The High-throughput Genomic and RNA Analysis (HGRA) Core for the Baylor College of Medicine (BCM) Intellectual and Developmental Disabilities Research Center (IDDRC) utilizes the resources and knowledge base of the Microarray Core Facility (MCF) at BCM. This newly named core represents a combination of two previously funded IDDRC cores (Core B2: Genomic Array Core and Core C4: Expression Array Core). As a new activity, the core will also offer next generation sequencing technology to users. Originally the Genomic Array Core was set up to offer array comparative genomic hybridization (aCGH) to users of the BCM-IDDRC. Since that time the BCM Medical Genetics Laboratories (a CLIA certified lab environment) developed a targeted aCGH platform which is called Chromosomal Microarray Analysis (CMA). In 2006, Dr. Lisa D. White became Technical Director of the CLIA CMA lab and many of the BCM-IDDRC researchers began using that laboratory for their aCGH. The switch to the CLIA lab has been stunningly successful and of immense benefit to the IDD community as illustrated by the large numbers of publications listed below. A very large number of new genetic etiologies for IDD have resulted from these efforts. The HGRA will continue to offer aCGH as a research activity for members of the BCM-IDDRC as an adjunct to the clinical efforts. The HGRA core will combine cutting edge technologies to provide state-of-the-art quality microarray-based and next generation sequencing-based services and analyses for both transcriptional and genomic profiling. The MCF was established in 1999 with funds from BCM, the National Cancer Institute and the National Eye Institute to develop microarray resources for BCM researchers. With the restructuring of the HGRA core, our purpose expands to providing assistance to BCM-IDDRC researchers in utilizing microarray technology, next generation sequencing technology, good experimental design, and data management and data analysis resources. We will begin offering next generation sequencing technology (Illumina Genome Analyzer II) to BCM-IDDRC members in March 2009.

National Institute of Health (NIH)
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Center Core Grants (P30)
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Special Emphasis Panel (ZHD1-MRG-C)
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Baylor College of Medicine
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Itami, Chiaki; Huang, Jui-Yen; Yamasaki, Miwako et al. (2016) Developmental Switch in Spike Timing-Dependent Plasticity and Cannabinoid-Dependent Reorganization of the Thalamocortical Projection in the Barrel Cortex. J Neurosci 36:7039-54
Herrera, José A; Ward, Christopher S; Wehrens, Xander H T et al. (2016) Methyl-CpG binding-protein 2 function in cholinergic neurons mediates cardiac arrhythmogenesis. Hum Mol Genet :
Machol, Keren; Jain, Mahim; Almannai, Mohammed et al. (2016) Corner fracture type spondylometaphyseal dysplasia: Overlap with type II collagenopathies. Am J Med Genet A :
Grafe, Ingo; Alexander, Stefanie; Yang, Tao et al. (2016) Sclerostin Antibody Treatment Improves the Bone Phenotype of Crtap(-/-) Mice, a Model of Recessive Osteogenesis Imperfecta. J Bone Miner Res 31:1030-40
Ure, Kerstin; Lu, Hui; Wang, Wei et al. (2016) Restoration of Mecp2 expression in GABAergic neurons is sufficient to rescue multiple disease features in a mouse model of Rett syndrome. Elife 5:
Radtke-Schuller, Susanne; Schuller, Gerd; Angenstein, Frank et al. (2016) Brain atlas of the Mongolian gerbil (Meriones unguiculatus) in CT/MRI-aided stereotaxic coordinates. Brain Struct Funct 221 Suppl 1:1-272
Fountain, Michael D; Aten, Emmelien; Cho, Megan T et al. (2016) The phenotypic spectrum of Schaaf-Yang syndrome: 18 new affected individuals from 14 families. Genet Med :
Patil, Vinit V; Guzman, Miguel; Carter, Angela N et al. (2016) Activation of extracellular regulated kinase and mechanistic target of rapamycin pathway in focal cortical dysplasia. Neuropathology 36:146-56
White, Janson; Beck, Christine R; Harel, Tamar et al. (2016) POGZ truncating alleles cause syndromic intellectual disability. Genome Med 8:3
Rajagopal, Abbhirami; Homan, Erica P; Joeng, Kyu Sang et al. (2016) Restoration of the serum level of SERPINF1 does not correct the bone phenotype in Serpinf1 null mice. Mol Genet Metab 117:378-82

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