Luigi Grasso, 58403 Barbara Ln, Rosemont, PA 19010

6602850, Aug 5, 2003

Jun 16, 2000

09/596377

Roy Clifford Levitt - Ambler PA
Luigi Grasso - Philadelphia PA
Nicholas C. Nicolaides - Boothwyn PA
Kenneth J. Holroyd - Collegeville PA

Genaera Corporation - Plymouth Meeting PA

A61K 3816

514 12, 514 2, 514 8, 514826, 514885

This invention relates to the diagnosis, treatment and methods for discovery of new therapeutics for atopic asthma and related disorders based on variants of Asthma Associated Factor 2. One embodiment of the invention is a variant of AAF2 wherein codon 173 is deleted resulting in the loss of glutamine 173 from the mature protein precursor. This single amino acid deletion results in a non-functional AAF2 protein and therefore the presence of this phenotype should be associated with less evidence of atopic asthma. Correspondingly, the lack of susceptibility to an asthmatic, atopic phenotype is characterized by the loss of glutamine at codon 173. The invention includes isolated DNA molecules which are variants of the wild type sequence as well as the proteins encoded by such DNA and the use of such DNA molecules and expressed protein in the diagnosis and treatment of atopic asthma.

6656736, Dec 2, 2003

Feb 21, 2001

09/788657

Nicholas C. Nicolaides - Boothwyn PA
Philip M. Sass - Audubon PA
Luigi Grasso - Philadelphia PA
Bert Vogelstein - Baltimore MD
Kenneth W. Kinzler - Bel Air MD

The Johns Hopkins University - Baltimore MD
Morphotek, Inc. - Exton PA

C12N 1574

435483, 4352542

Yeast cells are mutagenized to obtain desirable mutants. Mutagenesis is mediated by a defective mismatch repair system which can be enhanced using conventional exogenously applied mutagens. Yeast cells with the defective mismatch repair system are hypermutable, but after selection of desired mutant yeast strains, they can be be rendered genetically stable by restoring the mismatch repair system to proper functionality.

6737268, May 18, 2004

Nov 14, 2000

09/712691

Nicholas C. Nicolaides - Boothwyn PA
Luigi Grasso - Philadelphia PA
Philip M. Sass - Audubon PA

Morphotek, Inc. - Exton PA

C12N 1500

435325, 4353201, 435 691, 435455

Dominant negative alleles of human mismatch repair genes can be used to generate hypermutable cells and organisms. By introducing these genes into cells and transgenic animals, new cell lines and animal varieties with novel and useful properties can be prepared more efficiently than by relying on the natural rate of mutation. These methods are useful for generating genetic diversity within genes encoding for therapeutic antigens to produce altered polypeptides with enhanced antigenic and immunogenic activity. Moreover, these methods are useful for generating effective vaccines.

6808894, Oct 26, 2004

Nov 7, 2000

09/707468

Nicholas C. Nicolaides - Boothwyn PA
Luigi Grasso - Philadelphia PA
Philip M. Sass - Audubon PA

Morphotek, Inc. - Exton PA

C12N 1500

435 691, 435325, 4353201, 536 235, 536 245, 4241301

Dominant negative alleles of human mismatch repair genes can be used to generate hypermutable cells and organisms. By introducing these genes into cells and transgenic animals, new cell lines and animal varieties with novel and useful properties can be prepared more efficiently than by relying on the natural rate of mutation. These methods are useful for generating genetic diversity within immunoglobulin genes directed against an antigen of interest to produce altered antibodies with enhanced biochemical activity. Moreover, these methods are useful for generating antibody-producing cells with increased level of antibody production.

6825038, Nov 30, 2004

May 14, 2001

09/853646

Nicholas C. Nicolaides - Boothwyn PA
Philip M. Sass - Audubon PA
Luigi Grasso - Philadelphia PA
Bert Vogelstein - Baltimore MD
Kenneth W. Kinzler - Bel Air MD

The Johns Hopkins University - Baltimore MD
Morphotek, Inc. - Exton PA

C12N 1500

435440, 435455, 435465, 4353201, 435325

Dominant negative alleles of human mismatch repair genes can be used to generate hypermutable cells and organisms. By introducing these genes into cells and transgenic animals, new cell lines and animal varieties with novel and useful properties can be prepared more efficiently than by relying on the natural rate of mutation. The enhanced rate of mutation can be further augmented using mutagens. Moreover, the hypermutability of mismatch repair deficient cells can be remedied to stabilize cells or mammals with useful mutations.

6900370, May 31, 2005

Dec 28, 2000

09/749601

Nicholas C. Nicolaides - Boothwyn PA, US
Luigi Grasso - Philadelphia PA, US
Phillip M. Sass - Audubon PA, US
Ken Kinzler - Bel Air MD, US
Bert Vogelstein - Baltimore MD, US

John Hopkins University - Baltimore MD
Morphotek, Inc. - Philadelphia PA

C12N015/82
A01H005/00

800298, 435468, 435419, 800288

Blockade of mismatch repair in a plant can lead to hypermutation and a new genotype and/or phenotype. One approach used to generate hypermutable plants is through the expression of dominant negative alleles of mismatch repair genes in transgenic plants or derived cells. By introducing these genes into cells and transgenic plants, new cell lines and plant varieties with novel and useful properties can be prepared more efficiently than by relying on the natural rate of mutation. Moreover, methods to inhibit the expression and activity of endogenous plant MMR genes and their encoded products are also useful to generate hypermutable plants.

6921666, Jul 26, 2005

Aug 15, 2003

10/641068

Nicholas C. Nicolaides - Boothwyn PA, US
Philip M. Sass - Audubon PA, US
Luigi Grasso - Philadelphia PA, US
Bert Vogelstein - Baltimore MD, US
Kenneth W. Kinzler - Bel Air MD, US

The Johns Hopkins University - Baltimore MD
Morphotek - Philadelphia PA

C21N015/81

435483, 4352542

Yeast cells are mutagenized to obtain desirable mutants. Mutagenesis is mediated by a defective mismatch repair system which can be enhanced using conventional exogenously applied mutagens. Yeast cells with the defective mismatch repair system are hypermutable, but after selection of desired mutant yeast strains, they can be rendered genetically stable by restoring the mismatch repair system to proper functionality.

6982169, Jan 3, 2006

Jan 15, 2001

09/760285

Nicholas C. Nicolaides - Boothwyn PA, US
Luigi Grasso - Philadelphia PA, US
Philip M. Sass - Audubon PA, US

Morphotek, Inc. - Exton PA

C12N 15/00
C12N 1/16
A01N 27/00

435325, 4352542, 504357

Dominant negative alleles of human mismatch repair genes can be used to generate hypermutable cells and organisms. By introducing these genes into cells and transgenic animals, new cell lines and animal varieties with novel and useful properties can be prepared more efficiently than by relying on the natural rate of mutation. Methods of generating mutations in genes of interest and of making various cells mismatch repair defective through the use of chemicals to block mismatch repair in in vivo are disclosed.