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AKAP12 Overexpression Affects Cardiac Function via PDE8.
Circ Res
April 2024
Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, Germany (H.S., V.O.N.).
AKAP12 Upregulation Associates With PDE8A to Accelerate Cardiac Dysfunction.
Circ Res
April 2024
Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy (H.Q., M.R., Y.X., A.R.-A., H.Y.A., B.K.M.), University of Houston, TX.
Background: In heart failure, signaling downstream the β2-adrenergic receptor is critical. Sympathetic stimulation of β2-adrenergic receptor alters cAMP (cyclic adenosine 3',5'-monophosphate) and triggers PKA (protein kinase A)-dependent phosphorylation of proteins that regulate cardiac function. cAMP levels are regulated in part by PDEs (phosphodiesterases).
View Article and Find Full Text PDFMethyl protodioscin reduces c-Myc to ameliorate diabetes mellitus erectile dysfunction via downregulation of AKAP12.
Diabetes Res Clin Pract
December 2023
Hunan Engineering Research Center of Internet-Chinese and Western Medicine Collaboration-Health Service, Hunan University of Medicine, Huaihua 418000, Hunan Province, PR China; Department of Rehabilitation Medicine and Health Care, Hunan University of Medicine, Huaihua 418000, Hunan Province, PR China; College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha 410208, Hunan Province, PR China. Electronic address:
Article Synopsis
- Diabetes mellitus erectile dysfunction (DMED) is a common complication of diabetes, and the study aimed to evaluate the effectiveness of methyl protodioscin (MPD) as a treatment.
- In experiments with diabetic mice and vascular cells exposed to high glucose, MPD was found to enhance cell viability, reduce apoptosis, and alter key protein levels related to erectile function.
- The findings suggest that MPD improves erectile dysfunction in diabetic mice by regulating the interaction between c-Myc and AKAP12, indicating its potential as a natural remedy for DMED.
AKAP12 inhibits esophageal squamous carcinoma cell proliferation, migration, and cell cycle via the PI3K/AKT signaling pathway.
Mol Cell Probes
December 2023
Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Nantong University, The First People's Hospital of Nantong, 226001, Nantong, China. Electronic address:
Esophageal squamous cell carcinoma (ESCC) consistently ranks as one of the most challenging variants of squamous cell carcinomas, primarily due to the lack of effective early detection strategies. We herein aimed to elucidate the underlying mechanisms and biological role associated with A-kinase anchoring protein 12 (AKAP12) in the context of ESCC. Bioinformatic analysis had revealed significantly lower expression level of AKAP12 in ESCC tissue samples than in their non-cancerous counterparts.
View Article and Find Full Text PDFAKAP12 promotes cancer stem cell-like phenotypes and activates STAT3 in colorectal cancer.
Clin Transl Oncol
November 2023
Department of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, People's Republic of China.
Background: Cancer stem cells (CSCs) have unique biological characteristics, including tumorigenicity, immortality, and chemoresistance. Colorectal CSCs have been identified and isolated from colorectal cancers by various methods. AKAP12, a scaffolding protein, is considered to act as a potential suppressor in colorectal cancer, but its role in CSCs remains unknown.
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