Saint Louis University

Pharmacia Corporation

Smithkline Beecham Corporation

Rajeev Aurora

Stanton B Dotson

Anna Smith

Angel Baldan

Zachary Buchwald

Derk J Bergsma

Peter R Young

Catherine E Ellis

Jeffrey L Mooney

Yuan Zhu

Sherin Salaheldin Abdel-Meguid

John Edwin Tavis

Maureen J Donlin

Ronald B Frazier

George D Rose

Carolyn J Sympson

Preston Hensley

Stephanie F Guerrera

Cynthia L Woods

Hamideh Zakeri

Xianzhi Zhou

Jennifer Kiesel

Systems and methods for inhibiting atherosclerosis using FoxP3+ CD8 T-cells (Tc). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (Tc) through introduction of a low-dose of a RANK agonist such as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Pulsed introduction of low-dose RANKL as a therapy for diet-induced atherosclerosis

Systems and methods for inhibiting atherosclerosis using FoxP3+ CD8 T-cells (Tc). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (Tc) through introduction of a low-dose of a RANK agonist suck as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Pulsed introduction of low-dose RANKL as a therapy for atherosclerosis

Systems and methods for treating osteogenesis imperfecta using FoxP3+ CD8 T-cells (Tc). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (Tc) through introduction of a low-dose of a RANK agonist such as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Pulsed introduction of low-dose RANKL as a therapy for osteogenesis imperfecta

Systems and methods for inhibiting bone loss using FoxP3+ CD8 T-cells (Tc). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (Tc) through introduction of a low-dose of a RANK agonist such as RANKL. The RANKL was found to best work when provided in accordance with a schedule resulting in a pulsed administration.

Suppression of bone loss by introducing FoxP3+ CD8 T-cells (TcREG)

Systems and methods for inhibiting bone loss using FoxP3+ CD8 T-cells (Tc). Osteoclasts are induced to produce FoxP3+ CD8 T-cells (Tc) either in vivo or ex vivo. The FoxP3+ CD8 T-cells (Tc) are provided to the patient to subsequently regulate osteoclast function, thereby establishing a bi-directional regulatory loop between osteoclasts and FoxP3+ CD8 T-cells (Tc).

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Methods of identifying targets for designing a therapeutic agent are disclosed. These methods comprise: determining an amino acid sequence of one or more polypeptides of each isolate of a plurality of isolates of a biological system; identifying covariance pairs of amino acid residues; establishing a network comprising the covariance pairs; and identifying one or more hub residue positions, wherein a hub residue position comprises a target for designing a therapeutic agent if the hub residue position has a rank order in the 40percentile or greater. In other aspects, methods are disclosed for selecting a therapy for an infectious disorder. In various configurations, these methods comprise: determining amino acids occupying a plurality of diagnostic amino acid residue positions comprised by one or more polypeptides encoded by an infectious agent infecting a subject; and assigning the infectious agent infecting the subject to one covariance network selected from a plurality of covariance networks, wherein each network comprises a unique rank order of hubs with respect to the other networks, and whereby the therapy is selected on the basis of the covariance network assignment.

Sequence covariance networks, methods and uses therefor

Methionine aminopeptidases catalyse the co-translational removal of amino terminal methionine residues from nascent polypeptide chains. A newly-discovered enzyme, designated methionine aminopeptidase type-3 (MetAP-3), has a substrate specificity which is similar to MetAP-1 and MetAP-2, although it is not inhibited by fumagillin, an irreversible inhibitor of MetAP-2. MetAP-3 also preferentially localizes to mitochondria, unlike MetAP-1 and MetAP-2, which accumulate in the cytoplasm. One embodiment of the present invention relates to human cDNAs encoding polypeptides comprising MetAP-3. Other embodiments of the invention relate to nucleic acid molecules derived from these cDNAs, including complements, homologues, and fragments thereof, and methods of using these nucleic acid molecules, to generate polypeptides and fragments thereof. Other embodiments of the invention relate to antibodies directed against polypeptides comprising MetAP-3, and methods to screen for compounds or compositions that preferentially or specifically effect the activity of polypeptides comprising MetAP-3.

Human methionine aminopeptidase type 3

The present invention relates to a human cDNA encoding a methionine aminopeptidase type-3 (MetAP-3) protein. The invention also relates to nucleic acid molecules associated with or derived from this cDNA including complements, homologues and fragments thereof, and methods of using these nucleic acid molecules, to generate, for example, polypeptides and fragments thereof. The invention also provides methods of using the nucleic acids, for example, to produce a protein and fragments thereof and to screen for compounds or compositions that preferentially or specifically effect the activity of a MetAP-3 protein.

Methionine aminopeptidase type 3

EF-7 polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing EF-7 polypeptides and polynucleotides in therapy, and diagnostic assays for such.

Growing community of inventors

Wildwood, MO, United States of America

Rajeev Aurora