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Dipeptidyl peptidase DPF-3 is a gatekeeper of microRNA Argonaute compensation in animals

ABSTRACT: Dipeptidyl peptidase DPF-3 is a gatekeeper of microRNA Argonaute compensation in animals

PROVIDER: PRJNA1155651 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30510400.fastq.gz	Fastqsanger.gz
	SRR30510389.fastq.gz	Fastqsanger.gz
	SRR30510390.fastq.gz	Fastqsanger.gz
	SRR30510391.fastq.gz	Fastqsanger.gz
	SRR30510392.fastq.gz	Fastqsanger.gz

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Dipeptidyl peptidase DPF-3 is a gatekeeper of microRNA Argonaute compensation in animals

Project description:MicroRNAs (miRNAs) are essential regulators involved in multiple biological processes. To achieve their gene repression function, they are loaded in miRNA-specific Argonautes to form the miRNA-induced silencing complex (miRISC). Mammalians and C. elegans intriguingly possess more than one paralog of miRNA-specific Argonautes and the dynamic between them remains unclear. Here, using C. elegans as a model system, we report dipeptidyl peptidase DPF-3 as a new interactor of miRNA-specific Argonautes ALG-1 and ALG-2. Knockout of dpf-3 rescues miRNA-related defects observed in alg-1 null animals and allows ALG-2 to better compensate for the lack of its paralog through higher expression and activity. While DPF-3 can cleave a N-terminal dipeptide of ALG-2 in vitro, we show that it is likely not the molecular mechanism used by DPF-3 to regulate ALG-2. This study uncovers the importance of a dipeptidyl peptidase in the miRNA pathway and provide insights in miRNA-specific Argonautes regulation dynamics in animals.

2025-03-06 | GSE276186 | GEO

Dipeptidyl peptidase DPF-3 is a gatekeeper of microRNA Argonaute compensation in animals

Project description:MicroRNAs (miRNAs) are essential regulators involved in multiple biological processes. To achieve their gene repression function, they are loaded in miRNA-specific Argonautes to form the miRNA-induced silencing complex (miRISC). Mammals and C. elegans possess more than one paralog of miRNA-specific Argonautes but the dynamic between them remains unclear. Here, we report the conserved dipeptidyl peptidase DPF-3 as a new interactor of the miRNA-specific Argonautes ALG-1 and ALG-2 in C. elegans. Knockout of dpf-3 increases ALG-2 levels and miRISC formation in alg-1 null animals, thereby compensating for ALG-1 loss and rescuing miRNA-related defects observed. DPF-3 can cleave an ALG-2 N-terminal peptide in vitro but does not appear to rely on this catalytic activity to regulate ALG-2 in vivo. This study uncovers the importance of DPF-3 in the miRNA pathway and provides insights on how multiple miRNA Argonautes contribute to achieve proper miRNA-mediated gene regulation in animals.

2025-03-06 | PXD055867 | Pride

Dipeptidyl peptidase DPF-3 is a gatekeeper of microRNA Argonaute compensation in animals.

Project description:MicroRNAs (miRNAs) are essential regulators involved in multiple biological processes. To achieve their gene repression function, they are loaded in miRNA-specific Argonautes to form the miRNA-induced silencing complex (miRISC). Mammals and C. elegans possess more than one paralog of miRNA-specific Argonautes, but the dynamic between them remains unclear. Here, we report the conserved dipeptidyl peptidase DPF-3 as an interactor of the miRNA-specific Argonaute ALG-1 in C. elegans. Knockout of dpf-3 increases ALG-2 levels and miRISC formation in alg-1 loss-of-function animals, thereby compensating for ALG-1 loss and rescuing miRNA-related defects observed. DPF-3 can cleave an ALG-2 N-terminal peptide in vitro but does not appear to rely on this catalytic activity to regulate ALG-2 in vivo. This study uncovers the importance of DPF-3 in the miRNA pathway and provides insights into how multiple miRNA Argonautes contribute to achieving proper miRNA-mediated gene regulation in animals.

| S-EPMC11923051 | biostudies-literature

Dipeptidyl peptidase-IV is associated with decreased glioma growth

Project description:Effect of expression of dipeptidyl peptidase-IV (DPP-IV) in U373 cell line on uncontrolled cell proliferation and aberrant interactions with the brain extracellular matrix.

2011-12-31 | E-MTAB-583 | biostudies-arrayexpress

Deep quantification of substrate turnover definesprotease subsite cooperativity. Working title: Massively parallel mapping of dipeptidyl peptidase cleavage sites reveals substrate motifs

Project description:Proteases play a crucial role in processing or breaking down proteins. They exhibit varying levels of substrate specificity that determine their physiological or pharmacological functions. However, this specificity is not well-understood. To address this, we have developed hiMAPS (high-throughput mapping of protease cleavage sites), a mass spectrometry-based method that can survey tens of thousands of distinct peptides. By applying this approach to human DPP4 and C. elegans DPF-3, two prolyl peptidases from the Dipeptidyl Peptidase IV (DPPIV) family, we have derived quantitative models that confirm a strong preference for Pro and Ala in the penultimate (P1) position from the N-terminus, but also reveal differences in the relative preferences for other residues. The hiMAPS approach can be applied to other exoproteases using various cheap sources of highly diverse peptides. Additionally, we have observed that these proteases tolerate and accept substrates containing Thr and Ser at P1 position.

2024-11-01 | PXD042089 | Pride

Gene expression of cardiac tissues in dietary obese mice administered with a dipeptidyl peptidase-4 inhibitor

Project description:Dipeptidyl peptidase-4 (Dpp4) inhibitors are used worldwide to combat diabetes, however, their roles in cardiovascular disorders are yet to be defined. Here we show that a DPP4 inhibitor, linagliptin, contributes for the suppression of capillary rarefaction in cardiac tissues of dietary obese mice model. Imposing a high fat diet into mice induced capillary rarefaction and cardiac dysfunction. These pathologies associated with high DPP4 level in circulation, and the administration of linagliptin into dietary obese mice suppressed the development of capillary rarefaction and ameliorated cardiac dysfunction. Early growth response protein 1 (EGR1), known as an angiogenic transcription factor, is significantly reduced in the cardiac tissue upon metabolic stress, and this suppression was inhibited by the administration of linagliptin.

2017-04-27 | GSE98226 | GEO

Argonaute Alg-1 IP Caenorhabditis elegans

Project description:The Argonautes (AGOs) are widely expressed, evolutionarily conserved RNA binding proteins that play an important role in gene expression regulation. The AGOs bind to small regulatory noncoding RNAs such as micro RNAs (miRNAs), short interfering RNAs (siRNAs), Piwi-interacting RNAs (piRNAs) etc. The small regulatory noncoding RNAs serve the function of guiding the AGOs to the right target RNAs by complementary base pairing. Additionally, the AGOs interact with GW182 (TNRC6A/-B/-C) proteins and together with small RNAs, they form an effector ribonucleo protein complex named, RNA Induced Silencing Complex (RISC) that regulates several aspects of transcriptional and post-transcriptional gene expression. ALG-1 (Argonaute Like Gene) and ALG-2 are the AGO proteins in C. elegans that are required for miRNA mediated gene expression regulation. Our efforts towards the characterization of the protein complexes comprised of ALG-1 led to the identification of DPF-3, a conserved protease belonging to clinically relevant Di Peptidyl Peptidase IV family, as the novel interacting partner of ALG-1. We have further explored the role of DPF-3 in AGO regulation.

2025-03-06 | PXD060454 | Pride

miR-765 induces angiogenesis by inhibiting dipeptidyl peptidase 4 and increasing fibroblast growth factor 2

Project description:miR-765 induces angiogenesis by inhibiting dipeptidyl peptidase 4 and increasing fibroblast growth factor 2

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Foxp striatal compensation

Project description:Foxp striatal compensation

| PRJNA951694 | ENA

miR-765 induces angiogenesis by inhibiting dipeptidyl peptidase 4 and increasing fibroblast growth factor 2

Project description:Given that extracellular vesicles (EVs) secreted from stem cells contain angiogenic microRNAs (miRNAs), these EVs show equivalent angiogenic therapeutic effect to cell transplantation. This study aimed to identify the angiogenic miRNAs from several miRNAs involved in EVs secreted from stem cells. In human dental pulp stem cells (hDPSCs) under hypoxic culture, vascular endothelial growth factor (VEGF) involved in EVs increased. We hypothesized that angiogenic miRNAs increase in EVs that are secreted from hDPSCs under hypoxic culture compared with those under normoxic culture. In the first screening, the expression levels of miRNAs involved in EVs that were secreted from hDPSCs cultured under hypoxic and normoxic conditions were analyzed using miRNA array. In the second screening, 12 miRNAs were individually involved in EVs, and the growth of human aortic endothelial cells was assayed. In the third screening, miRNA-encapsulated EVs were injected in BALB/c mouse hindlimb ischemia model, followed by angiogenesis evaluation by blood flow analysis. Results showed that miR-765 is an angiogenic miRNA, targeting the 3′ untranslated region of dipeptidyl peptidase 4 (DPP4) and upregulating fibroblast growth factor 2 (FGF2) in vitro and in vivo. In conclusion, as an angiogenesis mechanism, miR-765 increased FGF2 expression levels by inhibiting DPP4.

2024-05-08 | GSE232178 | GEO

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