Wei G Gu10464 42Nd Ave, Corona, NY 11368

7241743, Jul 10, 2007

Jun 14, 2002

10/172706

Wei Gu - New York NY, US
Jian Yuan Luo - New York NY, US

The Trustees of Columbia University in the City of New York - New York NY

A01N 43/04

514 44

This invention provides methods for treating and for inhibiting the onset of cancer in a subject comprising administering an agent that inhibits the ability of Sir2α to inhibit p53-dependent apoptosis. This invention also provides a related method for inducing the death of a cell. This invention further provides a method for decreasing the amount of damage to a subject's cells caused by physical stress comprising administering agent that increases the amount of Sir2α in the subject's cells and/or the ability of Sir2α to inhibit p53-dependent apoptosis in the subject's cells. This invention further provides related methods for prolonging the life-span of a subject, decreasing the amount of damage to a cell caused by physical stress, and prolonging the life-span of a cell. Finally, this invention provides two articles of manufacture for performing the instant methods.

7358335, Apr 15, 2008

Apr 29, 2005

11/118524

Wei Gu - Paramus NJ, US

The Trustees of Columbia University in the City of New York - New York NY

C07K 5/10
G01N 33/53

530350, 435 71

The present invention relates to the mechanism of ARF-mediated cell growth suppression. ARF-BP1 is identified as a novel ubiquitin ligase, and a major component of ARF-containing nuclear complexes in human cells. The present invention discloses a novel mechanism of ARF-mediated p53 activation and that ARF-BP1 is a critical mediator of both p53-independent and p53-dependent tumor suppression functions of ARF. Inactivation of ARF-BP1 in normal cells stabilizes p53 and induces p53-dependent apoptosis. Inactivation of ARF-BP1, but not Mdm2, in p53-wildtype cells promotes cell growth inhibition in a manner reminiscent of ARF induction. ARF-BP1 directly binds and ubiquitinates p53 and inactivation of endogenous ARF-BP1 is crucial for ARF-mediated p53 stabilization in Mdm2-null cells. ARF-BP1 is advantageous over Mdm2 as a target for suppressing tumor cell growth regardless of p53 status.

7425538, Sep 16, 2008

Mar 30, 2002

10/113732

Wei Gu - New York NY, US
Muyang Li - New York NY, US

The trustess of Columbia University in the City of New York - New York NY

A61K 38/00
G01N 33/53

514 12, 435 6, 435 71, 435 723

The present invention provides methods for determining whether a subject has neoplasia, methods for assessing the efficacy of therapy to treat neoplasia in a subject, methods for assessing the prognosis of a subject who has neoplasia, and methods for treating neoplasia in a subject in need of treatment. The present invention further provides a kit for use in detecting neoplasia. Additionally, the present invention provides a pharmaceutical composition, comprising a modulator of HAUSP expression or a HAUSP protein and a pharmaceutically acceptable carrier. Also provided is a method for deubiquitinating p53 in a cell. The present invention is further directed to a method for identifying an agent that is reactive with p53, and the agent identified by this method. Furthermore, the present invention provides a method for treating a p53-associated condition in a subject in need of treatment. The present invention is also directed to a complex comprising p53 and HAUSP, and a mutant protein comprising the HAUSP amino acid sequence, in which Ser is substituted for Cys at amino acid residue 223.

7498134, Mar 3, 2009

Mar 29, 2004

10/813177

Wei Gu - New York NY, US
Muyang Li - New York NY, US

The Trustees of Columbia University in the City of New York - New York NY

C12Q 1/68
G01N 33/53

435 6, 435 71

The present invention provides methods for diagnosing neoplasia, assessing the efficacy of therapy to treat neoplasia, assessing the prognosis of a subject who has neoplasia, and treating neoplasia. The present invention also provides a kit for use in detecting neoplasia. The present invention further provides methods for deubiquitinating and/or stabilizing Mdm2 in a cell, and for modulating deubiquitination and/or stability of p53 in a cell. Additionally, the present invention provides a method for identifying a modulator of Mdm2-HAUSP interaction. Also provided is a modulator identified by this method, a pharmaceutical composition comprising the modulator, and use of the modulator in a method of treating neoplasia. The present invention further provides methods for identifying an agent that is reactive with Mdm2 and an agent that is reactive with HAUSP. Also provided are agents identified by these methods.

8043804, Oct 25, 2011

May 23, 2008

12/154503

Wei Gu - Paramus NJ, US

The Trustees of Columbia University in the City of New York - New York NY

C12Q 1/68

435 6

A novel complex is identified between the NAD-dependent deacetylase, SIRT1 and its novel inhibitor, DBC1. Provided herein are methods to identify a compound that inhibits the complexation between SIRT1 and DBC1. Exemplary methods comprise contacting either the complexation between DBC1 and SIRT1 with an agent being tested for its ability to inhibit the complexation between SIRT1 and DBC1. Also, provided are methods to identify a compound that increases the complexation between SIRT1 and DBC1. Exemplary methods comprise contacting either the complexation between DBC1 and SIRT1 with an agent being tested for its ability to increase the complexation between SIRT1 and DBC1. Further, methods are provided to increase or decrease SIRT1 activity by contacting the complexation between SIRT1 and DBC1 with a peptide that either decreases or increases the complexation between SIRT1 and DBC1. Further, methods are provided for the treatment of patients suffering from diseases including metabolic diseases including obesity and diabetes, and neurodegenerative disorders including Alzheimer's disease and Huntington's disease using compounds that inhibit the complexation between SIRT1 and DBC1.

2004002, Feb 12, 2004

Dec 6, 2002

10/313203

Wei Gu - Emerson NJ, US
Anatoly Nikolaev - New York NY, US

C12Q001/68
G01N033/53
C07H021/04
C07K014/47
C12P021/02
C12N005/06

435/006000, 435/069100, 435/320100, 435/325000, 530/350000, 536/023200

This invention provides an isolated p53-associated Parkin-like cytoplasmic protein (“Parc”) having use, for example, as an anti-cancer target. This invention also provides related recombinant proteins and nucleic acids such as vectors and anti-sense molecules. Further provided are anti-Parc antibodies, protein and antibody production methods, Parc-based screening assays, methods and compositions for decreasing Parc expression and treating subjects, diagnostic methods, and related kits.

2008011, May 22, 2008

Jul 9, 2007

11/825944

Wei Gu - New York NY, US
Jian Yuan Luo - New York NY, US

The Trustees of Colubia University - New York NY

A61K 31/70
C12N 5/08
A61P 35/00

514 44, 435375

This invention provides methods for treating and for inhibiting the onset of cancer in a subject comprising administering an agent that inhibits the ability of Sir2α to inhibit p53-dependent apoptosis. This invention also provides a related method for inducing the death of a cell. This invention further provides a method for decreasing the amount of damage to a subject's cells caused by physical stress comprising administering agent that increases the amount of Sir2α in the subject's cells and/or the ability of Sir2α to inhibit p53-dependent apoptosis in the subject's cells. This invention further provides related methods for prolonging the life-span of a subject, decreasing the amount of damage to a cell caused by physical stress, and prolonging the life-span of a cell. Finally, this invention provides two articles of manufacture for performing the instant methods.

2012007, Mar 22, 2012

Oct 20, 2011

13/278013

Wei Gu - Paramus NJ, US

C12Q 1/68
G01N 27/447
G01N 33/566
G01N 33/53
C12N 9/80

435 613, 435 71, 435 61, 435228, 435 792, 204450

A novel complex is identified between the NAD-dependent deacetylase, SIRT1 and its novel inhibitor, DBC1. Provided herein are methods to indentify a compound that inhibits the complexation between SIRT1 and DBC1. Exemplary methods comprise contacting either the complexation between DBC1 and SIRT1 with an agent being tested for its ability to inhibit the complexation between SIRT1 and DBC1. Also, provided are methods to identify a compound that increases the complexation between SIRT1 and DBC1. Exemplary methods comprise contacting either the complexation between DBC1 and SIRT1 with an agent being tested for its ability to increase the complexation between SIRT1 and DBC1. Further, methods are provided to increase or decrease SIRT1 activity by contacting the complexation between SIRT1 and DBC1 with a peptide that either decreases or increases the complexation between SIRT1 and DBC1. Further, methods are provided for the treatment of patients suffering from diseases including metabolic diseases including obesity and diabetes, and neurodegenerative disorders including Alzheimer's disease and Huntington's disease using compounds that inhibit the complexation between SIRT1 and DBC1.