Abstract: In certain embodiments, this present invention provides antibodies and Fc fusion proteins with enhanced pharmacokinetics, such as biotinylated antibodies or biotinylated Fc fusion polypeptides.

Abstract: In certain embodiments, this present invention provides antibodies and Fc fusion proteins with enhanced pharmacokinetics, such as biotinylated antibodies or biotinylated Fc fusion polypeptides.

Abstract: Provided herein are recombinant antibodies and antigen-binding portions thereof useful for binding to FcRn and blocking binding of FcRn to human serum albumin. The FcRn-binding proteins can be used to treat a variety of disorders including acute and chronic toxic exposure.

Abstract: In certain embodiments, this present invention provides antibodies and Fc fusion proteins with enhanced pharmacokinetics, such as biotinylated antibodies or biotinylated Fc fusion polypeptides.

Abstract: Provided herein are recombinant antibodies and antigen-binding portions thereof useful for binding to FcRn and blocking binding of FcRn to IgG Fc. The FcRn-binding proteins can be used to treat a variety of disorders including autoimmune disorders.

Abstract: Provided herein are recombinant antibodies and antigen-binding portions thereof useful for binding to FcRn and blocking binding of FcRn to IgG Fc. The FcRn-binding proteins can be used to treat a variety of disorders including autoimmune disorders.

Abstract: Provided herein are recombinant antibodies and antigen-binding portions thereof useful for binding to FcRn and blocking binding of FcRn to IgG Fc. The FcRn-binding proteins can be used to treat a variety of disorders including autoimmune disorders.

Abstract: In certain embodiments, this present invention provides antibodies and Fc fusion proteins with enhanced pharmacokinetics, such as biotinylated antibodies or biotinylated Fc fusion polypeptides.

Abstract: Provided herein are recombinant antibodies and antigen-binding portions thereof useful for binding to FcRn and blocking binding of FcRn to human serum albumin. The FcRn-binding proteins can be used to treat a variety of disorders including acute and chronic toxic exposure.

Abstract: Provided herein are recombinant antibodies and antigen-binding portions thereof useful for binding to FcRn and blocking binding of FcRn to IgG Fc. The FcRn-binding proteins can be used to treat a variety of disorders including autoimmune disorders.

Abstract: Methods and applications of Global Patter Recognition (GPR), including a system for analyzing the results of real-time polymerase chain reaction (RT-PCR) experiments employing micro-titer and/or microarray plates and robotic plate readers is described. The system employs a set of self-normalizing housekeeping primers or oligonucleotides on the plates/arrays and an algorithmic approach to normalizing expression data from all primers on the plate based on the reaction products of several of the self-normalizing gene primers oligonucleotides. Normalization is accomplished using simplex reactions involving these self-normalizing primers/oligonucleotides; the normalization parameters are then useable across all control and experimental reactions of the plate/array. A ranked list of genes whose amount of change is statistically significant can be determined. The accuracy of this list is enhanced by the data normalization aspect of the system. Other applications of GPR are also disclosed herein.

Abstract: In certain embodiments, this present invention provides antibodies and Fc fusion proteins with enhanced pharmacokinetics, such as biotinylated antibodies or biotinylated Fc fusion polypeptides.

Abstract: Methods and applications of Global Patter Recognition (GPR), including a system for analyzing the results of real-time polymerase chain reaction (RT-PCR) experiments employing micro-titer and/or microarray plates and robotic plate readers is described. The system employs a set of self-normalizing housekeeping primers or oligonucleotides on the plates/arrays and an algorithmic approach to normalizing expression data from all primers on the plate based on the reaction products of several of the self-normalizing gene primers oligonucleotides. Normalization is accomplished using simplex reactions involving these self-normalizing primers/oligonucleotides; the normalization parameters are then useable across all control and experimental reactions of the plate/array. A ranked list of genes whose amount of change is statistically significant can be determined. The accuracy of this list is enhanced by the data normalization aspect of the system. Other applications of GPR are also disclosed herein.

Abstract: A transgenic mouse is disclosed herein whose somatic and germ cells comprise a disrupted IL-21 receptor gene, the disruption being sufficient to inhibit the binding of IL-21 to an IL-21 receptor, and a disrupted IL-4 gene, the disruption being sufficient to inhibit the production of IL-4 or the binding of IL-4 to the IL-4 receptor. A mouse homozygous for the disrupted IL-21 receptor gene and homozygous for the disrupted IL-4 gene has diminished B cell function. A method is disclosed for altering a B cell activity. The method includes administering a therapeutically effective amount of an agent that interferes with the interaction of IL-21 with an IL-21 receptor, thereby altering the B cell activity. A method is also disclosed for of treating a subject with Job's disorder or atopic disease. A method is also disclosed for treating or preventing an allergic reaction in a subject. A method is also disclosed for treating a subject with an autoimmune or antibody mediated disorder.

Abstract: Disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene. The homozygous RcRn disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse in which exogenously administered IgG1 exhibits a substantially shorter half-life, as compared to the half-life of exogenously administered IgG1 in a wild-type mouse. The transgenic knockout mouse with a homozygous RcRn disruption is also unable to absorb maternal IgG in the prenatal or neonatal stage of development. Also disclosed is a transgenic knockout mouse comprising a homozygous FcRn disruption and a human FcRn transgene. The transgenic addition of human FcRn results in a substantial increase in the half-life of exogenously administered human IgG1. Methods of using the transgenic knockout mouse, and cells derived from them, are also disclosed.

Abstract: Systems and methods for performing rapid genomic DNA analysis of samples, such as control samples and experimental samples. In one aspect, the system makes use of genomic DNA input, rather than gene expression input such as mRNA and/or cDNA associated with mRNA. The systems and methods perform statistical analyses on data generated from the samples to determine which DNA sequences in an identified set of DNA sequences have a basis of variation in an experimental sample when compared to a control sample, and additionally provide a quantitative measure of this variation. The quantitative measure may be based on metrics such as copy number and/or fold-change. The systems and methods employ this statistical framework in DNA-based evaluation settings, including the evaluation/diagnosis of a pathological condition such as cancer or transgenic analysis of transgenic plants and animals.

Abstract: Disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene. The homozygous FcRn disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse in which exogenously administered IgG1 exhibits a substantially shorter half-life, as compared to the half-life of exogenously administered IgG1 in a wild-type mouse. The transgenic knockout mouse with a homozygous FcRn disruption is also unable to absorb maternal IgG in the prenatal or neonatal stage of development. Also disclosed is a transgenic knockout mouse comprising a homozygous FcRn disruption and a human FcRn transgene. The transgenic addition of human FcRn results in a substantial increase in the half-life of exogenously administered human IgG1. Methods of using the transgenic knockout mouse, and cells derived from them, are also disclosed.

Abstract: Disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene. The homozygous FcRn disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse in which exogenously administered IgG1 exhibits a substantially shorter half-life, as compared to the half-life of exogenously administered IgG1 in a wild-type mouse. The transgenic knockout mouse with a homozygous FcRn disruption is also unable to absorb maternal IgG in the prenatal or neonatal stage of development. Also disclosed is a transgenic knockout mouse comprising a homozygous FcRn disruption and a human FcRn transgenic. The transgenic addition of human FcRn results in a substantial increase in the half-life of exogenously administered human IgG1. Methods of using the transgenic knockout mouse, and cells derived from them, are also disclosed.

Abstract: A transgenic mouse is disclosed herein whose somatic and germ cells comprise a disrupted IL-21 receptor gene, the disruption being sufficient to inhibit the binding of IL-21 to an IL-21 receptor, and a disrupted IL-4 gene, the disruption being sufficient to inhibit the production of IL-4 or the binding of IL-4 to the IL-4 receptor. A mouse homozygous for the disrupted IL-21 receptor gene and homozygous for the disrupted IL-4 gene has diminished B cell function. A method is disclosed for altering a B cell activity. The method includes administering a therapeutically effective amount of an agent that interferes with the interaction of IL-21 with an IL-21 receptor, thereby altering the B cell activity. A method is also disclosed for of treating a subject with Job's disorder or atopic disease. A method is also disclosed for treating or preventing an allergic reaction in a subject. A method is also disclosed for treating a subject with an autoimmune or antibody mediated disorder.

Abstract: Disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene, wherein said homozygous disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse in which exogenously administered IgG1 exhibits a substantially shorter half-life, as compared to the half-life of exogenously administered IgG1 in a wild-type mouse. Also disclosed is a transgenic knockout mouse whose genome comprises a homozygous disruption in its endogenous FcRn gene, wherein said homozygous disruption prevents the expression of a functional FcRn protein, resulting in a transgenic knockout mouse which is unable to absorb maternal IgG in the prenatal or neonatal stage of development Methods of using the transgenic knockout mouse, and cells derived therefrom, are also disclosed.