Abstract: A method in which a mutant gene present in a gene pool mixedly with a large number of wild-type genes can be simply, inexpensively and sensitively detected is developed and provided. A clamping probe that is connected to a target nucleic acid molecule in two regions of first and second target nucleic acid complementary regions so that a wild-type target nucleic acid molecule and a mutant-type target nucleic acid molecule can be distinguished from each other depending on a difference in complementarity to these target nucleic acid molecules is provided.

Abstract: A method in which a mutant gene present in a gene pool mixedly with a large number of wild-type genes can be simply, inexpensively and sensitively detected is developed and provided. A clamping probe that is connected to a target nucleic acid molecule in two regions of first and second target nucleic acid complementary regions so that a wild-type target nucleic acid molecule and a mutant-type target nucleic acid molecule can be distinguished from each other depending on a difference in complementarity to these target nucleic acid molecules is provided.

Abstract: Provided are an improved double-stranded nucleic acid molecule involved in gene expression control mediated by a gene silencing mechanism, a method of producing the molecule, and a pharmaceutical composition comprising the double-stranded nucleic acid molecule. The double-stranded nucleic acid molecule for gene expression control comprises an antisense strand having a length of 18 to 28 nucleotides and a sense strand including a complementary moiety composed of a sequence sufficiently complementary to the antisense strand and a protruding single-stranded 5?-end moiety having a length of 2 to 100 nucleotides. The sense strand and the antisense strand form base pairs via the complementary moiety. The method produces such a double-stranded nucleic acid molecule, and the pharmaceutical composition contains such a double-stranded nucleic acid molecule as an active ingredient.

Abstract: The purpose of the present invention is to develop and provide a nucleic acid molecule that can specifically and efficiently inhibit the activity of a target RNAi molecule and can be produced safely at a low cost. Provided is a nucleic acid molecule for inhibiting the activity of a target RNAi molecule. The nucleic acid molecule comprises a single-stranded nucleic acid moiety that contains one unmodified DNA region composed of a nucleotide sequence completely or sufficiently complementary to a nucleotide sequence of a functional strand having the activity in the target RNAi molecule and a double-stranded nucleic acid moiety to be linked to at least one of the 5?-end and the 3?-end of the single-stranded nucleic acid moiety.

Abstract: The purpose of the present invention is to develop and provide a nucleic acid molecule that can specifically and efficiently inhibit the activity of a target RNAi molecule and can be produced safely at a low cost. Provided is a nucleic acid molecule for inhibiting the activity of a target RNAi molecule. The nucleic acid molecule comprises a single-stranded nucleic acid moiety that contains one unmodified DNA region composed of a nucleotide sequence completely or sufficiently complementary to a nucleotide sequence of a functional strand having the activity in the target RNAi molecule and a double-stranded nucleic acid moiety to be linked to at least one of the 5?-end and the 3?-end of the single-stranded nucleic acid moiety.

Abstract: Provided are an improved double-stranded nucleic acid molecule involved in gene expression control mediated by a gene silencing mechanism, a method of producing the molecule, and a pharmaceutical composition comprising the double-stranded nucleic acid molecule. The double-stranded nucleic acid molecule for gene expression control comprises an antisense strand having a length of 18 to 28 nucleotides and a sense strand including a complementary moiety composed of a sequence sufficiently complementary to the antisense strand and a protruding single-stranded 5?-end moiety having a length of 2 to 100 nucleotides. The sense strand and the antisense strand form base pairs via the complementary moiety. The method produces such a double-stranded nucleic acid molecule, and the pharmaceutical composition contains such a double-stranded nucleic acid molecule as an active ingredient.

Abstract: A mutant human prourokinase wherein a neutral amino acid in the epidermal growth factor (EGF) region of human prourokinase (human PUK) has been replaced with a basic amino acid, or an acidic amino acid has been replaced with a non-acidic amino acid, and a method for producing a mutant human PUK which comprises expression of mutant human PUK by cultivating a host transformed by a plasmid inserted with a DNA sequence coding for said mutant human PUK. By replacing a neutral amino acid in the EGF region of human PUK which is a fibrinolysin with a basic amino acid, or an acidic amino acid with a non-acidic amino acid, half-life in blood can be prolonged, and affinity for fibrin can be improved.

Abstract: A human prourokinase mutant in which the entire or a partial epidermal growth factor domain of human prourokinase is deleted or a partial epidermal growth factor domain of human prourokinase is replaced by one or more different amino acid residues, said mutant having a longer blood half-life than naturally occurring human prourokinase while retaining prourokinase enzymatic activity. In this human prourokinase mutant the region selected from the group consisting of: (a) from asparagine (10) to cysteine (42); (b) from asparagine (10) to aspartic acid (45); and (c) from asparagine (10) to threonine (49) is missing.