Abstract: Provided is a method of detecting the presence of an anti-Zika virus (ZIKV) antibody in a sample, including contacting a sample with a suspension having a plurality of microspheres wherein individual microspheres are conjugated to a peptide and the peptide includes a ZIKV peptide selected from the group including ZIKV NS1, ZIKV NS5, and ZIKV envelope protein, forming a first incubated suspension by incubating said sample with said suspension to permit binding of anti-ZIKV antibodies present in the sample to said microspheres, forming a second incubated suspension by contacting said first incubated suspension with an anti-ZIKV antibody detecting-reagent to permit binding of the anti-ZIKV antibody detecting reagent to said microspheres, removing from the second incubated suspension anti-ZIKV antibody detecting-reagent molecules that are not bound to said microspheres, and detecting the presence of anti-ZIKV antibody detecting-reagent molecules in the second incubated suspension.

Abstract: Disclosed is a method for producing a protein involving infecting a culture of eukaryotic cells with a recombinant vaccinia virus.

Abstract: Disclosed and claimed is the CaESS1 gene, portions thereof such as primers or probes, expression products therefrom, and methods for using the gene, and expression products; for instance, for diagnostic, therapeutic or preventive compositions.

Abstract: The invention relates to a novel Universal RT-coupled PCR strategy for the specific detection and accurate quantitation of mRNA. Claimed and disclosed are novel Universal reverse transcription (RT) primers, a specific primer mix containing the Universal RT-primers, a transcript specific forward primer and a reverse PCR primer identical to a unique tag sequence, and methods and kits thereof for avoiding the amplification of genomic DNA and/or pseudogenes.

Abstract: The invention provides compositions and methods for detecting the presence of SARS-coronavirus, for screening anti-SARS coronavirus agents and vaccines, and for reducing infection with plus-strand RNA viruses such as SARS-coronavirus.

Abstract: The invention provides compositions and methods for detecting the presence of SARS-coronavirus, for screening anti-SARS coronavirus agents and vaccines, and for reducing infection with plus-strand RNA viruses such as SARS-coronavirus.

Abstract: Provided is the active site of human gamma glutamyl hydrolase. The active site resides in amino acid residues 110, 171, 220 and 222 of SEQ ID NO:1. Thus provided is an inactive gamma glutamyl hydrolase protein, as well as a fragment thereof. A method of inactivating a gamma glutamyl hydrolase protein is also provided, as is a molecule capable of binding to one or more of amino acid residues 110, 171, 220 or 222 of SEQ ID NO:1 which can be used in such a method. A method for identifying a molecule that inactivates gamma glutamyl hydrolase is provided, as is a nucleic acid molecule encoding the inactive gamma glutamyl hydrolase.

Abstract: Provided is the active site of human gamma glutamyl hydrolase. The active site resides in amino acid residues 110, 171, 220 and 222 of SEQ ID NO:1. Thus provided is an inactive gamma glutamyl hydrolase protein, as well as a fragment thereof. A method of inactivating a gamma glutamyl hydrolase protein is also provided, as is a molecule capable of binding to one or more of amino acid residues 110, 171, 220 or 222 of SEQ ID NO:1 which can be used in such a method. A method for identifying a molecule that inactivates gamma glutamyl hydrolase is provided, as is a nucleic acid molecule encoding the inactive gamma glutamyl hydrolase.

Abstract: Disclosed and claimed is the CaESS1 gene, portions thereof such as primers or probes, expression products therefrom, and methods for using the gene, and expression products; for instance, for diagnostic, therapeutic or preventive compositions.

Abstract: The present invention is directed to nucleic acid molecules encoding a truncated human cyclin E protein, the truncated human cyclin E protein being a constitutively active form of human cyclin E protein. These truncated forms can be encoded by the nucleotide sequence of wild-type cyclin E, with a deletion therein to result in the truncated protein. Vectors and host cells containing the nucleic acid molecules are also provided. The invention further provides isolated fragments of the truncated cyclin E proteins, which fragments consist essentially of the deletion flanking regions of the wild-type cyclin E nucleotide sequence. Antisense nucleic acid molecules, and fragments thereof, to the truncated cyclin E protein and to the fragments thereof are also provided. Methods using the nucleic acid molecules, fragments thereof, antisense nucleic acid molecules, and fragments thereof, are provided. The antisense can be used therapeutically for inhibition of cyclin E activity.

Abstract: The present invention is directed to an isolated nucleic acid molecule encoding an interferon-.alpha.-induced protein, particularly the protein designated p36. Expression vectors and host cells comprising the nucleic acid molecule are also provided, as well as methods for increasing or decreasing the expression of the interferon-.alpha.-induced protein in host cells. DNA oligomers and antibodies specific for interferon-.alpha.-induced protein are provided, each of which can be used to detect interferon-.alpha.-induced protein in a sample. Methods for diagnosing immunodeficiency and autoimmune disease in an individual and methods for detecting the presence or past existence of lupus inclusions or interferon-.alpha. in a sample are also provided.

Abstract: The invention provides a method for separating target cells from a plurality of cells which is based on a reversible high affinity interaction between two molecules. The method comprises: forming a target cell/cell binding reagent/first molecule/second molecule/solid support complex, wherein the cell binding reagent is specific for target cells present within a plurality of cells and wherein the first molecule reversibly binds to the second molecule; removing non-target cells of the plurality of cells not attached to the solid support; and reversing the first molecule binding to the second molecule, thereby releasing the target cells as separate cells from the plurality of cells.

Abstract: What are disclosed are methods for modifying the genome of vaccinia virus to produce vaccinia mutants, particularly by the introduction into the vaccinia genome of exogenous DNA; modified vaccinia prepared by such methods; certain DNA sequences and unmodified and genetically modified microorganisms involved as intermediates in such methods; and methods for infecting cells and host animals with such vaccinia mutants to provoke the amplification of exogenous DNA and proteins encoded by the exogenous DNA, including antigenic proteins, by said cells and host animals.

Abstract: The present invention is directed to isolated nucleic acid molecules encoding gamma glutamyl hydrolase (GH). Expression vectors and host cells comprising the nucleic acid molecules are also provided, as well as methods for increasing or decreasing the expression of GH in host cells. The invention further provides a method of screening a substance for the ability of the substance to modify GH function, and a method for isolating other GH molecules. DNA oligomers and antibodies specific for GH are provided, each of which can be used to detect GH in a sample. Methods for decreasing deleterious side effects of antifolate treatment, increasing the levels of GH in cells of a patient, increasing the effectiveness of antifolate treatment, and monitoring progression of a tumor are further provided.

Abstract: The present invention is directed to an isolated nucleic acid molecule encoding an interferon-.alpha.-induced protein, particularly the protein designated p36. Expression vectors and host cells comprising the nucleic acid molecule are also provided, as well as methods for increasing or decreasing the expression of the interferon-.alpha.-induced protein in host cells. DNA oligomers and antibodies specific for interferon-.alpha.-induced protein are provided, each of which can be used to detect interferon-.alpha.-induced protein in a sample. Methods for diagnosing immunodeficiency and autoimmune disease in an individual and methods for detecting the presence or past existence of lupus inclusions or interferon-.alpha. in a sample are also provided.

Abstract: The present invention is directed to isolated nucleic acid molecules encoding gamma glutamyl hydrolase (GH). Expression vectors and host cells comprising the nucleic acid molecules are also provided, as well as methods for increasing or decreasing the expression of GH in host cells. The invention further provides a method of screening a substance for the ability of the substance to modify GH function, and a method for isolating other GH molecules. DNA oligomers and antibodies specific for GH are provided, each of which can be used to detect GH in a sample. Methods for decreasing deleterious side effects of antifolate treatment, increasing the levels of GH in cells of a patient, increasing the effectiveness of antifolate treatment, and monitoring progression of a tumor are further provided.

Abstract: The present invention relates to testing the efficacy of antimicrobial agents which inhibit intein function through genetic screens for monitoring the function of protein inteins, and isolating conditional mutants thereof.

Abstract: The present invention is directed to nucleic acid molecules encoding a truncated human cyclin E protein, the truncated human cyclin E protein being a constitutively active form of human cyclin E protein. These truncated forms can be encoded by the nucleotide sequence of wild-type cyclin E, with a deletion therein to result in the truncated protein. Vectors and host cells containing the nucleic acid molecules are also provided. The invention further provides isolated fragments of the truncated cyclin E proteins, which fragments consist essentially of the deletion flanking regions of the wild-type cyclin E nucleotide sequence. Antisense nucleic acid molecules, and fragments thereof, to the truncated cyclin E protein and to the fragments thereof are also provided. Methods using the nucleic acid molecules, fragments thereof, antisense nucleic acid molecules, and fragments thereof, are provided. The antisense can be used therapeutically for inhibition of cyclin E activity.

Abstract: The subject invention provides non-naturally occurring peptides capable of inhibiting growth factor-stimulated growth of cells. The peptide can be utilized to inhibit growth factor-stimulated growth, such growth factors including, for example, gonadotropins, peptide hormones, synthetic growth factors, and ligands, the ligand having a receptor that is a member of the steroid/thyroid hormone/vitamin receptor superfamily. Also provided are DNA sequences encoding the peptides and methods of producing and using the peptides.

Abstract: The subject invention provides non-naturally occurring peptides capable of inhibiting growth factor-stimulated growth of cells. The peptide can be utilized to inhibit growth factor-stimulated growth, such growth factors including, for example, gonadotropins, peptide hormones, synthetic growth factors, and ligands, the ligand having a receptor that is a member of the steroid/thyroid hormone/vitamin receptor superfamily. Also provided are DNA sequences encoding the peptides and methods of producing and using the peptides.