Pharmacia & Upjohn Company

University of Iowa Research Foundation

Steven L Roberds

Kevin P Campbell

Yoshihide Sunada

Richard D Anderson

Federica Piccolo

Rita M Huff

Jean-Claude Kaplan

Cara L Ruble

Marc Jeanpierre

Christopher W Benjamin

Alla M Karnovsky

Paul S Kaytes

The present invention provides novel ion channel polypeptides and polynucleotides that identify and encode them. In addition, the invention provides expression vectors, host cells and methods for their production. The invention also provides methods for the identification of ion channel agonists/antagonists, useful for the treatment of human diseases and conditions.

Human ion channel proteins

The present invention describes a recombinant rodent model for depression. More particularly, the rodent comprises cells expressing mutations in the WFS1 gene. The rodent is preferably a mouse heterologous for mutations in exon 8 of the WFS1 gene. Preferably, the mutations yield a non-functional wolframin protein that lacks all or some of it transmembrane regions. Methods and compositions for making and using the mouse and cells thereof are disclosed.

Mice heterozygous for WFS1 gene as mouse models for depression

The invention provides a method of identifying a therapeutic useful for treating or preventing asthma, which method includes the steps of contacting a identify compounds that inhibit the binding of human JAK2 protein to the &bgr;,first molecule comprising at least the N terminal 294 residues of JAK2 protein as shown in SEQ ID NO: 5 with a second molecule comprising at least 13 membrane proximal cytoplasmic amino acid residues of the &bgr;,subunit of the IL-3, IL-5, and GM-CSF receptors as shown in SEQ ID NO: 3 in the presence of a candidate compound to subunit of the IL-3, IL-5 and GM-CSF receptors. Compounds that block the signalling pathways of the IL-3, IL-5 and GM-CSF receptors may be of use in the treatment of asthma.

Method for identifying inhibitors of JAK2/cytokine receptor binding

Disclosed herein are compositions and methods for the detection of primary adhalinopathy. More specifically, disclosed herein are nucleic acid probes which hybridize specifically, under stringent hybridization conditions, to a mutant adhalin gene or the complement thereof, but not to the corresponding region of a wild-type adhalin gene. Also disclosed are methods for the detection of a mutation in the human adhalin gene which is responsible for primary adhalinopathy. Such methods include the use of the nucleic acid probes of the invention for detection of the myopathy by hybridization, as well as detection by direct DNA sequencing techniques.

Methods for detecting primary adhalinopathy

Disclosed are nucleic acid sequences encoding components of the dystrophin-glycoprotein complex. The components include dystroglycan, the 50 kDa protein component and the 59 kDa protein component. Also disclosed are compositions and methods which relate to the disclosed sequences.

Growing community of inventors

Mattawan, MI, United States of America

Steven L Roberds