Tracy Xiao Cui

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The regulation of c-fos transcription by GH involves multiple factors, including CCAAT/enhancer binding protein (C/EBP) beta. Knockdown of C/EBPbeta by RNA interference prevents stimulation of endogenous c-fos mRNA by GH, indicating a key role for C/EBPbeta in GH-stimulated c-fos transcription. GH rapidly increases the occupancy of both endogenous C/EBPbeta(More)
The transcription factor CCAAT/enhancer binding protein beta (C/EBPbeta) contains multiple acetylation sites, including lysine (K) 39. Mutation of C/EBPbeta at K39, an acetylation site in the transcriptional activation domain, impairs transcription of C/EBPbeta target genes in a dominant-negative fashion. Further, K39 of C/EBPbeta can be deacetylated by(More)
In examination of mechanisms regulating metabolic responses to growth hormone (GH), microarray analysis identified 561 probe sets showing time-dependent patterns of expression in GH-treated 3T3-F442A adipocytes. Biological functions significantly over-represented among GH-regulated genes include regulators of transcription at early times, and lipid(More)
TRAIL/Apo-2L, a novel cytokine, is a member of the tumor necrosis factor (TNF) family and serves as an extracellular signal triggering apoptosis. TRAIL/Apo-2L is capable of killing various transformed cells but not unstimulated primary T cells. In this study, five human glioma cells (U87, U118, U178, U563, and A172) were examined for their susceptibility to(More)
BACKGROUND Isolation of tracheal aspirate mesenchymal stromal cells (MSCs) from premature infants has been associated with increased risk of bronchopulmonary dysplasia (BPD). MSCs show high levels of mRNAs encoding matricellular proteins, non-structural extracellular proteins that regulate cell-matrix interactions and participate in tissue remodeling. We(More)
iii Recent findings have revealed a crucial contribution of the adhesion molecule neuroligin-1 to the precise organization and regulation of intercellular synaptic connections within the central nervous system, and disruption of neuroligin-1 signaling in vivo fosters cognitive abnormalities. Despite considerable recent progress, several uncertainties remain(More)
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