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TLR3 overexpression induces invasion of prostate cancer cells, whereas its activation triggers apoptosis

ABSTRACT: TLR3 overexpression induces invasion of prostate cancer cells, whereas its activation triggers apoptosis

PROVIDER: PRJNA771529 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16352000.fastq.gz	Fastqsanger.gz
	SRR16352001.fastq.gz	Fastqsanger.gz
	SRR16352002.fastq.gz	Fastqsanger.gz
	SRR16352003.fastq.gz	Fastqsanger.gz
	SRR16352004.fastq.gz	Fastqsanger.gz

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TLR3 overexpression induces invasion of prostate cancer cells, whereas its activation triggers apoptosis

Project description:Toll-like receptors are proteins that play an important role in the innate immune system. They are frequently detected in immune cells such as macrophages or dendritic cells. Their role has been in part studied in prostate cancer. However, in the present study we focus mostly on their functional significance at various types of cancer therapy resistance.

2022-05-19 | GSE185953 | GEO

Peptide occurring in Enterobacteriaceae triggers Streptococcus pneumoniae apoptosis

Project description:Peptide occurring in Enterobacteriaceae triggers Streptococcus pneumoniae apoptosis

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Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs) Fibroblast cells and PBMCs from donors with autosomal recessive (AR) complete TLR3 deficiency and autosomal dominant (AD) partial TLR3 deficiency were collected for microarray analysis to measure the transcriptional responsiveness of TLR3 in fibroblast and PBMCs. A total of 3 healthy controls, 1 AD TLR3-deficient patient, 1 AR TLR3-deficient patient, 1 AR UNC-93B-deficient patient, 1 MyD88 deficient patien were used in this study. The fibroblast cells were cultured in DMEM medium supplemented with 10% fetal calf serum (FCS). The PBMCs were cultured in RPMI medium complemented with 10% FCS. Different kinetics (2 hours and 8 hours) of poly(I:C) (25ug/ml, purchased from Amersham) stimulations were performed, aiming to define TLR3-inducible genes in these human cells. A stimulation of IL-1β (20ng/ml, purchased from R&D system Inc.) was used as a positive activation control with same kinetics of stimulations. A total of one million cells per stimulation were used for fibroblasts, and around 1.5 million cells per stimulation for PBMCs.

2011-11-02 | E-GEOD-30951 | biostudies-arrayexpress

Assessment of the impact of the TLR3 L412F variant in terms of TLR3-sensitive transcript induction

Project description:we assessed the impact of TLR3 L412F at endogenous cellular levels upon double stranded RNA (dsRNA) stimulation, by performing RNA-sequencing in primary fibroblasts from individuals homozygous for the ancestral allele (n =2) or homozygous for TLR3 L412F (n = 4) upon extracellular Poly(I:C) stimulation that activates the TLR3 pathway. The average response of TLR3 L412F homozygotes was significantly decreased (mean Δ log2 fold-change = 0.93; Wilcoxon p <10-16) compared to that of cells with the ancestral allele, approaching that of TLR3-deficient cells, used as negative control.

2023-01-13 | GSE216304 | GEO

Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs)

2011-11-02 | GSE30951 | GEO

Mitol dysfunction triggers apoptosis of hematopoietic stem cell via ER stress response

Project description:Mitol dysfunction triggers apoptosis of hematopoietic stem cell via ER stress response

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Isorhamnetin Inhibits Proliferation and Invasion and Induces Apoptosis Through the Mitochondria‑Dependent Apoptosis in Human Gastric Cancer Cells

Project description:Isorhamnetin Inhibits Proliferation and Invasion and Induces Apoptosis Through the Mitochondria‑Dependent Apoptosis in Human Gastric Cancer Cells

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microRNA expression profiling of small intestine of Tlr3+/+ and Tlr3-/- mice after total body g-irradiation

Project description:Microarray was performed to comprehensively examine microRNA induction in murine small intestine after exposure to total body g-irradiation. Small intestines were collected from Tlr3+/+ and Tlr3-/- mice at 0 and 6 hr after exposure to 10 Gy of total body g-irradiation. Samples were pooled from 3 mice. Total RNA was extracted and subjected to microRNA microarray analysis.

2015-02-01 | E-GEOD-42916 | biostudies-arrayexpress

Mitol dysfunction triggers apoptosis of hematopoietic stem cell via ER stress response

Project description:Cellular metabolism exceedingly determines hematopoietic stem cells (HSCs) divisional fate and functioning through organelles interaction upon stress-induced response. The outer mitochondrial membrane-localized E3 ubiquitin ligase Mitol/Marchf5 (encoded by Mitol gene) is known to regulate mitochondrial and endoplasmic reticulum (ER) interaction and promote cell survival. To investigate the precise functional involvement of Mitol in HSC maintenance, we analyzed MX1-cre inducible Mitol knockout mice. Mitol deletion in bone marrow (BM) leads to HSCs exhaustion and impairment of BM reconstitution capability. Moreover, Mitol deletion induced prolonged ER stress in HSCs, which triggers cellular apoptosis that is mainly regulated by IRE1a signaling. Inhibition of ER stress by KIRA6 could partially reduce apoptosis of long term-HSC. Our observations indicated that Mitol is principal to maintain hematopoietic homeostasis and protects HSCs from apoptosis mainly through ER function via IRE1a signaling.

2023-12-18 | GSE240788 | GEO

Impaired intrinsic immunity to HSV-1 in human iPSC-derived TLR3-deficient CNS cells

Project description:In the course of primary infection with herpes simplex virus 1 (HSV-1), children with inborn errors of the TLR3- and UNC-93B-dependent induction of IFN-α/β and/or IFN-λ immunity are prone to HSV-1 encephalitis (HSE) 1-3. The cells responsible for HSE in these children have yet to be identified. We tested the hypothesis that the pathogenesis of HSE involves non hematopoietic central nervous system (CNS)-resident cells. We derived induced pluripotent stem cells (iPSCs) from the dermal fibroblasts of TLR3- and UNC-93B-deficient patients and from controls. These iPSCs were allowed to differentiate into highly purified populations of neural stem cells (NSCs), neurons, astrocytes and oligodendrocytes. The induction of IFN-β and/or IFN-λ1 in response to poly(I:C) stimulation was dependent on TLR3 and UNC-93B in all cells tested. However, the induction of IFN-β and IFN-λ1 in response to HSV-1 infection was impaired selectively in UNC-93B-deficient neurons and oligodendrocytes. These cells were also much more susceptible to HSV-1 infection than control cells, whereas UNC-93B-deficient NSCs and astrocytes were not. The rescue of UNC-93B-deficient cells with the wild-type UNC93B1 allele demonstrated the genetic defect as the cause of the poly(I:C) and HSV-1 phenotypes. The viral infection phenotype was further rescued by treatment with exogenous IFN-α/β, but not IFN-λ1. TLR3-deficient neurons were also found to be susceptible to HSV-1 infection, a phenotype rescued by wild-type TLR3. Thus, impaired TLR3- and UNC-93B-dependent IFN-α/β intrinsic immunity to HSV-1 in the CNS, in neurons and oligodendrocytes in particular, may underlie the pathogenesis of HSE in children with TLR3 pathway deficiencies

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