Abstract: Provided are a method for fabricating a human nasal turbinate-derived mesenchymal stem cell-based 3D bioprinted construct, and a use thereof, wherein the human nasal turbinate-derived mesenchymal stem cell-based, 3D bioprinted construct is advantageous over conventional mesenchymal stem cell-based, 3D bioprinted constructs in that the former can survive and proliferate stably in vitro and/or in vivo and shows high osteogenic differentiation ability as well, therefore is expected to make a great contribution to the practical use of cellular therapeutic agents.

Abstract: The present disclosure provides a biomimetic cell culture apparatus that mimics interactions among organs in a human body. The present disclosure includes a plurality of culture units for culturing cells, a conduit for connecting the plurality of culture units to each other to form a circulating path, a pump unit disposed on the conduit for forming a flow in culture medium such that the culture medium circulates through the plurality of culture units, and an agitating module for agitating the plurality of culture units.

Abstract: The present disclosure provides a biomimetic cell culture apparatus that mimics interactions among organs in a human body. The present disclosure includes a plurality of culture units for culturing cells, a conduit for connecting the plurality of culture units to each other to form a circulating path, a pump unit disposed on the conduit for forming a flow in culture medium such that the culture medium circulates through the plurality of culture units, and an agitating module for agitating the plurality of culture units.

Abstract: The present invention relates to a cell culture container comprisng: an outer container of which an upper surface is open and into which a culture solution can be put; a container cover coupled to the upper end of the outer container to prevent the penetration of microorganisms; and an inner container which is placed inside the outer container, can put a culture solution, and can be separated from the outer container. The present invention relates to a cultivation culture system comprising: a plurality of the cell culture containers; circulation pipes for connecting each of the adjacent cell culture containers so as to allow the plurality of the cell culture containers to be interconnected and connecting a pair of the cell culture containers placed at both ends; and a circulation portion for supplying a culture solution and gas to a cell culture portion so as to circulate the same.

Abstract: The present invention relates to the E2EPF UCP-VHL interaction and the uses thereof, more precisely a method for increasing or reducing VHL activity or level by regulating UCP activity or level to inhibit cancer cell proliferation or metastasis or to increase angiogenesis. The inhibition of UCP activity is accomplished by any UCP activity inhibitor selected from a group consisting of a small interfering RNA (RNAi), an antisense oligonucleotide, and a polynucleotide complementarily binding to mRNA of UCP, a peptide, a peptide mimetics and an antibody, and a low molecular compound. In the meantime, the increase of angiogenesis is accomplished by the following mechanism; UCP over-expression is induced by a gene carrier and thus endogenous VHL is reduced, leading to the stabilization of HIF-1? which enhances VEGF activation based on the HIF-1? stabilization.

Abstract: The present invention relates to the E2EPF UCP-VHL interaction and the uses thereof, more precisely a method for increasing or reducing VHL activity or level by regulating UCP activity or level to inhibit cancer cell proliferation or metastasis or to increase angiogenesis. The inhibition of UCP activity is accomplished by any UCP activity inhibitor selected from a group consisting of a small interfering RNA (RNAi), an antisense oligonucleotide, and a polynucleotide complementarily binding to mRNA of UCP, a peptide, a peptide mimetics and an antibody, and a low molecular compound. In the meantime, the increase of angiogenesis is accomplished by the following mechanism; UCP over-expression is induced by a gene carrier and thus endogenous VHL is reduced, leading to the stabilization of HIF-1? which enhances VEGF activation based on the HIF-1? stabilization.

Abstract: The present invention relates to the E2EPF UCP-VHL interaction and the uses thereof, more precisely a method for increasing or reducing VHL activity or level by regulating UCP activity or level to inhibit cancer cell proliferation or metastasis or to increase angiogenesis. The inhibition of UCP activity is accomplished by any UCP activity inhibitor selected from a group consisting of a small interfering RNA (RNAi), an antisense oligonucleotide, and a polynucleotide complementarily binding to mRNA of UCP, a peptide, a peptide mimetics and an antibody, and a low molecular compound. In the meantime, the increase of angiogenesis is accomplished by the following mechanism; UCP over-expression is induced by a gene carrier and thus endogenous VHL is reduced, leading to the stabilization of HIF-1? which enhances VEGF activation based on the HIF-1? stabilization.

Abstract: The present invention relates to Enigma (PDLIM7)-Mdm2 interaction and use thereof. More particularly, it may induce an effective apoptosis of cancer cells by inhibition of an Enigma expression or an Enigma activity which induces Mdm2 destabilization and p53 activity; it may assess the prognosis of anti-cancer therapy by determining that Enigma, which is induced by SRF, is overexpressed in cancer tissues with Mdm2; it may screen anti-cancer activity substances by selecting a factor to inhibit specific binding between Enigma and Mdm2. Enigma-Mdm2 interaction and Enigma expression regulation may be utilized usefully for preventing cancers and developing therapeutic methods and anti-cancer agents.

Abstract: The present invention relates to Enigma (PDLIM7)-Mdm2 interaction and use thereof. More particularly, it may induce an effective apoptosis of cancer cells by inhibition of an Enigma expression or an Enigma activity which induces Mdm2 destabilization and p53 activity; it may assess the prognosis of anti-cancer therapy by determining that Enigma, which is induced by SRF, is overexpressed in cancer tissues with Mdm2; it may screen anti-cancer activity substances by selecting a factor to inhibit specific binding between Enigma and Mdm2. Enigma-Mdm2 interaction and Enigma expression regulation may be utilized usefully for preventing cancers and developing therapeutic methods and anti-cancer agents.

Abstract: The present invention relates to Enigma (PDLIM7)-Mdm2 interaction and use thereof. More particularly, it may induce an effective apoptosis of cancer cells by inhibition of an Enigma expression or an Enigma activity which induces Mdm2 destabilization and p53 activity; it may assess the prognosis of anti-cancer therapy by determining that Enigma, which is induced by SRF, is overexpressed in cancer tissues with Mdm2; it may screen anti-cancer activity substances by to selecting a factor to inhibit specific binding between Enigma and Mdm2. Enigma-Mdm2 interaction and Enigma expression regulation may be utilized usefully for preventing cancers and developing therapeutic methods and anti-cancer agents.

Abstract: The present invention relates to Enigma (PDLIM7)-Mdm2 interaction and use thereof. More particularly, it may induce an effective apoptosis of cancer cells by inhibition of an Enigma expression or an Enigma activity which induces Mdm2 destabilization and p53 activity; it may assess the prognosis of anti-cancer therapy by determining that Enigma, which is induced by SRF, is overexpressed in cancer tissues with Mdm2; it may screen anti-cancer activity substances by to selecting a factor to inhibit specific binding between Enigma and Mdm2. Enigma-Mdm2 interaction and Enigma expression regulation may be utilized usefully for preventing cancers and developing therapeutic methods and anti-cancer agents.