The Genome-wide RNAi Analysis Core is a newly established resource at BCM facilitated by the generous support of the Kleberg Foundation, BCM, and the Dept. of Biochemistry &Molecular Biology. While this Core became operational in May 2008, its support of the research programs of BCM and BCM-IDDRC investigators can already be seen by successful genetic screens ongoing in the Core. For instance. Dr. Westbrook is currently conducting a genetic screen for modifiers of REST, a master regulator of neural differentiation programs. This screen is designed to identify new pathways in nervous system function and development using the pooled shRNA-barcoding approach described above. In addition, Dr. Zoghbi's laboratory is in the process of performing a genetic screen for potential therapeutic targets in Spinocerebellar Ataxia type 1 (SCA1). This screen, which combines the shRNA library resource, high-throughput robotics, and flow cytometry of the Core, will identify new therapeutic targets for SCA1 and serve as a roadmap for finding treatments in other neurologic disorders. The potential for the Genome-wide RNAi Analysis Core to facilitate the objectives and research plans for numerous BCM-IDDRC investigators is evident from the proposed utilization by projects listed below. To gauge the level of demand for this newly proposed core among currently supported BCM-IDDRC investigators, a poll was taken. Nearly three quarters of investigators expressed enthusiasm for the core. Its availability will allow future BCM-IDDRC investigators to propose future projects that will take advantage of this type of screening facility. For those projects listed below in proposed utilization, there is immediate demand. It is likely based on the survey of BCM-IDDRC investigators who anticipate using the Core that demand will increase in future years. It is likely that additional

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Center Core Grants (P30)
Project #
5P30HD024064-24
Application #
8382001
Study Section
Special Emphasis Panel (ZHD1-MRG-C)
Project Start
Project End
Budget Start
2012-07-01
Budget End
2013-06-30
Support Year
24
Fiscal Year
2012
Total Cost
$202,634
Indirect Cost
$52,635
Name
Baylor College of Medicine
Department
Type
DUNS #
051113330
City
Houston
State
TX
Country
United States
Zip Code
77030
Kho, Jordan; Tian, Xiaoyu; Wong, Wing-Tak et al. (2018) Argininosuccinate Lyase Deficiency Causes an Endothelial-Dependent Form of Hypertension. Am J Hum Genet 103:276-287
Eblimit, Aiden; Zaneveld, Smriti Agrawal; Liu, Wei et al. (2018) NMNAT1 E257K variant, associated with Leber Congenital Amaurosis (LCA9), causes a mild retinal degeneration phenotype. Exp Eye Res 173:32-43
Lanzieri, Tatiana M; Chung, Winnie; Leung, Jessica et al. (2018) Hearing Trajectory in Children with Congenital Cytomegalovirus Infection. Otolaryngol Head Neck Surg 158:736-744
Madan, Simran; Kron, Bettina; Jin, Zixue et al. (2018) Arginase overexpression in neurons and its effect on traumatic brain injury. Mol Genet Metab 125:112-117
De Maio, Antonia; Yalamanchili, Hari Krishna; Adamski, Carolyn J et al. (2018) RBM17 Interacts with U2SURP and CHERP to Regulate Expression and Splicing of RNA-Processing Proteins. Cell Rep 25:726-736.e7
Reeber, Stacey L; Arancillo, Marife; Sillitoe, Roy V (2018) Bergmann Glia are Patterned into Topographic Molecular Zones in the Developing and Adult Mouse Cerebellum. Cerebellum 17:392-403
Gillentine, Madelyn A; Lupo, Philip J; Stankiewicz, Pawel et al. (2018) An estimation of the prevalence of genomic disorders using chromosomal microarray data. J Hum Genet 63:795-801
Jin, Haoxing Douglas; Demmler-Harrison, Gail J; Coats, David K et al. (2017) Long-term Visual and Ocular Sequelae in Patients With Congenital Cytomegalovirus Infection. Pediatr Infect Dis J 36:877-882
Beaudet, Arthur L (2017) Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: A hypothesis. Bioessays 39:
Marom, Ronit; Jain, Mahim; Burrage, Lindsay C et al. (2017) Heterozygous variants in ACTL6A, encoding a component of the BAF complex, are associated with intellectual disability. Hum Mutat 38:1365-1371

Showing the most recent 10 out of 709 publications