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PTBP1 is necessary for dendritic cells to regulate T cells homeostasis and antitumor immunity

ABSTRACT: PTBP1 is necessary for dendritic cells to regulate T cells homeostasis and antitumor immunity

PROVIDER: PRJNA642299 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12102210_1.fastq.gz	Fastqsanger.gz
	SRR12102210_2.fastq.gz	Fastqsanger.gz
	SRR12102211_1.fastq.gz	Fastqsanger.gz
	SRR12102211_2.fastq.gz	Fastqsanger.gz
	SRR12102212_1.fastq.gz	Fastqsanger.gz

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PTBP1 is necessary for dendritic cells to regulate T cells homeostasis and antitumor immunity

Project description:Dendritic cells (DCs) play an important role in innate and adaptive immunity. DCs could sense environment pathogens and tumors, presenting those antigens to T cells. PTBP1, an RNA-binding protein, the function in DCs is unknown. Here, we found PTBP1 specific deficiency in DCs could impair T cell homeostasis. PTBP1 deletion in DCs could enhance antitumor immunity and increase asthma exacerbation. Further studies demonstrate that PTBP1 negatively regulates the induction of a subset of IFN-response genes. These findings revealed the novel functions of PTBP1 in DCs and might be a potential therapeutic target for tumors.

2021-01-10 | GSE153401 | GEO

PTBP1 is necessary for dendritic cells to regulate T-cell homeostasis and antitumour immunity.

Project description:Dendritic cells (DCs) play an important role in linking innate and adaptive immunity. DCs can sense endogenous and exogenous antigens and present those antigens to T cells to induce an immune response or immune tolerance. During activation, alternative splicing (AS) in DCs is dramatically changed to induce cytokine secretion and upregulation of surface marker expression. PTBP1, an RNA-binding protein, is essential in alternative splicing, but the function of PTBP1 in DCs is unknown. Here, we found that a specific deficiency of Ptbp1 in DCs could increase MHC II expression and perturb T-cell homeostasis without affecting DC development. Functionally, Ptbp1 deletion in DCs could enhance antitumour immunity and asthma exacerbation. Mechanistically, we found that Pkm alternative splicing and a subset of Ifn response genes could be regulated by PTBP1. These findings revealed the function of PTBP1 in DCs and indicated that PTBP1 might be a novel therapeutic target for antitumour treatment.

| S-EPMC8044338 | biostudies-literature

The RNA binding protein PTBP1 is necessary for B cell selection in germinal centres

Project description:Antibody affinity maturation occurs in germinal centres (GC) where B cells cycle between the light zone (LZ) and the dark zone. In the LZ GC B cells bearing immunoglobulins with the highest affinity for antigen receive positive selection signals from T helper cells that promotes their rapid proliferation. Here we show that the RNA binding protein PTBP1 is necessary for the progression of GC B cells through late S-phase of the cell cycle and for affinity maturation. PTBP1 is required for the expression of the c-MYC-dependent gene programme induced in GC B cells receiving T cell help and directly regulates the alternative splicing of transcripts increased during positive selection to promote anabolic metabolism and cell proliferation.

2017-12-06 | GSE100969 | GEO

Proteome changes in PTBP1 deficient hematopoietic cells

Project description:Ribosomopathies constitute a range of disabling conditions associated with defective protein synthesis mainly affecting hematopoietic stem cells (HSCs) and erythroid development. Here we demonstrate that deletion of Polypyrimidine Tract Binding Protein 1 (PTBP1) in the hematopoietic compartment led to the development of a ribosomopathy-like condition. Specifically, loss of PTBP1 was associated with a decrease in HSC self-renewal, erythroid differentiation and protein synthesis. Consistent with its function as a splicing regulator, PTBP1 deficiency led to splicing defects in hundreds of genes and we demonstrate that the up-regulation of a specific isoform of CDC42 could partly mimic the protein synthesis defect associated with loss of PTBP1. Furthermore, PTBP1 deficiency was associated with a marked defect in ribosome biogenesis and a selective reduction in the translation of mRNAs encoding ribosomal proteins. Collectively, this work identifies PTBP1 as a key integrator of ribosomal functions and highlights the broad functional repertoire of RNA binding proteins.

2022-05-04 | PXD023879 | Pride

iiCLIP protocol benchmarking with PTBP1

Project description:We describe an improved individual nucleotide resolution CLIP protocol (iiCLIP), which can be completed within 4 days from UV crosslinking to libraries for sequencing. For benchmarking, we directly compared PTBP1 iiCLIP libraries with the iCLIP2 protocol produced under standardised conditions with 1 million HEK293 cells, and with public eCLIP and iCLIP PTBP1 data. There are 3 PTBP1 iiCLIP libraries, 1 input iiCLIP library and 1 PTBP1 iCLIP2 library produced in this study.

2022-08-01 | E-MTAB-10881 | biostudies-arrayexpress

Transcriptomic analysis of senescent cells upon PTBP1 knockdown.

Project description:IMR90 ER:RAS cells were stably transduced with either an empty vector or 2 deconvoluted shRNAs targeting PTBP1. Following selection with puromycin, the cells were treated with 4OHT to induce senescence. 6 days later the cells were collected for total mRNA analysis. PTBP1 is a regulator of alternative splicing. Our previous experiments had shown that PTBP1 depletion inhibits the expression of pro-inflammatory genes without affecting other senescence-associated phenotypes. By performing RNA-seq we confirmed those observations at a global level and analysed how PTBP1 knockdown alters alternative splicing as a potential mechanism of action.

2018-06-25 | GSE101750 | GEO

Detection of transcriptome changes caused by knockdown of Ptbp1 in U251 GBM cells

Project description:We demonstrated that knocking down Ptbp1 can reprogram GBM cells into neuron-like cells. In order to further explore the mechanism of Ptbp1 causing this phenomenon, we performed mRNA sequencing on U251 cells infected with sh-Luci-3d, sh-Ptbp1-3d and sh-Ptbp1-7d.

2022-06-01 | GSE189816 | GEO

4SU-iCLIP of MATR3 from HEK293 cells with or without PTBP1 depletion

Project description:The aim of the experiment was to compare binding of MATR3 in presence and absence of PTBP1. HEK293T cells were transfected with siRNA targeting PTBP1 and PTBP2 or control sequences and labelled with 4thio-uridine for 8 hours (100µM, crosslinking 2x400mJ/cm2 365nm UV light).

2018-05-01 | E-MTAB-6267 | biostudies-arrayexpress

Regulation of co-transcriptional splicing by RNA-binding protein PTBP1

Project description:We examined the role of PTBP1 in regulation of co-transcriptional splicing process by depleting this RNA-binding protein from embryonic stem cells using the auxin-inducible degron technology and analysing the total and chromatin-associated RNA fractions by RNA-seq. We also performed mNET-seq and ChIP-seq analyses using RNA polymerase II- and PTBP1-specific antibodies, respectively. Our data suggest that PTBP1 activates co-transcriptional splicing of hundreds of introns, a surprising effect given that PTBP1 is better known as a splicing repressor. Importantly, some co-transcriptionally activated introns fail to be spliced post-transcriptionally without PTBP1. In a striking example of this regulation, lasting retention of a PTBP1-dependent intron triggers nonsense-mediated decay of mRNAs encoding DNA methyltransferase DNMT3B, explaining their natural expression dynamics in development. Our further analyses suggest that this mechanism may protect differentiation-specific genes from aberrant methylation. We conclude that PTBP1-activated co-transcriptional splicing underlies biologically important decisions.

2023-01-08 | E-MTAB-11544 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of endothelial cells transfected with Ptbp1(wt), Ptbp1(T138A) or Ptbp1(T138E) plasmid Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of endothelial cells transfected with Ptbp1(wt), Ptbp1(T138A) or Ptbp1(T138E) plasmid Transcriptomes

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