV-1) infection in primary human fibroblasts. We compare several HSV-1 strains (wild-type, d109, d106) that induce cytokine responses and apoptosis, and place cGAS interactions in the context of temporal proteome alterations using isobaric-labeling mass spectrometry. Follow-up analyses establish a functional interaction between cGAS and 2â??-5â??-oligoadenylate synthase-like protein OASL. The OAS-like domain interacts with the cGAS Mab21 domain, while the OASL ubiquitin-like domain further inhibits cGAS-mediated interferon response. Our findings explain how cGAS may be inactively maintained in cellular homeostasis, with OASL functioning as a negative feedback loop for cytokine induction.

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Oligoadenylate synthetase-like (OASL) aggravated newcastle disease virus (NDV)-induced necroptosis in glioma cells

Project description:Newcastle disease virus (NDV) has emerged as an oncolytic agent in several cancers. Previous study has shown that NDV exerts cytolytic activity in glioma, however, the underlying mechanism has not been fully uncovered. Here the cytolytic activity of NDV in glioma and the associated mechanisms have been demonstrated. Infection with NDV inhibits cell proliferation and promotes cell apoptosis in LN229 cells. Further investigation showed that cytoplasmic organelle damage and cytoplasmic vacuolation were observed in LN229 cells after NDV infection. JC-1 staining assay proved that NDV caused cell apoptosis of LN229 cells by inducing mitochondrial dysfunction. We next speculated that NDV caused LN229 cells death through inducing necroptosis, but not ferroptosis, since the Fe2+ level did not alter after NDV infection. Furthermore, the NDV-caused cell death in LN229 cells was blocked by necroptosis inhibitor Nec1. Besides, RNA-seq analysis identified the different expression genes in NDV-infected LN229 cells. OASL, an antiviral gene, has been found to be directly induced by NDV infection. We also found that knockdown of OASL enhanced NDV infection-induced LN229 cells necroptosis. In summary, two aspects about cytolytic activity of NDV in glioma have been demonstrated. NDV presented cytolytic activity in glioma cells through inducing necroptosis. Additionally, targeting OASL may provide new strategy for enhancing necroptosis of glioma cells after NDV infection.

2023-05-01 | GSE227791 | GEO