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[A. Biochemistry/Molecular Biology] A-46



                     The Function of Nuclear Protein 1 in adipogenesis




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        Tatiana Patricia Mendes Duarte¹,²,³ , Tae-Hyun Kim¹,³ , Bo Kyung Yoon¹,²,³, Yoseob Lee¹,²,³, Nahee
                   Hwang¹,²,³, Kyu-Hye Chun¹,²,³, Jae-Won Kim¹,²,³, Mi-Young Kim¹,³, Jae-Woo Kim¹,²,³*

         ¹Biochemistry and Molecular Biology, Yonsei University college of medicine, Seoul 03722, Korea, ²Brain Korea 21

         PLUS Project for medical science, Yonsei University college of medicine, Seoul 03722, Korea, ³Chronic Intractable
             Disease for Systems Medicine Research Center, Yonsei University college of medicine, Seoul 03722, Korea





        Studying the  biological networks controlling adipogenesis may  facilitate  greater understanding of the
        pathophysiology of obesity. This study shows that Nuclear protein 1 is present in the white adipose tissue and
        increases its expression levels during adipogenesis. Nuclear protein 1 has been extensively studied in cancer, however,

        its role in metabolism and adipogenesis still has to be greatly explored. In early stage of adipogenesis, when Nuclear
        protein 1 is knocked down in 3T3-L1 cells, adipogenesis is shown to be impaired with Chop increase at day 0, which

        might constitute a cause for the adipogenesis impairment due to C/EBPβ activity inhibition. In addition, adipogenesis
        showed to become impaired and, cell death was also induced in treatment of Nuclear protein 1 inhibitor, ZZW-115.

        ZZW-115 treated cells showed to have mitochondria superoxide increased presence in relation to the control, and
        it was correlated with apoptosis, evidenced by pro-apoptotic BAX and PUMA increased expression in these cells.

        Similar results were verified when Nuclear protein 1 was knocked down at 2 days after induction of differentiation.
        Taken together, our study demonstrated that Nuclear protein 1 might have a role in protecting 3T3-L1 cells from

        Chop expression in early adipogenesis and ROS excessive production in late adipogenesis.
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