The Effects of Sidt2 on the Inflammatory Pathway in Mouse Mesangial Cells.
Animals
CRISPR-Cas Systems
Cytokines
/ metabolism
Gene Expression Profiling
Gene Expression Regulation
Glomerular Filtration Rate
I-kappa B Kinase
/ metabolism
Inflammation
/ metabolism
Lentivirus
/ genetics
Lipopolysaccharides
/ metabolism
Lysosomes
/ metabolism
MAP Kinase Signaling System
Mesangial Cells
/ metabolism
Mice
Mice, Knockout
NF-KappaB Inhibitor alpha
/ metabolism
Nucleotide Transport Proteins
/ metabolism
Signal Transduction
Transcription Factor RelA
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
Journal
Mediators of inflammation
ISSN: 1466-1861
Titre abrégé: Mediators Inflamm
Pays: United States
ID NLM: 9209001
Informations de publication
Date de publication:
2020
2020
Historique:
received:
07
03
2020
accepted:
02
05
2020
entrez:
23
6
2020
pubmed:
23
6
2020
medline:
10
7
2021
Statut:
epublish
Résumé
In patients with chronic kidney disease, the abnormal activation of inflammatory pathways is usually an important factor leading to renal fibrosis and further deterioration of renal function. Finding effective intervention targets of the inflammatory signaling pathway is an important way to treat chronic kidney disease. As a newly discovered lysosomal membrane protein, the correlation between SID1 transmembrane family member 2 (Sidt2) and the inflammatory signaling pathway has not been reported. The aim of this study was to investigate the effect of Sidt2 on inflammation by inhibiting the expression of the
Identifiants
pubmed: 32565723
doi: 10.1155/2020/3560793
pmc: PMC7275211
doi:
Substances chimiques
Cytokines
0
Lipopolysaccharides
0
Nucleotide Transport Proteins
0
Rela protein, mouse
0
Sidt2 protein, mouse
0
Transcription Factor RelA
0
Tumor Necrosis Factor-alpha
0
NF-KappaB Inhibitor alpha
139874-52-5
I-kappa B Kinase
EC 2.7.11.10
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
3560793Informations de copyright
Copyright © 2020 Hui Sun et al.
Déclaration de conflit d'intérêts
The authors declare no conflicts of interest.
Références
J Biol Chem. 1979 Mar 10;254(5):1537-9
pubmed: 762154
Am J Cardiol. 2006 Jan 16;97(2A):20A-27A
pubmed: 16442933
Mol Cell Biochem. 2018 Aug;445(1-2):169-178
pubmed: 29368095
Immunol Rev. 2017 May;277(1):113-127
pubmed: 28462531
Circ J. 2011;75(12):2739-48
pubmed: 22067929
Contrib Nephrol. 2017;191:32-43
pubmed: 28910789
J Surg Res. 2012 Nov;178(1):339-45
pubmed: 22883438
Nat Immunol. 2017 Mar 22;18(4):374-384
pubmed: 28323260
Mol Cell Biol. 2019 Oct 11;39(21):
pubmed: 31427458
ACS Cent Sci. 2018 Aug 22;4(8):982-995
pubmed: 30159395
J Surg Res. 2012 May 15;174(2):326-33
pubmed: 21392794
Molecules. 2018 Dec 26;24(1):
pubmed: 30587838
Shock. 2010 Apr;33(4):436-41
pubmed: 19730166
Arterioscler Thromb Vasc Biol. 2019 Apr;39(4):719-730
pubmed: 30816805
Int Rev Cell Mol Biol. 2018;335:41-84
pubmed: 29305014
Nat Rev Immunol. 2017 Sep;17(9):545-558
pubmed: 28580957
J Biol Chem. 2008 Aug 1;283(31):21487-94
pubmed: 18541524
Immunol Rev. 2009 Mar;228(1):273-87
pubmed: 19290934
Autophagy. 2018;14(2):181-189
pubmed: 28738171
Sci Signal. 2011 Jul 05;4(180):ra44
pubmed: 21730326
Sci Signal. 2009 Jul 28;2(81):pe47
pubmed: 19638614
Front Physiol. 2017 Oct 24;8:829
pubmed: 29114233
Annu Rev Physiol. 2015;77:57-80
pubmed: 25668017
J Cell Physiol. 2017 Feb;232(2):381-390
pubmed: 27191060
Exp Ther Med. 2020 Mar;19(3):1997-2007
pubmed: 32104259
Cold Spring Harb Perspect Biol. 2009 Dec;1(6):a001651
pubmed: 20457564
Inflammation. 2018 Dec;41(6):2149-2159
pubmed: 30069662
Int Rev Immunol. 2015;34(5):415-31
pubmed: 25075736