• Title, Summary, Keyword: AKAP12

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Akap12beta supports asymmetric heart development via modulating the Kupffer's vesicle formation in zebrafish

  • Kim, Jeong-gyun;Kim, Hyun-Ho;Bae, Sung-Jin
    • BMB Reports
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    • v.52 no.8
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    • pp.526-531
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    • 2019
  • The vertebrate body plan is accomplished by left-right asymmetric organ development and the heart is a representative asymmetric internal organ which jogs to the left-side. Kupffer's vesicle (KV) is a spherical left-right organizer during zebrafish embryogenesis and is derived from a cluster of dorsal forerunner cells (DFCs). Cadherin1 is required for collective migration of a DFC cluster and failure of DFC collective migration by Cadherin1 decrement causes KV malformation which results in defective heart laterality. Recently, loss of function mutation of A-kinase anchoring protein 12 (AKAP12) is reported as a high-risk gene in congenital heart disease patients. In this study, we demonstrated the role of $akap12{\beta}$ in asymmetric heart development. The $akap12{\beta}$, one of the akap12 isoforms, was expressed in DFCs which give rise to KV and $akap12{\beta}$-deficient zebrafish embryos showed defective heart laterality due to the fragmentation of DFC clusters which resulted in KV malformation. DFC-specific loss of $akap12{\beta}$ also led to defective heart laterality as a consequence of the failure of collective migration by cadherin1 reduction. Exogenous $akap12{\beta}$ mRNA not only restored the defective heart laterality but also increased cadherin1 expression in $akap12{\beta}$ morphant zebrafish embryos. Taken together, these findings provide the first experimental evidence that $akap12{\beta}$ regulates heart laterality via cadherin1.

Lack of Relation of AKAP12 with p53 and Bcl-2 in Colorectal Carcinoma

  • Suren, Dinc;Yildirim, Mustafa;Alikanoglu, Arsenal Sezgin;Kaya, Vildan;Yildiz, Mustafa;Dilli, Utku Donem;Sezer, Cem
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.8
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    • pp.3415-3418
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    • 2014
  • Background: AKAP12 inhibits oncogenic proliferation, invasion, chemotaxis and neovascularization. Bcl-2 and p53 are two important apoptotic markers that play roles in apoptotic processes. It has been found that AKAP12 blocks the cell cycle and induces apoptosis in fibrosarcoma cells. In our study we assessed the relationship of AKAP12 with apoptotic markers, Bcl-2 and p53. Materials and Methods: Our study included 45 cases that were histopathologically diagnosed with colorectal carcinoma from the tissue samples acquired by surgical resection. AKAP 12, Bcl-2, and p53 expression was examined by immunohistochemistry. Results: A total of 45 colorectal adenocarcinoma patients - 17 (37.8%) females and 28 (62.2%) males - were included in this study. AKAP12 expression was found to be negative in 8 patients (17.8%), and positive in 37 patients (82.2%). Bcl-2 was found positive in 6 patients (13.3%) and p53 in 29 patients (55.6%). AKAP12 expression had no significant relation with Bcl-2 and p53 expression (p:0.939, p:0.079, respectively). Conclusions: Although various studies have pointed to apoptotic activity of AKAP12, the literature is limited regarding relations with p53 or Bcl-2 expression. In the present study, we found no relation in colorectal carcinomas.