Shyamal D Desai

US Patent:

20100111874, May 6, 2010

Filed:

Mar 17, 2008

Appl. No.:

12/532375

Inventors:

Leroy F. Liu - Bridgewater NJ, US
Shyamal Desai - Somerset NJ, US
Johnson Yin-Nam Lau - Newport Beach CA, US

Assignee:

University of Medicine and Dentistry of New Jresey - Somerset NJ

International Classification:

A61K 49/00
A61K 31/203
A61K 38/21
A61K 38/19
A61K 31/4375
C12Q 1/68
G01N 33/53
G01N 33/574
A61P 35/00

US Classification:

424 92, 514559, 424 854, 424 851, 514283, 435 6, 435 721, 435 723

Abstract:

The present invention provides methods for detecting and treating cancer. In some embodiments, levels of ISG15 are determined, and topoisomerase I and II inhibitors as well as other DNA-damaging agents plus agents that increase the expression of ISG15 are selected and administered.

US Patent:

20210320969, Oct 14, 2021

Filed:

Mar 29, 2021

Appl. No.:

17/215980

Inventors:

- Baton Rouge LA, US
Shyamal D. Desai - Metairie LA, US

International Classification:

H04L 29/08

Abstract:

This invention is directed to compositions and methods for detecting proteinopathies.

US Patent:

20180120334, May 3, 2018

Filed:

Nov 17, 2017

Appl. No.:

15/816998

Inventors:

- BATON ROUGE LA, US
Shyamal D. Desai - Metairie LA, US

International Classification:

G01N 33/68
A61K 31/52
A61K 31/713

Abstract:

This invention is directed to compositions and methods for detecting proteinopathies.

US Patent:

20170196871, Jul 13, 2017

Filed:

Mar 21, 2017

Appl. No.:

15/464473

Inventors:

Shyamal D. Desai - Metairie LA, US

Assignee:

Board of Supervisors of Louisiana State University and Agricultural and Mechanical College - New Orleans LA

International Classification:

A61K 31/52
G01N 33/68

Abstract:

ATM kinase is shown to regulate proteasome-mediated protein turnover through suppression of the expression of the ubiquitin-like protein ISG15 (Interferon Stimulated Gene 15). Silencing of the ISG15 pathway restored both the ubiquitin and autophagy pathways, and the UV-mediated degradation of their substrates in A-T cells. The ATM kinase negatively regulates the ISG15 pathway, and the constitutively elevated ISG15 pathway induces proteinopathy in A-T cells, and in A-T patients. These findings indicate that proteasome-mediated protein degradation is impaired in A-T cells due to elevated expression of the ISG15 conjugation pathway, which contributes to progressive neurodegeneration in A-T patients. The ISG15 pathway is a new target for both detection and treatment of A-T. Inhibitors if ISG15 expression can be used to inhibit or attenuate neurodegeneration in A-T patients. In addition, an inhibitor of the early phase of autophagy, 3-MA, was shown to be effective in decreasing the impaired proteasome-mediated protein degradation in A-T cells, and thus would be effective in decreasing the neurodegeneration in A-T patients.

US Patent:

20160216279, Jul 28, 2016

Filed:

Nov 29, 2012

Appl. No.:

13/688384

Inventors:

Shyamal D. Desai - Metairie LA, US

International Classification:

G01N 33/68
A61K 31/52
A61K 31/713

Abstract:

ATM kinase is shown to regulate proteasome-mediated protein turnover through suppression of the expression of the ubiquitin-like protein ISG15 (Interferon Stimulated Gene 15). Silencing of the ISG15 pathway restored both the ubiquitin and autophagy pathways, and the UV-mediated degradation of their substrates in A-T cells. The ATM kinase negatively regulates the ISG15 pathway, and the constitutively elevated ISG15 pathway induces proteinopathy in A-T cells, and in A-T patients. These findings indicate that proteasome-mediated protein degradation is impaired in A-T cells due to elevated expression of the ISG15 conjugation pathway, which contributes to progressive neurodegeneration in A-T patients. The ISG15 pathway is a new target for both detection and treatment of A-T Inhibitors if ISG15 expression can be used to inhibit or attenuate neurodegeneration in A-T patients. In addition, an inhibitor of the early phase of autophagy, 3-MA, was shown to be effective in decreasing the impaired proteasome-mediated protein degradation in A-T cells, and thus would be effective in decreasing the neurodegeneration in A-T patients.