ArticleExperimental cell research2012
Carbonic anhydrase III regulates peroxisome proliferator-activated receptor-γ2.
Article in Experimental cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- Osteoblast-derived CAR3 synergizing with collagen and bone sialoprotein enhances bone formation.International journal of oral science · 2026Article
- Fragment-Derived Nicotinic Acid Analogues Inhibit hCA III and DownregulateBiomolecules · 2026Article
- Preliminary Study on Polymerization between Hemoglobin and Enzymes during the Preparation of PolyHb-SOD-CAT-CA.Doklady. Biochemistry and biophysics · 2024Article
- Enzyme Inhibitors as Multifaceted Tools in Medicine and Agriculture.Molecules (Basel, Switzerland) · 2024Review
- Carbonic Anhydrase 3 is required for cardiac repair post myocardial infarction via Smad7-Smad2/3 signaling pathway.International journal of biological sciences · 2024Article
- Carbonic anhydrases III and IX are new players in the crosstalk between adrenocortical carcinoma and its altered adipose microenvironment.Journal of endocrinological investigation · 2023Article
- Protein Targets of Acetaminophen Covalent Binding in Rat and Mouse Liver Studied by LC-MS/MS.Frontiers in chemistry · 2021Article
- Synthesis and evaluation of 2,4,5-trisubstitutedthiazoles as carbonic anhydrase-III inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Deletion of metal transporter Zip14 (Slc39a14) produces skeletal muscle wasting, endotoxemia, Mef2c activation and induction of miR-675 and Hspb7.Scientific reports · 2020Article
- Transgenic expression of carbonic anhydrase III in cardiac muscle demonstrates a mechanism to tolerate acidosis.American journal of physiology. Cell physiology · 2019Article
- Carbonic anhydrase III protects osteocytes from oxidative stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- COAmerican journal of respiratory cell and molecular biology · 2017Article
- Anti-Atherosclerotic Action of Agmatine in ApoE-Knockout Mice.International journal of molecular sciences · 2017Article
- Article
- Hepatic proteomic analysis revealed altered metabolic pathways in insulin resistant Akt1(+/-)/Akt2(-/-) mice.Metabolism: clinical and experimental · 2015Article
- Probing the surface of human carbonic anhydrase for clues towards the design of isoform specific inhibitors.BioMed research international · 2015Review
- Multilayered genetic and omics dissection of mitochondrial activity in a mouse reference population.Cell · 2014Article
- Proteomics of genetically engineered mouse mammary tumors identifies fatty acid metabolism members as potential predictive markers for cisplatin resistance.Molecular & cellular proteomics : MCP · 2013Article
- Specificity and heterogeneity of terahertz radiation effect on gene expression in mouse mesenchymal stem cells.Scientific reports · 2013Article
- Carbonic anhydrases III and IV autoantibodies in rheumatoid arthritis, systemic lupus erythematosus, diabetes, hypertensive renal disease, and heart failure.Clinical & developmental immunology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Carbonic anhydrase III (CAIII) is an isoenzyme of the CA family. Because of its low specific anhydrase activity, physiological functions in addition to hydrating CO(2) have been proposed. CAIII expression is highly induced in adipogenesis and CAIII is the most abundant protein in adipose tissues. The function of CAIII in both preadipocytes and adipocytes is however unknown. In the present study we demonstrate that adipogenesis is greatly increased in mouse embryonic fibroblasts (MEFs) from CAIII knockout (KO) mice, as demonstrated by a greater than 10-fold increase in the induction of fatty acid-binding protein-4 (FABP4) and increased triglyceride formation in CAIII(-/-) MEFs compared with CAIII(+/+) cells. To address the underlying mechanism, we investigated the expression of the two adipogenic key regulators, peroxisome proliferator-activated receptor-γ2 (PPARγ2) and CCAAT/enhancer binding protein-α. We found a considerable (approximately 1000-fold) increase in the PPARγ2 expression in the CAIII(-/-) MEFs. Furthermore, RNAi-mediated knockdown of endogenous CAIII in NIH 3T3-L1 preadipocytes resulted in a significant increase in the induction of PPARγ2 and FABP4. When both CAIII and PPARγ2 were knocked down, FABP4 was not induced. We conclude that down-regulation of CAIII in preadipocytes enhances adipogenesis and that CAIII is a regulator of adipogenic differentiation which acts at the level of PPARγ2 gene expression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.