• Molecules and Cells
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• 제37권4호
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• pp.314-321
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• 2014

CDK2 is a key regulator of cell cycle progression. In this study, we screened for miRNAs targeting CDK2 using a luciferase-3'-untranslated region reporter assay. Among 11 hit miRNAs, miR-509-3p reduced CDK2 protein levels and significantly inhibited cancer cell growth. Microarray, Western blotting, and luciferase reporter analyses revealed additional targets of miR-509-3p, including Rac1 and PIK3C2A. Overexpression of miR-509-3p induced G1 cell-cycle arrest and inhibited colony formation and migration. RNAi experiments indicated that the growth-inhibitory effects of miR-509-3p may occur through down-regulation of CDK2, Rac1, and PIK3C2A. Targeting of multiple growth regulatory genes by miR-509-3p may contribute to effective anti-cancer therapy.

• 한국산림과학회지
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• 제103권2호
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• pp.182-188
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• 2014

ISSR 표지를 이용하여 전나무 6개 집단의 유전다양성과 유전구조를 분석하였다. 6개 ISSR primer로 유전다양성을 추정한 결과, 집단별 다형성 유전자좌의 비율은 평균 85.6%, 이형접합도 기대치($H_e$)는 0.288로 나타났다. AMOVA 결과, 전체 유전변이에서 5.6%는 집단간, 94.4%는 집단내 개체간 차이에 기인하는 것으로 나타났다. 베이즈 추론에 근거한 유전분화는 ${\theta}^{II}$와 $G_{ST}$가 각각 0.045, 0.038로, 근연교배 정도는 0.509로 추정되었다. Mental 검증에서 집단간 지리적 거리가 멀수록 유전적으로 상이한 것으로 판명되었다(r = 0.74, P < 0.05). UPGMA 방법과 PCA 결과에 따라서 남원, 청도, 문경 집단을 한 군집으로, 인제, 홍천, 평창 집단을 다른 군집으로 나눌 수 있었다. 베이즈 군집분석에서는 유전변이 분포에 따라서 남원, 문경 집단이 한 군집으로 인제, 홍천, 평창, 청도 집단이 다른 한 군집으로 묶여서 2개의 상위 군집으로 나뉘었다. 빈도주의 분석에 따른 '군집'을 반영한 AMOVA 결과에서 전체 유전변이의 3.9%를 군집의 영향으로 설명할 수 있었으며, 전나무 집단의 지리적 분포는 베이즈 분석보다는 UPGMA 방법에 의한 구분과 일치하는 것으로 나타났다.

• Biomolecules & Therapeutics
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• 제32권5호
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• pp.509-522
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• 2024

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.