Arch Development Corporation

Other

Graeme I Bell

Kazuki Yasuda

Terry Reisine

Yuichiro Yamada

Susumu Seino

Hiroto Furuta

Yukio Horikawa

Michael S German

Nancy J Cox

Lori Sussel

Philippe Froguel

Nathalie Vionnet

Stephan Menzel

Simon J Pilkis

Markus Stoffel

Habib Zouali

Jun Takeda

Craig L Hanis

Daniel Cohen

Naohisa Oda

Gilberto Velho

Kazuya Yamagata

Naohisha Oda

Pamela J Kaisaki

The invention relates generally to compositions of and methods for obtaining opioid receptor polypeptides. The invention relates as well to polynucleotides encoding opioid receptor polypeptides, the recombinant vectors carrying those sequences, the recombinant host cells including either the sequences or vectors, and recombinant opioid receptor polypeptides. By way of example, the invention discloses the cloning and functional expression of at least three different opioid receptor polypeptides. The invention includes as well, methods for using the isolated, recombinant receptor polypeptides in assays designed to select and improve substances capable of interacting with opioid receptor polypeptides for use in diagnostic, drug design and therapeutic applications.

Methods of identifying agonists and antagonists of opioid receptors

The invention relates generally to compositions of and methods for obtaining opioid receptor polypeptides. The invention relates as well to polynucleotides encoding opioid receptor polypeptides. More specifically, the invention relates to polynucleotides encoding kappa opioid receptor polypeptides, the recombinant vectors carrying those sequences, the recombinant host cells including either the sequences or vectors, and recombinant opioid receptor polypeptides. By way of example, the invention discloses the cloning and functional expression of at least three different opioid receptor polypeptides. The invention includes as well, methods for using the isolated, recombinant receptor polypeptides in assays designed to select and improve substances capable of interacting with opioid receptor polypeptides for use in diagnostic, drug design and therapeutic applications.

Nucleic acids encoding kappa opioid receptors

The present invention features a human Nkx-2.2 polypeptide and nucleotide sequences encoding Nkx-2.2 polypeptides. In a particular aspect, the polynucleotide is the nucleotide sequence of SEQ ID NO:1. In addition, the invention features polynucleotide sequences that hybridize under stringent conditions to SEQ ID NO:1. In related aspects the invention features expression vectors and host cells comprising polynucleotides that encode a human Nkx-2.2 polypeptide. The present invention also relates to antibodies that bind specifically to a human Nkx-2.2 polypeptide, and methods for producing human Nkx-2.2 polypeptides.

Human Nkx-2.2 polypeptide-encoding nucleotide sequences

The present invention relates generally to the field of diabetes. More particularly, it concerns the identification of genes responsible for NIDDM1 for use in diagnostic and therapeutic applications. The present invention demonstrates that the NIDDM1 locus is, in fact, the calpain 10 gene. The invention further relates to the discovery that analysis of mutations in calpain genes and gene products can be diagnostic for type 2 diabetes. The invention also contemplates methods of treating diabetes in view of the fact that calpain mutations can cause diabetes. Further, the invention relates to novel polynucleotides of the NIDDM1 locus and polypeptides encoded by such polynucleotides.

Polynucleotides encoding calpain 10

The present invention relates generally to the fields diabetes. More particularly, it concerns the identification of genes responsible for NIDDM for use in diagnostics and therapeutics. The present invention demonstrates that the MODY3 locus is, in fact, the HNF1&agr; gene, MODY4 locus is the HNF1&bgr; and the MODY1 locus is the HNF4&agr; gene. The invention further relates to the discovery that analysis of mutations in the HNF1&agr;, HNF1&bgr; and HNF4&agr; genes can be diagnostic for diabetes. The invention also contemplates methods of treating diabetes in view of the fact that HNF1&agr;, HNF1&bgr; and HNF4&agr; mutations can cause diabetes.

Mutations in the diabetes susceptibility genes hepatocyte nuclear factor (HNF) 1 alpha (&agr;), HNF1&bgr; and HNF4&agr;

The invention relates generally to compositions of and methods for using polynucleotides encoding kappa opioid receptors. In addition to such polynucleotides themselves, the invention relates to expression vectors comprising polynucleotides encoding kappa opioid receptors, recombinant host cells comprising such polynucleotides, and processes for preparing kappa opioid receptor polypeptides.

Polynucleotides encoding KAPPA opiod receptors

The invention relates generally to compositions of and methods for obtaining somatostatin receptors. The invention relates as well to the DNA sequences encoding somatostatin receptors, the recombinant vectors carrying those sequences, the recombinant host cells including either the sequences or vectors, and recombinant somatostatin receptor polypeptides. By way of example, the invention discloses the cloning and functional expression of at least three different somatostatin receptors, SSTR1, SSTR2 and SSTR3 from two different mammalian sources. The invention includes as well, methods for using the isolated, recombinant receptor polypeptides in assays designed to select and improve substances capable of interacting with somatostatin receptor polypeptides for use in diagnostic, drug design and therapeutic applications.

Somatostatin receptors

The invention relates to the observed tight linkage between DNA polymorphisms in the glucokinase gene (GCK) on the short arm of chromosome 7, and NIDDM in a cohort of sixteen French families having MODY. It further relates to identification of mutations in GCK and their linkage with diabetes in particular families are disclosed. This invention provides the first evidence implicating specific mutations in a gene involved in glucose metabolism in the pathogenesis of NIDDM. The invention further discloses the isolation and characterization of human pancreatic .beta.-cell GCK and a method for searching for mutations that cause early-onset NIDDM. To assess the effect of these mutations on glucokinase activity, a method is disclosed for generating an .alpha.-carbon backbone model for human glucokinase based on the crystal structure of the structurally-related yeast hexokinase B. Thus, in its most general sense, the invention relates to a method for detecting a propensity to develop early-onset, non-insulin-dependent diabetes mellitus.

Detection of glucokinase-linked early-onset non-insulin-dependent

Isolated DNA encoding a somatostatin receptor

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Chicago, IL, United States of America

Graeme I Bell