RAJINDER K KAUL
Medical Practice at 123, Miami, FL
License number
Florida 33684
Issued Date
May 31, 1995
Effective Date
Sep 28, 2000
Expiration Date
Jun 30, 1998
Category
Health Care
Type
Clinical Laboratory Personnel
Address
Address
7305 SW 123Rd St, Miami, FL 33156
Professional information
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Aspartoacylase Gene, Protein, And Methods Of Screening For Mutations Associated With Canavan Disease
Aspartoacylase Gene, Protein, And Methods Of Screening For Mutations Associated With Canavan Disease
US Patent:
7217547, May 15, 2007
Filed:
Oct 1, 2001
Appl. No.:
09/965807
Inventors:
Reuben Matalon - Coral Gables FL, US
Rajinder Kaul - Miami FL, US
Guang Ping Cao - Miami FL, US
Kuppareddi Balamurugan - Miami FL, US
Rajinder Kaul - Miami FL, US
Guang Ping Cao - Miami FL, US
Kuppareddi Balamurugan - Miami FL, US
Assignee:
Miami Children's Hospital - Miami FL
International Classification:
C12N 9/00, C07K 14/00, A61K 38/46
US Classification:
435183, 530350, 424 946
Abstract:
Canavan disease, an autosomal recessive leukodystrophy, is caused by deficiency of aspartoacylase and accumulation of N-acetylaspartic acid in brain. Human aspartoacylase (ASP) cDNA spanning 1,435 bp has been cloned and expressed in. A base change, a854>c, has been found in 85% of the 34 Canavan alleles tested so far, which results in a missense glu285>ala mutation that is predicted to be part of the catalytic domain of aspartoacylase. The invention therefore provides nucleic acid sequences, genes, polypeptides, antibodies, vectors containing the gene, host cells transformed with vectors containing the gene, animal models for the disease, methods for expressing the polypeptide, genetic screening methods and kits, diagnostic methods and kits, methods of treating Canavan disease and methods of genetic therapy for the disease.
Aspartoacylase Gene, Protein, And Methods Of Screening For Mutations Associated With Canavan Disease
Aspartoacylase Gene, Protein, And Methods Of Screening For Mutations Associated With Canavan Disease
US Patent:
2007002, Feb 1, 2007
Filed:
Oct 3, 2006
Appl. No.:
11/541665
Inventors:
Reuben Matalon - Coral Gables FL, US
Rajinder Kaul - Miami FL, US
Guang Cao - Miami FL, US
Kuppareddi Balamurugan - Miami FL, US
Rajinder Kaul - Miami FL, US
Guang Cao - Miami FL, US
Kuppareddi Balamurugan - Miami FL, US
International Classification:
C12Q 1/68, G01N 33/53, C07H 21/04, C12P 21/06, C12N 9/80
US Classification:
435006000, 435069100, 435228000, 435320100, 435325000, 536023200, 435007100
Abstract:
Canavan disease, an autosomal recessive leukodystrophy, is caused by deficiency of aspartoacylase and accumulation of N-acetylaspartic acid in brain. Human aspartoacylase (ASP) cDNA spanning 1,435 bp has been cloned and expressed in . A base change, a854>c, has been found in 85% of the 34 Canavan alleles tested so far, which results in a missense glu285>ala mutation that is predicted to be part of the catalytic domain of aspartoacylase. The invention therefore provides nucleic acid sequences, genes, polypeptides, antibodies, vectors containing the gene, host cells transformed with vectors containing the gene, animal models for the disease, methods for expressing the polypeptide, genetic screening methods and kits, diagnostic methods and kits, methods of treating Canavan disease and methods of genetic therapy for the disease.
Aspartoacylase Gene, Protein, And Methods Of Screening For Mutatons Associated With Canavan Disease
Aspartoacylase Gene, Protein, And Methods Of Screening For Mutatons Associated With Canavan Disease
US Patent:
5679635, Oct 21, 1997
Filed:
Sep 9, 1994
Appl. No.:
8/302449
Inventors:
Reuben Matalon - Coral Gables FL
Rajinder Kaul - Miami FL
Guang Ping Gao - Miami FL
Kuppareddi Balamurugan - Miami FL
Rajinder Kaul - Miami FL
Guang Ping Gao - Miami FL
Kuppareddi Balamurugan - Miami FL
Assignee:
Miami Children's Hospital Research Institute, Inc. - Miami FL
International Classification:
C12Q 168, C12P 1934, C07H 2102, C07H 2104
US Classification:
435 6
Abstract:
Canavan disease, an autosomal recessive leukodystrophy, is caused by deficiency of aspartoacylase and accumulation of N-acetylaspartic acid in brain. Human aspartoacylase (ASP) cDNA spanning 1,435 bp has been cloned and expressed in E. coli. A base change, a854>c, has been found in 85% of the 34 Canavan alleles tested so far, which results in a missense glu285>ala mutation that is predicted to be part of the catalytic domain of aspartoacylase. Several additional mutations have also been identified. The invention therefore provides nucleic acid sequences, genes, polypeptides, antibodies, vectors containing the gene, host cells transformed with vectors containing the gene, animal models for the disease, methods for expressing the polypeptide, genetic screening methods and kits, diagnostic methods and kits, methods of treating Canavan disease and methods of genetic therapy for the disease.