Abstract: The present application provides novel binding proteins, including human binding proteins that specifically bind to the human ErbB2.

Abstract: Methods and compositions for treating and diagnosing cancer and screening for agents for such treatment and diagnosis are provided. The methods involve screening for agents that modulate the activity or expression of FOXM1, which has been discovered herein to play a role in cell growth and cell cycle regulation. Methods for treating cancer, methods for modulating the activity or expression of FOXM1, methods for diagnosing a subject that has or is at risk of developing cancer, and pharmaceutical compositions are also provided.

Abstract: The present application provides novel binding proteins, including human binding proteins that specifically bind to the human ErbB2.

Abstract: Methods of screening for agents for treating asthma are provided. The methods involve screening for agents that decrease the production or activity of a RegIII protein that has been discovered herein to play a role in producing the symptoms and pathological complications involved in asthma. Methods of treating asthma, as well as screening for and treating with inhibitors of a RegIII protein are also provided.

Abstract: The present invention provides compositions and methods useful for detecting or treating asthma or other allergic or inflammatory diseases. In one aspect, the methods of the present invention include inhibiting the activity or expression of a component of an arginine metabolic pathway in tissues affected by asthma or other allergic or inflammatory diseases. In many embodiments, the component being inhibited is a cationic amino acid transporter, an arginase, or a component downstream of the arginase. In many other embodiments, the activity or expression of the component is inhibited by an agent that binds to the component. In still many other embodiments, the activity or expression of the component is inhibited by an agent that binds a polynucleotide encoding the component.

Abstract: Mutagenesis of the gene encoding homoserine dehydrogenase (hom) for production of the amino acid threonine is described. The mutation causes an alteration in the carboxy terminus of the enzyme that interferes with end-product inhibition by threonine. The lack of end-product inhibition causes an overproduction of threonine.

Abstract: The present invention is a method for the isolation and characterization of C. glutamicum genes involved in amino acid biosynthesis, specifically, encoding hom, thrB, and thrC, and sequences regulating their expression. Techniques for modifying or replacing these sequences and means for facilitating further isolations and characterizations, including promoter probe vectors which are useful in screening for high efficiency and regulatable promoters and repressors, are also disclosed.A C. glutamicum genomic library was constructed by cleaving chromosomal DNA with restriction enzymes, inserting the DNA fragments into an appropriate vector, and transforming the resulting recombinant molecules (rDNA) into C. glutamicum. Amino acid biosynthetic genes hom, thrB, and thrC, encoding homoserine dehydrogenase, homoserine kinase, and threonine synthetase, respectively, were isolated by complementation of C. glutamicum auxotrophs. The hom-thrB genes were subcloned on a 3.