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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Lietman, Caressa D; Marom, Ronit; Munivez, Elda et al. (2015) A transgenic mouse model of OI type V supports a neomorphic mechanism of the IFITM5 mutation. J Bone Miner Res 30:489-98
Han, Kihoon; Chen, Hogmei; Gennarino, Vincenzo A et al. (2015) Fragile X-like behaviors and abnormal cortical dendritic spines in cytoplasmic FMR1-interacting protein 2-mutant mice. Hum Mol Genet 24:1813-23
Haltom, Amanda R; Lee, Tom V; Harvey, Beth M et al. (2014) The protein O-glucosyltransferase Rumi modifies eyes shut to promote rhabdomere separation in Drosophila. PLoS Genet 10:e1004795
Grafe, Ingo; Yang, Tao; Alexander, Stefanie et al. (2014) Excessive transforming growth factor-? signaling is a common mechanism in osteogenesis imperfecta. Nat Med 20:670-5
Wu, Chia-Shan; Morgan, Daniel; Jew, Chris P et al. (2014) Long-term consequences of perinatal fatty acid amino hydrolase inhibition. Br J Pharmacol 171:1420-34
Stashi, Erin; Lanz, Rainer B; Mao, Jianqiang et al. (2014) SRC-2 is an essential coactivator for orchestrating metabolism and circadian rhythm. Cell Rep 6:633-45
Sillitoe, Roy V; George-Jones, Nicholas A; Millen, Kathleen J et al. (2014) Purkinje cell compartmentalization in the cerebellum of the spontaneous mutant mouse dreher. Brain Struct Funct 219:35-47
Yamamoto, Shinya; Jaiswal, Manish; Charng, Wu-Lin et al. (2014) A drosophila genetic resource of mutants to study mechanisms underlying human genetic diseases. Cell 159:200-14
Zhu, Gengzhen; Li, Yujing; Zhu, Fei et al. (2014) Coordination of engineered factors with TET1/2 promotes early-stage epigenetic modification during somatic cell reprogramming. Stem Cell Reports 2:253-61
Homan, Erica P; Lietman, Caressa; Grafe, Ingo et al. (2014) Differential effects of collagen prolyl 3-hydroxylation on skeletal tissues. PLoS Genet 10:e1004121

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