Abstract: The present invention is to construct a DNA replication reaction system which is excellent in versatility and is easily used. An amino acid sequence of a PCNA monomer which is one of factors involved in DNA replication is prepared so that amino acid residues causing mutual charge repulsion constitute a site which causes, when an N terminal region of the PCNA monomer and a C terminal region of another PCNA monomer act as an interface to form a multimeric complex, an intermolecular interaction of the monomers in an interface region of the monomers.

Abstract: The present application provides a method for predicting the functional site of a protein using data of the entire proteins of an organism of which genome data or cDNA data is known. More specifically, the present application provides a method for predicting a protein functional site, comprising the steps of calculating the frequency of occurrence of an oligopeptide in the entire proteins, calculating the value of each amino-acid residue contributing to the frequency of occurrence as the representative value of the function, and predicting the protein functional site by using the representative value of function as an indicator. The present also provides a system for predicting a functional site for automatically performing said methods.

Abstract: A method is described for enhancing degradation of telomerase. This method includes inhibiting the binding of TERT (telomerase catalytic subunit) to USP21, the binding of NEDD8-conjugated TERT to USP21, or the NEDD8 deconjugation by USP21 from NEDD8-conjugated TERT. A method of inhibiting telomerase activity is also described. The method includes utilizing the method of enhancing the degradation. A method of identifying a compound that inhibits the binding or the NEDD8 deconjugation is further described. An agent for inhibiting telomerase activity is described. An agent for preventing and/or treating diseases attributable to the enhanced telomerase activity is described and includes an inhibitory agent. Also, a method of preventing and/or treating diseases is described and includes using the inhibition method or the inhibitory agent. Further, a reagent kit is described.

Abstract: The present invention was aimed at reducing transcription activating activity of MITF-M to inhibit production of BCL2 gene product and thereby to allow treatment and/or prevention of melanoma The present invention provided a method of inhibiting production of BCL2 gene product and an agent for inhibiting the same, which inhibit binding of protein selected from a group consisting of HLF, ELK4 and CLOCK to MITF-M, a method of inducing cell death of melanoma cells, an agent for inducing the same, an agent for treating and/or preventing diseases accompanied by enhanced production of BCL2 gene product, such as melanoma, a method of treating and/or preventing the diseases, a method of identifying any one of the following compounds: a compound that inhibits the aforementioned binding; a compound that inhibits production of BCL2 gene product; and a compound that increases sensitivity of melanoma to melanoma drugs, as well as a reagent kit.

Abstract: The present invention found the interaction of CREBL1 and HNF-4? with HtrA2 and revealed for the first time that CREBL1, ATF6, and HNF-4? are degraded by active HtrA2. In addition, the present invention provides a means for inhibiting the degradation of at least one of CREBL1, ATF6, and HNF-4?, comprising inhibiting the function of HtrA2; a means for preventing and/or treating diabetes, comprising inhibiting the degradation by HtrA2 of at least one of CREBL1, ATF6, and HNF-4?; a means for preventing cell death (for example, pancreatic ? cell death), comprising inhibiting the degradation by HtrA2 of CREBL1 and/or ATF6; a means for preventing and/or treating type 2 diabetes, comprising inhibiting the degradation by HtrA2 of HNF-4?; and a reagent kit.

Abstract: PAK4 and JIK, both of which bind to MKK7 and directly phosphorylate MKK7, were found in the present invention. The present invention provides an inhibitor of c-Jun phosphorylation caused by JNK3 and a method for inhibiting the same, and an agent for preventing and/or treating a disorder attributable to c-Jun phosphorylation caused by JNK3 and a method for preventing and/or treating the same, all of which comprise inhibiting one member selected from the following: the binding of PAK4 to MKK7, the phosphorylation of MKK7 by PAK4, the binding of JIK to MKK7, and the phosphorylation of MKK7 by JIK. Further, the present invention provides a method for identifying a compound that inhibits the binding of PAK4 to MKK7, the phosphorylation of MKK7 caused by PAK4, the binding of JIK to MKK7, or the phosphorylation of MKK7 caused by JIK, as well as the compound obtained thereby.

Abstract: The task is to provide protein interaction inhibitors and/or detection method for interaction inhibitors related to regulation of T cell activation and production of IL-2. The present invention provides inhibitors of interaction between PKC theta and KPNA1, and inhibitors of interaction between KPNA1 and NF-kappaB. Inhibitors of interaction is defined as an candidate compound demonstrating the inhibition of interaction by assaying whether interaction has occurred or not between 2 types of protein and the candidate compound under the conditions allowing interaction of each combination. The detection kit is equipped with samples providing proteins of combinations to be interacted.

Abstract: The present application provides a method for predicting the functional site of a protein using data of the entire proteins of an organism of which genome data or cDNA data is known. More specifically, the present application provides a method for predicting a protein functional site, comprising the steps of calculating the frequency of occurrence of an oligopeptide in the entire proteins, calculating the value of each amino-acid residue contributing to the frequency of occurrence as the representative value of the function, and predicting the protein functional site by using the representative value of function as an indicator. The present also provides a system for predicting a functional site for automatically performing said methods.

Abstract: It is an object of the present invention to find a protein interacting with Granzyme B and to provide a means for preventing and/or treating diseases caused by the decomposition of the above protein by Granzyme B. The present invention provides a method of using Golgin-160 as a substrate of Granzyme B; a method for screening an inhibitor of the interaction of Granzyme B with Golgin-160 and/or an inhibitor of the decomposition of Golgin-160 by Granzyme B; various types of agent which comprise an inhibitor of the interaction of Granzyme B with Golgin-160 and/or an inhibitor of the decomposition of Golgin-160 by Granzyme B; and a method for preventing and/or treating various diseases which comprises a step of inhibiting the interaction of Granzyme B with Golgin-160 and/or the decomposition of Golgin-160 by Granzyme B.

Abstract: A method and an agent for inhibiting the oligomerization of procaspase-1, a method and an agent for inhibiting the activation of procaspase-1, a method and an agent for inhibiting the production of caspase-1, a method of preventing and/or treating an inflammatory disease, and an agent for preventing and/or treating an inflammatory disease, all of which comprise inhibiting the binding of NOD2 to procaspase-1; a method of identifying a compound that inhibits the binding of NOD2 to procaspase-1; and a reagent kit for use in the identifying method are provided.

Abstract: The present invention provides a method for inhibiting the activation of telomerase and an agent for inhibiting the activation of telomerase, a method for inhibiting telomerase activity and an agent for inhibiting telomerase activity, a method for preventing and/or a method for treating a cancer disease, an agent for preventing and/or an agent for treating a cancer disease, all of which comprises inhibiting the binding of MAPKAPK3 to TERT that is a catalytic subunit of telomerase or inhibiting the phosphorylation of TERT by active MAPKAPK3; a method of identifying a compound that inhibits the binding of MAPKAPK3 to TERT or a compound that inhibits the phosphorylation of TERT by active MAPKAPK3; and a reagent kit.

Abstract: PAK4 and JIK, both of which bind to MKK7 and directly phosphorylate MKK7, were found in the present invention. The present invention provides an inhibitor of c-Jun phosphorylation caused by JNK3 and a method for inhibiting the same, and an agent for preventing and/or treating a disorder attributable to c-Jun phosphorylation caused by JNK3 and a method for preventing and/or treating the same, all of which comprise inhibiting one member selected from the following: the binding of PAK4 to MKK7, the phosphorylation of MKK7 by PAK4, the binding of JIK to MKK7, and the phosphorylation of MKK7 by JIK. Further, the present invention provides a method for identifying a compound that inhibits the binding of PAK4 to MKK7, the phosphorylation of MKK7 caused by PAK4, the binding of JIK to MKK7, or the phosphorylation of MKK7 caused by JIK, as well as the compound obtained thereby.

Abstract: Based on the finding that m-calpain or ?-calpain degrades hepatocyte nuclear factor 4? (HNF-4?), hepatocyte nuclear factor 1? (HNF-1?) and insulin promoter factor 1 (IPF-1), which form transcription factor networks involved in expression of glucose metabolism-related genes in pancreatic ? cells, the following have been provided: a method for degradation of these transcription factors; a method for inhibiting the degradation and an agent for inhibiting the degradation; a method for enhancing production of the gene product of a gene on which these factors act as transcription factors and an agent for enhancing the same; an agent for preventing and/or treating a disease attributable to the degradation of these transcription factors and a method for preventing and/or treating the disease; a method for identifying a compound that inhibits the degradation of these transcription factors by calpain; a compound obtained by the identification method; and a reagent kit including calpain, these transcription factors, pol

Abstract: A method for promoting insulin gene transcription, which comprises the step of inhibiting binding of IPF1 and any one of proteins selected from the following group: (i) HNF3G, (ii) PHF1, and (iii) DLX4; and a method for screening a substance that promotes insulin gene transcription, which comprises the step of bringing a test substance into contact with IPF1 and/or any one of proteins selected from the following group under a condition that allows the binding of IPF1 and said protein and then determining whether or not the test substance inhibits the binding of IPF1 and said protein by detecting presence or absence, or change of a signal and/or a marker generated by the binding of IPF1 and said protein in a system in which the signal and/or the marker can be detected: (i) HNF3G, (ii) PHF1, and (iii) DLX4.

Abstract: A novel protein involved in cell-death and a gene encoding the protein, the use thereof to screen for an anti-cell-death factor for use in the treatment of a disorder caused by excessive cell-death or to screen for a remedy for a disorder caused by aberrant suppression of cell-death, and the screening method are provided. Human HtrA2 and human HtrA2-expressing cells and animals to screen for an anti-cell-death factor for use in the treatment of a disorder caused by excessive cell-death, a method for screening for an anti-cell-death factor for use in the treatment of disorder caused by excessive cell-death, and a method for screening for a remedy for a disorder caused by aberrant suppression of cell-death.

Abstract: It was discovered that hepatitis B virus x interacting protein (XIP) is cleaved and degraded by caspase-1, and the cleavage recognition site of XIP was also discovered. Based on these findings, the present invention provides a method and composition for inhibiting the degradation of XIP, more particularly, inhibiting the degradation of XIP caused by caspase-1, preventing and/or treating a disease attributable to the degradation of XIP, inhibiting the replication and/or transcription of hepatitis B virus, preventing and/or treating hepatitis B, and preventing and/or treating hepatic cancer caused by hepatitis B virus.

Abstract: PAK4 and JIK, both of which bind to MKK7 and directly phosphorylate MKK7, were found in the present invention. The present invention provides an inhibitor of c-Jun phosphorylation caused by JNK3 and a method for inhibiting the same, and an agent for preventing and/or treating a disorder attributable to c-Jun phosphorylation caused by JNK3 and a method for preventing and/or treating the same, all of which comprise inhibiting one member selected from the following: the binding of PAK4 to MKK7, the phosphorylation of MKK7 by PAK4, the binding of JIK to MKK7, and the phosphorylation of MKK7 by JIK. Further, the present invention provides a method for identifying a compound that inhibits the binding of PAK4 to MKK7, the phosphorylation of MKK7 caused by PAK4, the binding of JIK to MKK7, or the phosphorylation of MKK7 caused by JIK, as well as the compound obtained thereby.

Abstract: An electrical actuator has a DC motor which is provided with a rotor having a permanent magnet for forming a plurality of magnetic poles around a periphery thereof and a stator having a plurality of energizing coils and being disposed around a periphery of the rotor to thereby generate a rotary force for the rotor. In mounting this DC motor on a heat-generating member which generates radiant heat, a member for shielding radiant heat from a heat-generating member is disposed between the DC motor and the heat generating member. In this manner, the radiant heat from the heat-generating member is prevented from reaching the DC motor, whereby the problems in the DC motor associated with the radiant heat can be prevented.

Abstract: Method predicting whether protein or polypeptide interacts with another one by the steps of decomposition, database searching, sequence alignment and frequency determination; recording medium for carrying out the method; and obtained proteins.

Abstract: All DNA's of a mutant of a sequencing target organic species (e.g., a resistant bacterium, a tumor cell, or a virus) are extracted, and shotgun libraries are generated for the DNA's. DNA fragments are sequentially fetched from these libraries, and each fragment is subjected to sequencing using an automated DNA sequencer. Fragment sequence information such as base sequences of the respective DNA fragments of the mutant output from the sequencer is stored in a fragment sequence database.