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RISS 인기검색어
- 검색키워드
- 저자 : Irwin H. Gelman (검색결과 2 건)
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Role of A-Kinase Anchoring Protein 12 in the Central Nervous System
Shintaro Kimura,Josephine Lok,Irwin H. Gelman,Eng H. Lo,Ken Arai 대한신경과학회 2023 Journal of Clinical Neurology Vol.19 No.4
A-kinase anchoring protein (AKAP) 12 is a scaffolding protein that anchors various signaling proteins to the plasma membrane. These signaling proteins include protein kinase A, protein kinase C, protein phosphatase 2B, Src-family kinases, cyclins, and calmodulin, which regulate their respective signaling pathways. AKAP12 expression is observed in the neurons, astrocytes, endothelial cells, pericytes, and oligodendrocytes of the central nervous system (CNS). Its physiological roles include promoting the development of the blood–brain barrier, maintaining white-matter homeostasis, and even regulating complex cognitive functions such as long-term memory formation. Under pathological conditions, dysregulation of AKAP12 expression levels may be involved in the pathology of neurological diseases such as ischemic brain injury and Alzheimer’s disease. This minireview aimed to summarize the current literature on the role of AKAP12 in the CNS.
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Lee, Hye Shin,Choi, Jinhyeok,Son, Taekwon,Lee, Eun Ji,Kim, Jeong-Gyun,Ryu, Soo Hyung,Lee, Danbi,Jang, Myoung Kuk,Yu, Eunsil,Chung, Young-Hwa,Gelman, Irwin H.,Kim, Kyu-Won D.A. Spandidos 2018 Oncology letters Vol.16 No.5
<P>AKAP12 belongs to A-kinase anchoring protein (AKAP) family of scaffold proteins and is known as a tumor suppressor in several human cancer types. Its role as a tumor suppressor in hepatocellular carcinoma (HCC) was proposed due to its downregulation and epigenetic modification in human HCC; however, the effect of its deficiency on liver injuries, such as liver fibrosis and cancer has been poorly studied. By analyzing tumor and non-tumor tissues of 15 patients with HCC, it was confirmed that AKAP12 expression was downregulated in human HCC as compared with adjacent non-tumor tissues. Immunohistochemical staining of mouse liver tissue for AKAP12 revealed that its sinusoidal expression was diminished in capillarized endothelium after 8 weeks of thioacetamide (TAA) administration. AKAP12 deficiency resulted in the promotion of ductular response of biliary epithelial cells, whereas overall fibrosis and myofibroblast activation were comparable between genotypes after short-term TAA treatment. The mRNA expressions of some fibrosis-related genes such as those encoding epithelial cell adhesion molecule, collagen type 1 α1 and elastin were upregulated in liver tissues of AKAP12-knockout mice. Long-term administration of TAA for 26 weeks led to the development of liver tumors; the incidence of tumor development was higher in AKAP12-deficient mice than in wild-type littermates. Together, these results suggest that AKAP12 functions as a tumor suppressor in liver cancer and is associated with the regulation of hepatic non-parenchymal cells.</P>
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