David W Beach

US Patent:

6486131, Nov 26, 2002

Filed:

Jan 30, 1998

Appl. No.:

09/016750

Inventors:

David H. Beach - Huntington Bay NY
Douglas J. Demetrick - E. Northport NY
Manuel Serrano - Mill Neck NY
Gregory J. Hannon - Huntington NY

Assignee:

Cold Spring Harbor Laboratory - Cold Spring Harbor NY

International Classification:

A61K 3170

US Classification:

514 44, 424 932, 4353201, 435325, 435455

Abstract:

The present invention relates to the discovery in eukaryotic cells, particularly mammalian cells, of a novel family of cell-cycle regulatory proteins (âCCR-proteinsâ). As described herein, this family of proteins includes a polypeptide having an apparent molecular weight of 16 kDa, and a polypeptide having an apparent molecular weight of approximately 15 kDa, each of which can function as an inhibitor of cell-cycle progression, and therefore ultimately of cell growth. Thus, similar to the role of p21 to the p53 checkpoint, the subject CCR-proteins may function coordinately with the cell-cycle regulatory protein, retinoblastoma (RB). Furthermore, the CCR-protein family includes a protein having an apparent molecular weight of 13. 5 kDa (hereinafter âp13. 5â). The presumptive role of p13.

US Patent:

6566054, May 20, 2003

Filed:

Aug 30, 1996

Appl. No.:

08/706322

Inventors:

David H. Beach - Huntington Bay NY
Manuel Serrano - Mill Neck NY

Assignee:

Cold Spring Harbor Laboratory - Cold Spring Harbor NY

International Classification:

C12Q 168

US Classification:

435 6, 435 71, 435 772

Abstract:

The present invention relates to the discovery in eukaryotic cells, particularly mammalian cells, of mutant cyclin dependent kinase (CDK) proteins. These proteins fail to bind to CDK-inhibitory proteins and thus lead to aberrant cell growth. Herein, screening assays are described to identify CDK mutant proteins and the uses of these mutant proteins as tumor vaccines is described.

US Patent:

6503742, Jan 7, 2003

Filed:

Sep 8, 1999

Appl. No.:

09/392163

Inventors:

David Beach - Huntington Bay NY
Maureen G. Caligiuri - Huntington NY
Bradley Nefsky - Highland Park NJ

Assignee:

Cold Spring Harbor Laboratory - Cold Spring Harbor NY

International Classification:

C12N 1552

US Classification:

435183, 4353201, 4352523, 435325, 536 232

Abstract:

The present invention relates to the discovery in eukaryotic cells of a ubiquitin ligases. These proteins are referred to herein collectively as âpubâ proteins for Protein UBiquitin ligase, and individually as h-pub1, h-pub2 and s-pub1 for the human pub1 and pub2 and pub1 clones, respectively. Pub1 proteins apparently play a role in the ubiquitination of the mitotic activating tyrosine phosphatase cdc25, and thus they may regulate the progression of proliferation in eukaryotic cells by activating the cyclin dependent kinase complexes. In disruption of s-pub1 elevates the level of cdc25 protein in vivo increasing the activity of the tyrosine kinases, wee1 and mik1, required to arrest the cell-cycle. Loss of wee1 function in an cell carrying a disruption in the s-pub1 gene results in a lethal premature entry into mitosis; such lethal phenotype can be rescued by the loss of cdc25 function. An ubiquitin thioester adduct of s-pub1 can be isolated from and disruption of s-pub1 dramatically reduces ubiquitination of cdc25.

US Patent:

7005258, Feb 28, 2006

Filed:

Oct 30, 2000

Appl. No.:

09/699580

Inventors:

David H. Beach - Huntington Bay NY, US
Konstantin Galaktionov - Cold Spring Harbor NY, US

Assignee:

The National Institutes of Health - Bethesda MD

International Classification:

C12Q 1/68
C07H 21/04

US Classification:

435 6, 536 245

Abstract:

Two previously undescribed human cdc25 genes, designated cdc25 A and cdc25 B, which have been shown to have an endogenous tyrosine phosphatase activity that can be specifically activated by B-type cyclin, in the complete absence of cdc2 are described. As a result of this work, new approaches to regulating the cell cycle in eukaryotic cells and, particularly, to regulating the activity of tyrosine specific phosphatases which play a key role in the cell cycle are available. Applicant's invention relates to methods of regulating the cell cycle and, specifically, to regulating activation of cdc2-kinase, through alteration of the activity and/or levels of tyrosine phosphatases or through alteration of the interaction of components of MPF. More specifically, the invention relates to inhibiting transcription or translation of mammalian CDC25A genes using oligonucleotides.

US Patent:

7425617, Sep 16, 2008

Filed:

Jan 30, 1998

Appl. No.:

09/016869

Inventors:

David H. Beach - Huntington Bay NY, US
Douglas J. Demetrick - Northport NY, US
Manuel Serrano - Mill Neck NY, US
Gregory J. Hannon - Huntington NY, US

Assignee:

Cold Spring Harbor Laboratory - Cold Spring Harbor NY

International Classification:

C07K 16/00

US Classification:

5303871, 5303881, 5303891

Abstract:

The present invention relates to the discovery in eukaryotic cells, particularly mammalian cells, of a family of cell-cycle regulatory proteins (“CCR-proteins”). As described herein, this family of proteins includes a polypeptide having an apparent molecular weight of 16 kDa, and a polypeptide having an apparent molecular weight of approximately 15 kDa, each of which can function as an inhibitor of cell-cycle progression, and therefore ultimately of cell growth. The present invention comprises antibodies directed to such CCR-proteins.

US Patent:

7550561, Jun 23, 2009

Filed:

Apr 14, 1994

Appl. No.:

08/227371

Inventors:

David H. Beach - Huntington Bay NY, US
Douglas J. Demetrick - E. Northport NY, US
Manuel Serrano - Mill Neck NY, US
Gregory J. Hannon - Huntington NY, US

Assignee:

Cold Spring Harbor Laboratory - Cold Spring Harbor NY

International Classification:

C12Q 1/68
C12P 21/04
C07K 14/435

US Classification:

530350, 530324, 530352, 530395, 530402, 530403, 435 6, 435 691, 435 697

Abstract:

The present invention relates to the discovery in eukaryotic cells, particularly human cells, a novel polypeptide of 16 kDa (hereinafter “p16” or “p16”) can function as an inhibitor of cell cycle progression, and therefore ultimately of cell growth, and that similar to the role of p21 and p53, the p16 protein may function coordinately with the cell cycle regulatory protein, retinoblastoma (Rb).

US Patent:

7691632, Apr 6, 2010

Filed:

Aug 20, 2008

Appl. No.:

12/195135

Inventors:

David H. Beach - Huntington Bay NY, US
Douglas J. Demetrick - Northport NY, US
Manuel Serrano - Mill Neck NY, US
Gregory J. Hannon - Huntington NY, US

Assignee:

Cold Spring Harbor Laboratory - Cold Spring Harbor NY

International Classification:

C07K 16/00

US Classification:

435810, 5303871

Abstract:

The present invention relates to the discovery in eukaryotic cells, particularly mammalian cells, of a family of cell-cycle regulatory proteins (“CCR-proteins”). As described herein, this family of proteins includes a polypeptide having an apparent molecular weight of 16 kDa, and a polypeptide having an apparent molecular weight of approximately 15 kDa, each of which can function as an inhibitor of cell-cycle progression, and therefore ultimately of cell growth. The present invention comprises antibodies directed to such CCR-proteins. The present invention is directed to a kit for detecting the level of cyclin-dependent kinase inhibitor p16 gene expression comprising antibodies directed to a p16 protein.

US Patent:

20030100489, May 29, 2003

Filed:

Sep 4, 2001

Appl. No.:

09/947206

Inventors:

David Beach - Huntington Bay NY, US
Douglas Demetrick - E. Northport NY, US
Manuel Serrano - Mill Neck NY, US
Gregory Hannon - Huntington NY, US

International Classification:

A61K038/55
C12N009/99

US Classification:

514/012000, 435/184000, 435/069200, 435/320100, 435/325000

Abstract:

The present invention relates to the discovery in eukaryotic cells, particularly mammalian cells, of a novel family of cell-cycle regulatory proteins (“CCR-proteins”). As described herein, this family of proteins includes a polypeptide having an apparent molecular weight of 16 kDa, and a polypeptide having an apparent molecular weight of approximately 15 kDa, each of which can function as an inhibitor of cell-cycle progression, and therefore ultimately of cell growth. Thus, similar to the role of p21 to the p53 checkpoint, the subject CCR-proteins may function coordinately with the cell-cycle regulatory protein, retinoblastoma (RB). Furthermore, the CCR-protein family includes a protein having an apparent molecular weight of 13.5 kDa (hereinafter “p13.5”). The presumptive role of p13.5, like p16 and p15, is in the regulation of the cell-cycle.