PARN is essential to GSIS in beta cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1044780 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26942083_1.fastq.gz | Fastqsanger.gz | |||
| SRR26942083_2.fastq.gz | Fastqsanger.gz | |||
| SRR26942084_1.fastq.gz | Fastqsanger.gz | |||
| SRR26942084_2.fastq.gz | Fastqsanger.gz | |||
| SRR26942085_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:To investigated the function of PARN in beta cells, we generated the specific deletion of Parn in beta cells.
2024-11-20 | GSE248559 | GEO
Project description:To investigated the function of PARN in beta cells, we generated the specific deletion of Parn in beta cells.
2024-11-20 | GSE248389 | GEO
Project description:PARN is essential to GSIS in beta cell
| PRJNA1043657 | ENA
Project description:The previous results suggest that PARN is involved in the early steps of miR-29a maturation. To identify factors that associate with and could recruit PARN to polyadenylated pri-miR-29a transcripts, we performed immunoprecipitation experiments in extracts of NCI-H520 cells with PARN antibody, followed by mass spectrometry. Of the identified proteins, we focused on cleavage and polyadenylation specificity factor 6 (CPSF6), the 68 kDa larger component of the mammalian cleavage factor I (CFIm), which is essential for the early steps of mRNA 3 ́ end processing and the selection of multiple poly(A) sites
2026-03-07 | PXD064050 | Pride
Project description:Class switch recombination (CSR) is a programmed DNA recombination process that enables B cells to switch the isotype of antibodies they produce, thereby generating high-affinity immunoglobulins essential for adaptive immunity. Of note, systemic lupus erythematosus (SLE) frequently arises in the context of hypersensitivity; however, the precise mechanisms underlying its pathogenesis remain incompletely understood. Here, we demonstrate that poly(A)-specific ribonuclease (PARN), an RNA-binding protein, acts as a critical regulator of CSR. In antibody-secreting cells, loss of PARN impairs CSR, resulting in a reduced proportion of cells producing post-switched immunoglobulin isotypes. Mechanistically, PARN specifically binds to the enhancer motif UGUA and the polyadenylation signal AAUAAA. PARN subsequently promotes transcript 3’ UTR shortening through alternative polyadenylation to regulate RNA stability. Depletion of PARN contributes to widespread 3’ UTR lengthening across the transcriptome, significantly affecting the Foxp1 transcript, and consequently impedes CSR efficiency. We further identified PTBP1 and PABP1 as cofactors that functionally cooperate with PARN to suppress CSR. Analysis of human datasets further reveals that Parn expression is elevated in patients with SLE. In an SLE mouse model, targeted Parn knockout in B lymphocytes undergoing CSR alleviates disease severity. This study unveils PARN as a key modulator of CSR in B cells, highlighting its therapeutic potential in SLE.
2026-07-15 | GSE313542 | GEO
Project description:Class switch recombination (CSR) is a programmed DNA recombination process that enables B cells to switch the isotype of antibodies they produce, thereby generating high-affinity immunoglobulins essential for adaptive immunity. Notably, systemic lupus erythematosus (SLE) frequently arises in the context of hypersensitivity; however, the precise mechanisms underlying its pathogenesis remain incompletely understood. Here, we demonstrate that poly(A)-specific ribonuclease (PARN), an RNA-binding protein, acts as a critical regulator of CSR. In antibody-secreting cells, loss of PARN impairs CSR, resulting in a reduced proportion of cells producing post-switched immunoglobulin isotypes. Mechanistically, PARN specifically binds to the enhancer motif UGUA and the polyadenylation signal AAUAAA. PARN subsequently promotes transcript 3’ UTR shortening through alternative polyadenylation to regulate RNA stability. Depletion of PARN contributes to widespread 3’ UTR lengthening across the transcriptome, notably affecting the Foxp1 transcript, and consequently impedes CSR efficiency. We further identified PTBP1 and PABP as cofactors that functionally cooperate with PARN to suppress CSR. Analysis of human datasets further reveals that Parn expression is elevated in patients with SLE. In an SLE mouse model, targeted Parn knockout in B lymphocytes undergoing CSR alleviates disease severity. This study unveils PARN as a key modulator of CSR in B cells, highlighting its therapeutic potential in SLE.
2026-07-15 | GSE312680 | GEO
Project description:Class switch recombination (CSR) is a programmed DNA recombination process that enables B cells to switch the isotype of antibodies they produce, thereby generating high-affinity immunoglobulins essential for adaptive immunity. Of note, systemic lupus erythematosus (SLE) frequently arises in the context of hypersensitivity; however, the precise mechanisms underlying its pathogenesis remain incompletely understood. Here, we demonstrate that poly(A)-specific ribonuclease (PARN), an RNA-binding protein, acts as a critical regulator of CSR. In antibody-secreting cells, loss of PARN impairs CSR, resulting in a reduced proportion of cells producing post-switched immunoglobulin isotypes. Mechanistically, PARN specifically binds to the enhancer motif UGUA and the polyadenylation signal AAUAAA. PARN subsequently promotes transcript 3’ UTR shortening through alternative polyadenylation to regulate RNA stability. Depletion of PARN contributes to widespread 3’ UTR lengthening across the transcriptome, significantly affecting the Foxp1 transcript, and consequently impedes CSR efficiency. We further identified PTBP1 and PABP1 as cofactors that functionally cooperate with PARN to suppress CSR. Analysis of human datasets further reveals that Parn expression is elevated in patients with SLE. In an SLE mouse model, targeted Parn knockout in B lymphocytes undergoing CSR alleviates disease severity. This study unveils PARN as a key modulator of CSR in B cells, highlighting its therapeutic potential in SLE.
2026-07-15 | GSE313461 | GEO
Project description:Class switch recombination (CSR) is a programmed DNA recombination process that enables B cells to switch the isotype of antibodies they produce, thereby generating high-affinity immunoglobulins essential for adaptive immunity. Of note, systemic lupus erythematosus (SLE) frequently arises in the context of hypersensitivity; however, the precise mechanisms underlying its pathogenesis remain incompletely understood. Here, we demonstrate that poly(A)-specific ribonuclease (PARN), an RNA-binding protein, acts as a critical regulator of CSR. In antibody-secreting cells, loss of PARN impairs CSR, resulting in a reduced proportion of cells producing post-switched immunoglobulin isotypes. Mechanistically, PARN specifically binds to the enhancer motif UGUA and the polyadenylation signal AAUAAA. PARN subsequently promotes transcript 3’ UTR shortening through alternative polyadenylation to regulate RNA stability. Depletion of PARN contributes to widespread 3’ UTR lengthening across the transcriptome, significantly affecting the Foxp1 transcript, and consequently impedes CSR efficiency. We further identified PTBP1 and PABP1 as cofactors that functionally cooperate with PARN to suppress CSR. Analysis of human datasets further reveals that Parn expression is elevated in patients with SLE. In an SLE mouse model, targeted Parn knockout in B lymphocytes undergoing CSR alleviates disease severity. This study unveils PARN as a key modulator of CSR in B cells, highlighting its therapeutic potential in SLE.
2026-07-15 | GSE313464 | GEO
Project description:Class switch recombination (CSR) is a programmed DNA recombination process that enables B cells to switch the isotype of antibodies they produce, thereby generating high-affinity immunoglobulins essential for adaptive immunity. Of note, systemic lupus erythematosus (SLE) frequently arises in the context of hypersensitivity; however, the precise mechanisms underlying its pathogenesis remain incompletely understood. Here, we demonstrate that poly(A)-specific ribonuclease (PARN), an RNA-binding protein, acts as a critical regulator of CSR. In antibody-secreting cells, loss of PARN impairs CSR, resulting in a reduced proportion of cells producing post-switched immunoglobulin isotypes. Mechanistically, PARN specifically binds to the enhancer motif UGUA and the polyadenylation signal AAUAAA. PARN subsequently promotes transcript 3’ UTR shortening through alternative polyadenylation to regulate RNA stability. Depletion of PARN contributes to widespread 3’ UTR lengthening across the transcriptome, significantly affecting the Foxp1 transcript, and consequently impedes CSR efficiency. We further identified PTBP1 and PABP1 as cofactors that functionally cooperate with PARN to suppress CSR. Analysis of human datasets further reveals that Parn expression is elevated in patients with SLE. In an SLE mouse model, targeted Parn knockout in B lymphocytes undergoing CSR alleviates disease severity. This study unveils PARN as a key modulator of CSR in B cells, highlighting its therapeutic potential in SLE.
2026-07-15 | GSE313463 | GEO
Project description:To understand the role of PARN we have employed miRNAs microarray expression profiling as a discovery platform to identify miRNAs whose expression is regulated by PARN
2026-03-10 | GSE207372 | GEO