mouse renal tubular epithelial tcmk 1 cells (ATCC)
ATCC is a verified supplier 
ATCC manufactures this product 
96
Structured Review
ATCC
mouse renal tubular epithelial tcmk 1 cells
Mouse Renal Tubular Epithelial Tcmk 1 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 208 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+renal+tubular+epithelial+tcmk+1+cells/TCMK-1/pm41218270-62-0-10
Average 96 stars, based on 208 article reviews
Mouse Renal Tubular Epithelial Tcmk 1 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 208 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+renal+tubular+epithelial+tcmk+1+cells/TCMK-1/pm41218270-62-0-10
Average 96 stars, based on 208 article reviews
mouse renal tubular epithelial tcmk 1 cells - by Bioz Stars,
2026-09
96/100 stars
Images
Related Articles
other:Article Title: Complement 3 activates the renal renin-angiotensin system by induction of epithelial-to-mesenchymal transition of the nephrotubulus in mice. Article Snippet: Xueli Zhou, Noboru Fukuda, Hiroyuki Matsuda, Morito Endo, Xiaofei Wang, Kosuke Saito, Takahiro Ueno, Taro Matsumoto, Koichi Matsumoto, Masayoshi Soma, Naohiko Kobayashi, and Akira Nishiyama Division of Nephrology, Hypertension, and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan; Advanced Research Institute of the Sciences and Humanities, Nihon University, Tokyo, Japan; Department of General Medicine, Nihon University School of Medicine, Tokyo, Japan; Faculty of Human Health Science, Hachinohe University, Hachinohe, Aomori, Japan; Division of Cell Regeneration and Transplantation, Department of Advanced Medicine, Nihon University School of Medicine, Tokyo, Japan; Department of Cardiovascular Medicine, Dokkyo Medical University, Tochigi, Japan; and Department of Pharmacology, Kagawa University School of Medicine, Takamatsu, Kagawa, Japan Article Title: Sodium fluoride induces nephrotoxicity via oxidative stress-regulated mitochondrial SIRT3 signaling pathway Article Snippet: Article Title: Mo 2 C nanozyme targets citrate synthase to treat acute kidney injury through alleviating oxidative stress and dysfunction of energy metabolism. Article Snippet: Acute kidney injury (AKI), characterized by rapid renal dysfunction, lacks effective therapies due to its complex pathophysiology involving oxidative stress and mitochondrial damage.. Molybdenum carbide (Mo2C) nanozymes show promise through their tunable catalytic properties and reactive oxygen species (ROS)-scavenging capacity.. To elucidate the metabolic basis of their therapeutic effects, we employed metabolomics analysis for molecularlevel metabolic profiling, combined with evaluation in lipopolysaccharide (LPS)-, cisplatin (CP)-, and ischemiareperfusion injury (IRI)-induced AKI models and TCMK-1 cell validation. Cell Culture:Article Title: NOX4 mediates the renoprotection of remote ischemic preconditioning against acute kidney injury by inhibiting NF-κB signaling and tubular apoptosis. Article Snippet: Acute kidney injury (AKI) is a clinical syndrome characterized by an abrupt loss of kidney function and is associated with increased morbidity and mortality.. Remote ischemic preconditioning (rIPC) is a nonpharmacological intervention involving brief episodes of ischemia in distal tissues, which may provide protection from kidney injury, but its underlying mechanism remain elusive.. In a previous study, we demonstrated that NOX4 can serve as a potential therapeutic target in AKI and is associated with the upregulation of inflammation and apoptosis. |