{"database":"ENA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Pharmacology, Department of Pharmacology, Shandong University"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA430704"],"scientific_name":["Mus musculus"],"long_description":["Although there is significant progress in understanding the structure and function of NLRC5, a member of the NOD like receptor (NLR) family, in the context of MHC class I gene expression, the functions of NLRC5 in innate and adaptive immune responses beyond the regulation of MHC class I genes remain controversial and unresolved. In particular, the role of NLRC5 in the kidney keeps unknown. In this study, we found that NLRC5 was significantly upregulated in the kidney from mice with renal ischemia/reperfusion injury (IRI). NLRC5 deficient (NLRC5-/-) mice significantly ameliorated renal injury as evidenced by decreased serum creatinine levels, improved morphological injuries, and reduced inflammatory responses versus wild type mice. Similar protective effects were also observed in cisplatin-induced acute kidney injury (AKI). Mechanistically, NLRC5 contributed to renal injury by promoting tubular epithelial cell apoptosis and reducing inflammatory responses which is associated with, at least in part, the negative regulation of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1). To determine the relative contribution of NLRC5 expression by parenchymal cells or leukocytes to renal damage during IRI, we generated bone marrow (BM) chimeric mice. NLRC5-/- mice engrafted with WT hematopoietic cells had significantly lower serum creatinine and less tubular damage than WT mice reconstituted with NLRC5-/- BM, suggesting that NLRC5 signaling in renal parenchymal cells plays the dominant role in mediating renal damage. Collectively, modulation of NLRC5-mediated pathway may have important therapeutic implications for patients with AKI. Overall design: NLRC5-/- mice and age-matched C57BL/6 wild type (WT) mice were used in this study, We established a bilateral renal ischemia model for 30min and mice were sacrificed after reperfusion at 48h."],"repository":["ENA"],"description_synonyms":["mmCGM1a, 3.4.22.-, CD66a Antigen, Laboratory, Acute renal failure, Mus domesticus, Renal Insufficiency, mini-ICE, CASP-14, protein, Cell-CAM 105, House Mouse, Renal Failures, MHVR1, Renal Injury, C CAM1, House, Acute Renal Insufficiencies, Antigen, Mus musculus domesticus, Biliary Glycoprotein A, Kidney Injuries, ARF, Biliary Glycoprotein I, acute kidney injury, Mice, A, AK220210, Acute Kidney Insufficiency, Acute Renal Insufficiency, Kidney Insufficiencies, C-CAM1, Acute Kidney Insufficiencies, kidney failure, I, Swiss, Acute Kidney Injuries, Kidney Insufficiency, acute renal failure, CellCAM, Swiss Mice, Cell CAM 105, NOD27, AKI, Nonspecific Cross Reacting Antigen 160, Acute Renal Injury, Carcinoembryonic Antigen Related Cell Adhesion Molecule 1, Acute Renal Failure, CellCAM 105, Acute kidney failure, Acute Renal Injuries, Biliary, CD66a, Hv-2, single organism signaling., AI451557, Renal Injuries, Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1, Renal Failure, CASP14, mouse, Mhv-1, mmCGM2, mmCGM1, Glycoprotein A, CEA-Related Cell Adhesion Molecule 1, Mus, BGP, Bgp, Glycoprotein I, Mini-ICE, Protein, Cc1, CEACAM1, MHVR, CLR16.1, Acute Kidney Failures, Acute Renal Failures, mCEA1, acute, Mus musculus, Hv2, Caspase-14 subunit p10, bb-1, Kidney Failures, Kidney Failure, mice, Kidney Injury, Swiss Mouse, NOD4, House Mice, Caspase-14 subunit p19, Cea-7, CEA Related Cell Adhesion Molecule 1, MICE, Cea-1, C-CAM protein, Laboratory Mice, domesticus, C-CAM, BGPI, Acute Kidney Failure, Acute, Cea7, Nonspecific Cross-Reacting Antigen 160, signalling process, Cea1, Cell-CAM, Mouse, 105, Biliary Glycoprotein, BGP1, Bgp1, Renal Insufficiencies, C CAM protein, Laboratory Mouse"],"name_synonyms":["mmCGM1a, 3.4.22.-, CD66a Antigen, Laboratory, Acute renal failure, Mus domesticus, Renal Insufficiency, mini-ICE, CASP-14, protein, Cell-CAM 105, House Mouse, Renal Failures, MHVR1, Renal Injury, C CAM1, House, Acute Renal Insufficiencies, Antigen, Mus musculus domesticus, Biliary Glycoprotein A, Kidney Injuries, ARF, Biliary Glycoprotein I, acute kidney injury, Mice, A, AK220210, Acute Kidney Insufficiency, Acute Renal Insufficiency, Kidney Insufficiencies, C-CAM1, Acute Kidney Insufficiencies, kidney failure, I, Swiss, Acute Kidney Injuries, Kidney Insufficiency, acute renal failure, CellCAM, Swiss Mice, Cell CAM 105, NOD27, AKI, Nonspecific Cross Reacting Antigen 160, Acute Renal Injury, Carcinoembryonic Antigen Related Cell Adhesion Molecule 1, Acute Renal Failure, CellCAM 105, Acute kidney failure, Acute Renal Injuries, Biliary, CD66a, Hv-2, single organism signaling., AI451557, Renal Injuries, Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1, Renal Failure, CASP14, mouse, Mhv-1, mmCGM2, mmCGM1, Glycoprotein A, CEA-Related Cell Adhesion Molecule 1, Mus, BGP, Bgp, Glycoprotein I, Mini-ICE, Protein, Cc1, CEACAM1, MHVR, CLR16.1, Acute Kidney Failures, Acute Renal Failures, mCEA1, acute, Mus musculus, Hv2, Caspase-14 subunit p10, bb-1, Kidney Failures, Kidney Failure, mice, Kidney Injury, Swiss Mouse, NOD4, House Mice, Caspase-14 subunit p19, Cea-7, CEA Related Cell Adhesion Molecule 1, MICE, Cea-1, C-CAM protein, Laboratory Mice, domesticus, C-CAM, BGPI, Acute Kidney Failure, Acute, Cea7, Nonspecific Cross-Reacting Antigen 160, signalling process, Cea1, Cell-CAM, Mouse, 105, Biliary Glycoprotein, BGP1, Bgp1, Renal Insufficiencies, C CAM protein, Laboratory Mouse"],"additional_accession":[]},"is_claimable":false,"name":"NLRC5 deficiency protects against acute kidney injury in mice by mediating CEACAM1 signaling","description":"NLRC5 deficiency protects against acute kidney injury in mice by mediating CEACAM1 signaling","dates":{"last_updated":"2025-09-24","first_public":"2018-03-01"},"accession":"PRJNA430704","cross_references":{"GEO":["GSE109374"],"taxon":["10090"]}}