Abstract: There is provided a cooperative driving control method based on a vehicle security status. The cooperative driving method according to an embodiment includes: identifying a security status of a cooperative driving target vehicle; determining a cooperative driving strategy according to the identified security status; and controlling driving according to the determined cooperative driving strategy. Accordingly, cooperative driving may be performed or excluded based on a security status of a target vehicle, so that an accident may be prevented from being caused by cooperative driving with a problematic vehicle, and safety of a driver and an occupant may be guaranteed.

Abstract: The present invention provides a method of manufacturing an animal model of non-alcoholic liver disease by using correlation among metabolic dysregulations through AKT regulation by Hippo signaling, and an animal model prepared by the method above, and a screening method of a therapeutic agent by using the animal model.

Abstract: A method of controlling a vehicle to redundantly protect a driver, includes determining whether the vehicle has entered a shoulder of a road based on a Global Positioning System (GPS) information; and based on a result of the determining, controlling a Light Emitting Diode (LED) projector based on a first internal information of the vehicle, and transmitting a second internal information different from the first internal information to a server.

Abstract: The present invention provides a method of manufacturing an animal model of non-alcoholic liver disease by using correlation among metabolic dysregulations through AKT regulation by Hippo signaling, and an animal model prepared by the method above, and a screening method of a therapeutic agent by using the animal model.

Abstract: Mechanisms regulating cell proliferation stop and differentiation initiation during the development stage of mammalian embryo, and the proteins involved therein, are presented. Differentiation regulators, methods of regulating differentiation, transgenic organisms with loss of expression of the differentiation regulator, and methods of preparing the transgenic organisms, are provided.

Abstract: Mechanisms regulating cell proliferation stop and differentiation initiation during the development stage of mammalian embryo, and the proteins involved therein, are presented. Differentiation regulators, methods of regulating differentiation, transgenic organisms with loss of expression of the differentiation regulator, and methods of preparing the transgenic organisms, are provided.

Abstract: Disclosed is a complex of the 11 kDa Ca2+ binding protein of 11 and Hepatitis B virus polymerase (HBVPol) which moves to Promyelocytic Leukemia Nuclear Body (PMLNB). Furthermore, the present invention discloses a method for controlling movement of the HBVPol/p11 complex into the nucleus of HepG2 cell with adjusting of intracellular Ca2+ ion concentration by administrating an agent for controlling calcium ion concentration in HepG2 cells.

Abstract: There is provided a cell line that is prepared by transforming HEK293 cell with a human Kir2.1 gene using a retrovirus expression system, wherein the HEK293 expresses a stable ?1G T-type calcium channel. The cell line responds sensitively to KCl and forms an appropriate level of the membrane voltage so that the cell signaling pathway may be investigated by the molecular biological and biochemical studies.

Abstract: There is provided a cell line that is prepared by transforming HEK293 cell with a human Kir2.1 gene using a retrovirus expression system, wherein the HEK293 expresses a stable ?1G T-type calcium channel. The cell line responds sensitively to KCl and forms an appropriate level of the membrane voltage so that the cell signaling pathway may be investigated by the molecular biological and biochemical studies.

Abstract: Disclosed is a complex of the 11 kDa Ca2+ binding protein of 11 and Hepatitis B virus polymerase (HBVPol) which moves to Promyelocytic Leukemia Nuclear Body (PMLNB). Furthermore, the present invention discloses a method for controlling movement of the HBVPol/p11 complex into the nucleus of HepG2 cell with adjusting of intracellular Ca2+ ion concentration by administrating an agent for controlling calcium ion concentration in HepG2 cells.

Abstract: The present invention relates to identification of the consensus sequence phosphorylated by ATM kinase. This, in turn, permitted identification of ATM kinase target proteins, and development of a convenient assay system for ATM kinase phosphorylation using fusion polypeptides as substrates. The assay system is adaptable to screening for ATM modulators, particularly inhibitors. In a specific embodiment, the substrate recognition sequence and mutagenized variants of this sequence were incorporated in a GST fusion protein and assayed for phosphorylation by ATM kinase. This assay system is useful in screening for ATM inhibitors. ATM function assays were validated using an ATM-kinase dead dominant-negative mutant.

Abstract: The present invention relates to identification of the consensus sequence phosphorylated by ATM kinase. This, in turn, permitted identification of ATM kinase target proteins, and development of a convenient assay system for ATM kinase phosphorylation using fusion polypeptides as substrates. The assay system is adaptable to screening for ATM modulators, particularly inhibitors. In a specific embodiment, the substrate recognition sequence and mutagenized variants of this sequence were incorporated in a GST fusion protein and assayed for phosphorylation by ATM kinase. This assay system is useful in screening for ATM inhibitors. ATM function assays were validated using an ATM-kinase dead dominant-negative mutant.

Abstract: The present invention relates to identification of the consensus sequence phosphorylated by ATM kinase. This, in turn, permitted identification of ATM kinase target proteins, and development of a convenient assay system for ATM kinase phosphorylation using fusion polypeptides as substrates. The assay system is adaptable to screening for ATM modulators, particularly inhibitors. In a specific embodiment, the substrate recognition sequence and mutagenized variants of this sequence were incorporated in a GST fusion protein and assayed for phosphorylation by ATM kinase. This assay system is useful in screening for ATM inhibitors. ATM function assays were validated using an ATM-kinase dead dominant-negative mutant.

Abstract: The present invention discloses MmRad51-deficient transgenic mice and mouse cells, as well as MmRad51/p53-deficient transgenic mice and mouse cells. Also described is a method of screening for proteins that rescue the senescence phenotype in MmRad51/p53-deficient cells.

Abstract: Ku deficient cells and transgenic animals are described that comprise at least one allele of the XRCC5 gene that has been mutated by targeted disruption. Fibroblasts derived from XRCC5 mutant embryos and mice were found to prematurely age. These cells displayed decreased growth, slow entry into S phase, altered colony size distribution that favored small colonies, short life span and morphology characteristic of terminal differentiation. Mutant cells were also hypersensitive to .gamma.-radiation. The tissue culture data was at least partly reproduced in vivo because mutant mice grew slower than control littermates. The XRCC5 mutation, designated xrcc5.sup.M1, was a deletion of nucleotides 701-964 that shifted the reading frame. xrcc5.sup.M1 is expected to be null because the deleted allele produced no detectable transcript and because lymphocyte development and V(D)J recombination was severely disrupted.