Celastrol targets adenylyl cyclase-associated protein 1 to reduce macrophages-mediated inflammation and ameliorates high fat diet-induced metabolic syndrome in mice

Metabolic syndrome is a clustering of metabolic disorder with unclear molecular mechanism. Increasing studies have found that the pathogenesis and progression of metabolic syndrome are closely related to inflammation. Here, we report celastrol, a traditional Chinese medicine, can improve high fat diet-induced metabolic syndrome through suppressing resistin-induced inflammation. Mechanistically, celastrol binds to adenylyl cyclase associated protein 1 (CAP1) and inhibits the interaction between CAP1 and resistin, which restrains the cyclic adenylate monophosphate (cAMP)-protein kinase A (PKA)-nuclear factor kappa-B (NF-

The eukaryotic expression,intracellular location and functions of human CAP1 / 西安交通大学学报(医学版)

Objective To construct the recombinant eukaryotic expression plasmids of human adenylyl cyclase-associated protein 1 (CAP1)and to explore its intracellular location and functions.Methods By using Hela cDNA as the template,the cDNAs encoding CAP1 was amplified by PCR and inserted into pCMV-Myc vector to construct the recombinant plasmid.The recombinant plasmid was transfected into 293 cells using lipofectamine 2000.The protein expression and the intracellular location of the inserted gene were confirmed by Western blotting and immunofluorescence,respectively.Scratch-repair experiment was used to detect the cancer cells’ migration ability.Results The recombinant eukaryotic expression plasmid of human CAP1 was successfully constructed and transfected into eukaryote cells.The recombinant plasmid was successfully expressed in eukaryote cells.CAP1 was located in the cytoplasm.The results of scratch-repair experiment showed that the overexpression of CAP1 could significantly inhibit the cells’ migration.Conclusion CAP1 recombinant plasmid was successfully expressed in eukaryotic cells.CAP1 protein was located in the cytoplasm.The overexpression of CAP1 inhibited cell migration. The present study provides important experimental evidence for further study on CAP1.

Candida albicans transcription factor Cap1p: An update / 第二军医大学学报

Cap1p, encoded by CAP1, is a basic region-teucine zipper (bZip) transcription factor in Candida albicans. It has been proven to play important roles in both drug resistance and oxidative stress. Within the AP-1 family, Caplp belongs to the same subgroup which also includes Yap1p, Yap2p, and Pap1p. The function of Cap1p is regulated by a nuclear localization mechanism. In recent years, some target genes of CapIp have been discovered and the differences as well as similarities between Cap1p and Yap1p have been revealed. However, the role of Caplp in the drug resistance of Candida albicans still needs to be further investigated. Currently drug resistance and oxidative stress are the 2 focuses in the research of fungal pathogens, making Cap1p very important in the future study. The authors have been involved in Cap1p research for a long time and this review introduces the current progress in the area.

Candida albicans transcription factor Cap1p: an update / 第二军医大学学报

Cap1p, encoded by CAP1, is a basic region-leucine zipper (bZip) transcription factor in Candida albicans. It has been proven to play important roles in both drug resistance and oxidative stress. Within the AP-1 family, Cap1p belongs to the same subgroup which also includes Yap1p, Yap2p, and Pap1p. The function of Cap1p is regulated by a nuclear localization mechanism. In recent years, some target genes of Cap1p have been discovered and the differences as well as similarities between Cap1p and Yap1p have been revealed. However, the role of Cap1p in the drug resistance of Candida albicans still needs to be further investigated. Currently drug resistance and oxidative stress are the 2 focuses in the research of fungal pathogens, making Cap1p very important in the future study. The authors have been involved in Cap1p research for a long time and this review introduces the current progress in the area.