Cross-species comparative gene expression profiling was performed to identify differentially expressed genes conserved in aggressive B lymphomas.
Identification of candidate B-lymphoma genes by cross-species gene expression profiling.
Sex, Specimen part
View SamplesGene expression profiles of rescue with wild type or SUMO double mutant TRIM24 after shRNA mediated knockdown of TRIM24 in MCF7 cell line Overall design: Gene expression profiles of rescue with wild type TRIM24 and SUMO double mutant, 3 replicate each
Cross-talk between chromatin acetylation and SUMOylation of tripartite motif-containing protein 24 (TRIM24) impacts cell adhesion.
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View SamplesRNA sequencing was performed to examine differential gene expression profiles in the ring gland of PG-specific Séance RNAi animals versus control. Overall design: Drosophila larvae with PG-specific knockdown of Séance and control animals were carefully staged at the larval L2/L3 molt. Ring glands were dissected at 44 hours L3. RNA isolated from ring glands were subject to RNA sequencing. Differential gene expression profiles were compared between control and RNAi animals.
Cooperative Control of Ecdysone Biosynthesis in <i>Drosophila</i> by Transcription Factors Séance, Ouija Board, and Molting Defective.
Specimen part, Subject
View SamplesUsp22, a component of the SAGA complex, is over expressed in highly aggressive cancers, but the normal functions of this deubiquitinase are not well defined. We determined that loss of Usp22 in mice results in embryonic lethality due to defects in extra-embryonic placental tissues and failure to establish proper vascular interactions with the maternal circulatory system. These phenotypes arise from abnormal gene expression patterns that reflect defective kinase signaling, including TGFß and several receptor tyrosine kinase (RTK) pathways. Usp22 deletion in endothelial cells and pericytes induced from embryonic stem cells also hinders these signaling cascades with detrimental effects on cell survival and differentiation as well as ability to form vessels. Our findings provide new insights to Usp22 functions during development that may offer clues to its role in disease states. Overall design: To determine changes in gene expression profile upon Usp22 loss in the developing placenta, RNA from day E9.5 placentas from wild-type and Ups22-/- mice s was isolated for deep sequencing, in triplicates and duplicates respectively. Key genes identified from RNAseq were validated by qRT-PCR using RNA from the same samples that were used for sequencing.
USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta.
Cell line, Subject
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