HUDA ZOGHBI, MD
Medical Practice at Fannin St, Houston, TX

6709817, Mar 23, 2004

Sep 7, 2000

09/657013

Huda Y. Zoghbi - Houston TX
Ignatia B. Van den Veyver - Bellaire TX
Ruthie Amir - Haifa, IL
Uta Francke - Los Altos Hills CA

Baylor College of Medicine - Houston TX

C12Q 168

435 6

The present invention relates to the identification of mutations in a gene encoding a methyl-CpG-binding domain containing protein or alterations in its corresponding protein in neurodevelopmental disease. The protein acts in a complex to regulate transcriptional repression through methylated CpG dinucleotides. Methods to screen mutations in said gene or alterations in said protein related to neurodevelopmental disease are provided. Methods to treat a vertebrate with said disease are also provided.

2001003, Oct 18, 2001

Jun 19, 2001

09/884384

Huda Zoghbi - Houston TX, US
Harry Orr - Minneapolis MN, US
Christopher Cummings - San Francisco CA, US

A01K067/00, A01K067/027

800/013000, 800/018000

The present invention provides a novel method for treating neurodegenerative disease in mammals. This method involves the introduction of a therapeutic effective amount of a chaperone, a chaperone-like-compound or a compound which increases proteasome activity into the neurological system of the mammal. There is also a novel method for screening for compounds having chaperone-like activity or having activity to increase proteasome activity. The screening works in either cultured cells or animal models.

2001002, Oct 4, 2001

May 28, 1999

09/321916

HUDA Y. ZOGHBI - HOUSTON TX, US
HARRY T. ORR - MINNEAPOLIS MN, US
DONALD B. DEFRANCO - PITTSBURGH PA, US
MICHAEL A. MANCINI - HOUSTON TX, US
DAVID STENOIEN - HOUSTON TX, US
CHRISTOPHER J. CUMMINGS - HOUSTON TX, US

A61K048/00, A01K067/00

514/044000, 514/002000, 800/013000

The present invention provides a novel method for treating neurodegenerative disease in mammals. This method involves the introduction of a therapeutic effective amount of a chaperone, a chaperone-like-compound or a compound which increases proteasome activity into the neurological system of the mammal. There is also a novel method for screening for compounds having chaperone-like activity or having activity to increase proteasome activity. The screening works in either cultured cells or animal models.

2002019, Dec 19, 2002

Dec 5, 2001

10/004717

Huda Zoghbi - Houston TX, US
Qi Yang - The Woodlands TX, US

C12Q001/68, G01N033/567, C12N005/08

435/006000, 435/366000, 435/007210

Compositions and methods are disclosed for the therapeutic use of an atonal-associated nucleic acid or amino acid sequence. Also, an animal heterozygous for an atonal-associated gene inactivation is also disclosed having at least one atonal-associated nucleic acid sequence replaced by insertion of a heterologous nucleic acid sequence used to detect expression driven by an atonal-associated promoter sequence, wherein the inactivation of the atonal-associated nucleic acid sequence prevents expression of the atonal-associated gene.

2004007, Apr 22, 2004

Jul 14, 2003

10/618869

Edward Faeldt - Backefors, SE
Luis Serrano - Heidelberg, DE
Cayetano Gonzalez - Madrid, DE
Christian Boulin - Wiesloch, DE
Christopher Cummings - Brookline MA, US
Juan Botas - Houston TX, US
Huda Zoghbi - Houston TX, US

G06K009/00

382/128000

A method of system is provided for assaying specimens. In connection with such system or method, plural multi-pixel target images of a field of view are obtained at different corresponding points in time over a given sample period. A background image is obtained using a plural set of the plural target images. For a range of points in time, the background image is removed from the target images to produce corresponding background-removed target images. Analysis is performed using at least a portion of the corresponding background-removed target images to identify visible features of the specimens. A holding structure is provided to hold a set of discrete specimen containers. A positioning mechanism is provided to position a plural subset of the containers to place the moving specimens within the plural subset of the containers within a field of view of the camera.

6838444, Jan 4, 2005

Jun 1, 2000

09/585645

Huda Y. Zoghbi - Houston TX, US
Hugo J. Bellen - Houston TX, US
Nessan A. Bermingham - Houston TX, US
Bassem Hassan - Houston TX, US
Nissim Ben-Arie - Mevaseret Zion, IL

Baylor College of Medicine - Houston TX

A61K 3170, C07H 2102, C12N 1500

514 44, 536 231, 4353201

Compositions and methods are disclosed for the therapeutic use of an atonal-associated nucleic acid or amino acid sequence. Also, an animal heterozygous for an atonal-associated gene inactivation is also disclosed having at least one atonal-associated nucleic acid sequence replaced by insertion of a heterologous nucleic acid sequence used to detect expression driven by an atonal-associated promoter sequence, wherein the inactivation of the atonal-associated nucleic acid sequence prevents expression of the atonal-associated gene.

5741645, Apr 21, 1998

Jun 6, 1995

8/469802

Harry T. Orr - Minneapolis MN
Laura P. W. Ranum - St. Paul MN
Ming-Yi Chung - Minneapolis MN
Huda Y. Zoghbi - Houston TX

Regents of the University of Minnesota - Minneapolis MN

C12Q 168, C12P 1934, C07H 2104

435 6

The present invention provides an isolated DNA sequence of the short arm of chromosome 6 which is located within the autosomal dominant spinocerebellar ataxia type 1 gene. This isolated DNA sequence is preferably located within a 3. 36 kb EcoRI fragment, i. e. , an EcoRI fragment containing about 3360 base pairs, of the SCA1 gene. The isolated sequence preferably contains a CAG repeat region. The number of CAG trinucleotide repeats (n) is. ltoreq. 36, preferably n=19-36, for normal individuals. For an affected individual n>36, preferably n. gtoreq. 43.

5834183, Nov 10, 1998

Jun 28, 1994

8/267803

Harry T. Orr - Minneapolis MN
Laura P. W. Ranum - St. Paul MN
Ming-yi Chung - Minneapolis MN
Huda Y. Zoghbi - Houston TX

Regents of the University of Minnesota - Minneapolis MN

C12Q 168, C12P 1934, C07H 2104

435 6

The present invention provides an isolated DNA molecule of the autosomal dominant spinocerebellar ataxia type 1 gene, which is located within the short arm of chromosome 6. This isolated DNA molecule is preferably located within a 3. 36 kb EcoRI fragment, i. e. , an EcoRI fragment containing about 3360 base pairs, of the SCA1 gene. The isolated sequences contain a CAG repeat region. The number of CAG trinucleotide repeats (n) is. ltoreq. 36, preferably n=19-36, for normal individuals. For an affected individual n>36, preferably n. gtoreq. 43.

2004004, Mar 4, 2004

Jun 11, 2003

10/459188

Huda Zoghbi - Houston TX, US
Kei Watase - Houston TX, US
Christopher Cummings - Brookline MA, US

A01K067/027

800/018000

The present invention utilizes a “knock-in” approach to provide a transgenic mammal containing integrated into its genome a repeating nucleotide sequence encoding a polyglutamine comprising at least about 154, preferably at least about 160, 200, 300, 400, 500, and up to 600 or more contiguous glutamine residues. The transgenic mammals normally display observable phenotypic changes. As such, they may serve as a model for disease processes in humans for such diseases as spinobulbar muscular atrophy (SBMA), Huntington's disease (HD), dentatorubral pallidoluysian atrophy (DRPLA), and the spinocerebellar ataxias types 1, 2, 3, 6, 7, and 17. As a result of displaying pathology indicative of a human disease, the efficacy of an agent for treating human disease may be tested in the transgenic mammals.