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Genome-wide analysis of Nrdc-binding sites by ChIP-seq in mouse embryonic fibroblasts

ABSTRACT: Nardilysin (Nrdc) is a metallopeptidase of M16 family, which has been recently identified as a transcriptional coregulator. Here, we characterize the role of Nrdc in transcriptional regulation by genome-wide analysis using ChIP-seq and transcriptome.

ORGANISM(S): Mus musculus

PROVIDER: GSE90107 | GEO | 2017/10/23

SECONDARY ACCESSION(S): PRJNA354481

REPOSITORIES: GEO

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Transcriptome analysis in Nrdc-deficient MEF using RNA-seq

Project description:Nardilysin (Nrdc) is a metallopeptidase of M16 family, which has been recently identified as a transcriptional coregulator. Here, we characterize the role of Nrdc in transcriptional regulation by genome-wide analysis using ChIP-seq and transcriptome.

2017-10-23 | GSE90108 | GEO

Expression profiles of Nrdc-depleted pancreas

Project description:Pancreatic ductal adenocarcinoma (PDA) is the devastating disease in urgent need to identify new strategies for diagnosing and treating. Chronic pancreatitis is a risk factor for PDA in humans. Nardilysin (Nrdc, NRDC), a zinc peptidase of the M16 family has been shown to promote cancer cell growth in vitro. Here, we report that pancreatic deletion of Nrdc dramatically accelerates formation of pancreatic intraepithelial neoplasia (PanIN) and invasive PDA in the presence of oncogenic Kras. Nrdc was expressed in the nucleus of pancreatic acinar cells and pancreatic deletion of Nrdc was dispensable for pancreatic development in mice, but led to spontaneous chronic pancreatitis concomitant with acinar-to-ductal conversion, fibrotic change, infiltrated inflammatory cells, increased apoptosis, and atrophic pancreas in adult mice. Ex vivo acinar cell explants culture experiments showed that acinar-to-ductal conversion was not induced through a cell autonomous mechanism and that expression of several chemokines, including Cxcl10, was markedly up-regulated in Nrdc-null pancreatic acinar cells. Microarray analysis revealed that pathways implicated in pancreatitis and tumorigenesis, including chemotaxis, NF-κB and Erk1/2 signaling, were up-regulated in Nrdc-cKO pancreata compared with WT controls. Finally, immunostaining for NRDC revealed absence of NRDC expression in a subset of human PanINs and PDAs. These data demonstrate a previously unappreciated tumor suppressive function of Nrdc in the pancreas through suppressing chronic pancreatitis with acinar-to-ductal conversion in mice.

2017-05-31 | GSE99438 | GEO

Gene expression profiles after knockdown of Nardilysin in TMK-1 gastric cancer cells

2011-05-16 | GSE29144 | GEO

Gene expression profiles after knockdown of Nardilysin in TMK-1 gastric cancer cells

Project description:Nardilysin (NRDc), a metalloendopeptidase of the M16 family, has been reported to promote the ectodomain shedding and resulting activation of various growth factors and cytokines, but its role in cancer biology have not been elucidated. Microarray experiments were performed to analyze the chnages of gene expression profiles after knockdown of NRDc by microRNA (miR)-based RNA interference (RNAi). RNAi experiments were perfomed using BLOCK-iT Pol II miR RNAi Expression Vector Kit with EmGFP (Invitrogen). TMK-1 cells stably expressing conrol or NRDc-targeting miR vector were established.

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Exercise Training-induced Extracellular miR-136-3p Modulates Glucose Uptake and Myogenesis through Targeting of NRDC in Human Skeletal Muscle

Project description:We identified several exercise training-responsive miRNAs within exosome-rich EVs in serum, including miR-136-3p. In human myotubes, miR-136-3p enhanced glucose uptake and targeted the nardilysin convertase (NRDC) gene. To search miR-136-3p and NRDC relating function in human myotubes, we performed transcriptome analysis.

2025-10-31 | GSE282291 | GEO

Nrdc-deficient MEF

Project description:Nrdc-deficient MEF

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Nardilysin-Regulated Scission Mechanism Activates Polo-like Kinase 3 to Suppress the Development of Pancreatic Cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) develops through step-wise genetic and molecular alterations including Kras mutation and inactivation of apoptotic pathways. Here, we find that development of anoikis resistance and metastasis of KrasG12D-driven PDAC in mice is accelerated by deleting Plk3, explaining the often reduced Plk3 expression in human PDAC. Importantly, a 41 kDa Plk3 (p41Plk3) that contained the entire kinase domain at the N-terminus (1-353 aa) is activated by scission of the precursor p72Plk3 at Arg354 by metalloendopeptidase Nardilysin (NRDC), and the resulting p32Plk3 C-terminal Polo-box domain (PBD) was quickly removed by proteasome degradation preventing the p41Plk3 inhibition by PBD. We found that p41Plk3 is the activated form of Plk3 that regulates a feedforward mechanism to promote anoikis and suppress PDAC and metastasis. p41Plk3 phosphorylates c-Fos on Thr164, which in turn, induces expression of Plk3 and pro-apoptotic genes. These findings uncovered an NRDC-regulated post-translational mechanism (PTM) that activates Plk3, establishing a prototypic regulation by scission mechanism.

2023-12-23 | PXD042993 | Pride

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Project description:IP-MS analysis against endogenous NRDC using megakaryocyte cell lysates.

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ChIP-MS of GR and GR-DZn in mouse embryonic fibroblasts

Project description:The Glucocorticoid Receptor (GR) is both one of the most widely used clinical drug targets and a very potent metabolic regulator. GR belongs to the nuclear hormone receptor family of ligand-gated transcription factors that govern mammalian physiology. Upon ligand binding, GR enters the nucleus to regulate gene expression both positively and negatively. It is known to bind to consensus DNA sequences termed glucocorticoid response elements (GREs), but the mechanisms determining transcriptional activation versus repression remain an unresolved molecular paradox. Prevailing models suggest that tethering of GR to AP-1 or NF-κB via protein-protein interactions, rather than direct DNA binding, specifies negative regulation. However, here we show that the repression of inflammatory genes as well as all other glucocorticoid responses, require direct DNA binding of GR. Generating GR point mutant mice that retain the ability to tether via protein-protein interactions while unable to recognize DNA sequences, we demonstrate that response element recognition via the Zinc finger is absolutely required for both transcriptional activation and repression. We have used ChIP-Seq and RNA-Seq in inflammatory and metabolic cells and tissues together with proteomics to reveal that DNA binding of GR is necessary for the assembly of a functional SWI/SNF coregulator complex. Generally, the desired anti-inflammatory actions of GR are attributed to the silencing of inflammatory genes, while its adverse effects are believed to result from the transcriptional upregulation of metabolic targets. Our findings not only challenge classical models and dogmas of GR mediated gene regulation, but will provide an important basis for the development of novel immunosuppressants with reduced side effect profiles.

2020-07-07 | PXD013772 | Pride

Training-induced exosomal miR-136-3p modulates mitochondrial functions by targeting NRDC in human skeletal muscle.

Project description:Training-induced exosomal miR-136-3p modulates mitochondrial functions by targeting NRDC in human skeletal muscle.

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