US2016122769A1PendingUtilityA1

Method of screening for chaperonin modulator

Assignee: POSTECH ACAD IND FOUNDPriority: Aug 24, 2011Filed: Jan 7, 2016Published: May 5, 2016
Est. expiryAug 24, 2031(~5.1 yrs left)· nominal 20-yr term from priority
A61P 25/16A61P 25/28A61P 25/14G01N 2500/04C12N 2310/14A61K 45/00G01N 2800/2821C12Q 1/6883C12Q 1/485C12N 2320/30C12Q 2600/136A61K 31/7088C12Q 1/25G01N 2500/02A61K 31/713C12N 15/1137G01N 33/573C12Q 1/6809G01N 2800/2835A61P 25/00C12Q 2600/158C12Q 2600/178G01N 33/68G01N 33/53
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Claims

Abstract

The present invention relates to a method of screening for modulator of chaperonin that is involved in protein aggregation inducing neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and Huntington's disease, use of the chaperonin modulator screened by the method for prevention and treatment of neurodegenerative diseases. According to the present invention, novel negative chaperonin modulator is provided, and chaperonin modulator may be more rapidly and conveniently screened with the negative modulator as a target. Furthermore, by using the screened material, neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and Huntington's disease may be effectively prevented or treated without concern for cell death due to autophagy, which is the existing method of removing protein aggregate.

Claims

exact text as granted — not AI-modified
What is claimed is: 
     
         1 . A method of screening for a TRiC/CCT modulator comprising
 1) preparing candidate material and at least one selected from the group consisting of VRK2 and COP1;   2) measuring the expression amount or enzyme activity of COP1, or the binding between the VRK2 and COP1; and   3) treating COP1 with the candidate material and measuring a change in the expression amount or the enzyme activity of COP1, or the binding between the VRK2 and COP1; and   4) determining the candidate material as a material that increases the amount or stability of TRiC/CCT protein if the expression amount or enzyme activity of COP1 has been decreased compared to untreated control,   determining the candidate material as a material that decreases the amount or stability of TRiC/CCT protein if the expression amount or enzyme activity of COP1 has been increased compared to untreated control, or   determining the candidate material as a material that increases the expression amount or stability of TRiC/CCT protein if binding between the VRK2 and COP1 is inhibited by treatment of the candidate material.   
     
     
         2 . A method for preventing or treating a neurodegenerative disease comprising administering a material that increases an expression amount or a stability of TRiC/CCT protein, screened by the method of  claim 1 , as an active ingredient, to a subject in need. 
     
     
         3 . The method for preventing or treating a neurodegenerative disease according to  claim 2 , wherein the material that increases the amount or the stability of TRiC/CCT protein is one or more selected from the group consisting of double stranded siVRK2 consisting of a single stranded siVRK2 (SEQ ID NO: 1) and a complementary strand thereof, double stranded siCOP1 consisting of a single stranded siCOP1 (SEQ ID NO: 2) and a complementary strand thereof, and double stranded siRBX1 consisting of a single stranded siRBX1 (SEQ ID NO: 3) and a complementary strand thereof. 
     
     
         4 . The method for preventing or treating a neurodegenerative disease according to  claim 2 , wherein the material that increases the amount or the stability of TRiC/CCT protein is contained at an amount of 0.0001 to 99.9 wt %. 
     
     
         5 . The method for preventing or treating a neurodegenerative disease according to  claim 2 , wherein the neurodegenerative disease is Alzheimer's disease, Parkinson's disease, or Huntington's disease.

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