Expression profiling HeLa DOCK6 knockout clones 1 and 45 compared to wild type cells
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ABSTRACT: We described a striking divergence between the phenotypes arising from acute (siDOCK6) and chronic (DOCK6 KO cells) depletion is highly suggestive of a suppression mechanism that buffers the prolonged absence of DOCK6. To identify the factor(s) that compensate for the lack of DOCK6 activity, we compared the expression profiles of two independent DOCK6 KO HeLa clones (KO1 and KO45) with wild type control cells. See related experiment: E-MTAB-5067
Project description:We described a striking divergence between the phenotypes arising from acute (siDOCK6) and chronic (DOCK6 KO cells) depletion is highly suggestive of a suppression mechanism that buffers the prolonged absence of DOCK6. This mechanism is probably also active in AOS patients who harbor homozygous loss-of-function mutations in DOCK6 because the actin organization patterns in their fibroblasts resemble those of DOCK6 KO cells (Shaheen et al., 2011). To identify the factor(s) that compensate for the lack of DOCK6 activity, we compared mRNA profiles of fibroblasts isolated from an AOS patient who harbored a homozygous 4 base pair deletion in the DOCK6 gene (c.1362_1365delAACT, p.Thr455Serfs*24; RefSeq accession number: NM_020812.2) with two healthy controls (Shaheen et al., 2011)
Project description:We find that 499 genes are up-regulated and 457 are down-regulated in response to over-expression of JADE1, while 397 genes are up-regulated and 385 are down-regulated after HBO1 knock-down. For each condition - HBO1 siRNA treatment or JADE1 over-expression - two biological replicates were analyzed in duplicate.
Project description:Epithelial ovarian cancer (EOC) is the leading cause of death among all gynecological malignancies due to high rate of disease relapse. Disease relapse in cancer patients after clinical remission are often referred to tumor dormancy. Here we identify the RNA polymerase II transcriptional Mediator subunit 12 (MED12) as an important molecular regulator of tumor dormancy. We found that MED12 knock-out (KO) could induce dormancy of EOC cells in vitro and in vivo. Mechanistically, microarray analysis showed that MED12 KO decreased the expression of EGFR. Hierarchical cluster assays of the differentially expressed genes between SKOV3 KO1#_Vector and SKOV3 KO1#_MED12 cells
Project description:This SuperSeries is composed of the following subset Series: GSE33007: Genome-wide map of HBO1 in cancer derived human cell line GSE33220: Effects of the JADE-HBO1 complex on gene expression Refer to individual Series
Project description:Mex3a is an RNA binding protein of unknown function. To elucidate the contribution of Mex3a to tumoral heterogeneity, Mex3a KO organoids engineered by CRISPR were sequenced in three different conditions. Live organoids (DAPI negative) were sorted in Control, after 2 days of FOLFIRI and after 5 days of treatment. Two WT organoids (parental and a derived clone) and two KO (KO1 and KO2, two independent clones) were used for this experiment.
Project description:We used the CRISPR/Cas9 technique to construct nbr1-KO lines (KO1 and KO3) in order to test the effects of AtNBR1 depletion. Reduced expression of several ABA-up regulated genes were observed in shoots of the two KO lines. Grant number: 2014/15/B/NZ3/04854 Grant funding source: National Science Centre (Poland) Grantee Name: Agnieszka Sirko Grant title: Upstream regulators and cellular targets of the selective autophagy cargo receptor AtNBR1 in different phases of sulfur deficiency in plants.
Project description:We used the CRISPR/Cas9 technique to construct nbr1-KO lines (KO1 and KO3) in order to test the effects of AtNBR1 depletion. Reduced expression of several ABA-up regulated genes were observed in shoots of the two KO lines. Grant number: 2014/15/B/NZ3/04854 Grant funding source: National Science Centre (Poland) Grantee Name: Agnieszka Sirko Grant title: Upstream regulators and cellular targets of the selective autophagy cargo receptor AtNBR1 in different phases of sulfur deficiency in plants.
Project description:The ACBP knockout were created by targeted disruption of the gene in mice. The expression profiling was performed on liver tissue from ACBP-/- (KO) and +/+ (WT) mice at the age of 21 days, which in our study is the time immediately before weaning. The mice used for this experiment were taken directly away from their mother. Thus, having free access to chow and breast milk until sacrificed at 8-11am 15 ACBP-/- and 15 +/+ control mice divided into 6 groups (KO1, KO2, KO3, WT1, WT2 and WT3) with 5 individuals in each group were used for this study.
Project description:The experiment is intended to test the effect of the Cripsr/Cas9 deletion of the H2AFJ gene encoding the histone variant H2A.J on the transcriptome of luminal breast cancer T47D cells in conditions of proliferation, and after proliferative arrest induced by treating the cells with 5 µm tamoxifen for 4 days. Two independent H2A.J-KO cell lines were analyzed: KO1 and KO18.
Project description:Members of the Nuclear mRNA Export Factor (NXF) family are implicated in nuclear export and/or cytoplasmic transport of mRNAs in eukaryotic cells. We previously proposed NXF5 to be involved in cognitive development and aimed to study its functional role further using a mouse model. The syntenic region of the human Xcen-GLA-NXF5-NXF2-NXF3-BEX4-Xqter in the mouse is Xcen-Gla-Nxf2-Nxf7-Nxf3-Bex4-Xqter strongly indicating that mouse Nxf2 is the homolog of human NXF5. However, our functional analyses demonstrated that mouse Nxf7 is actually the functional homolog of NXF5. Both orthologs are expressed in brain, although at low levels, show predominant cytoplasmic localization, and present a granular staining in neuronal dendrites, all indicative for a role in cytoplasmic mRNA transport or metabolism. The mouse and human Nxf2/NXF2 proteins on the other hand, show highest expression in testis, and mostly nuclear staining with incorporation in the nuclear membrane, suggesting a predominant role in nuclear mRNA export. Based on these findings we generated an Nxf7 knockout mouse, which was viable and fertile and no gross anatomical changes or morphological brain abnormalities were detected. Detailed behavioral analysis demonstrated that Nxf7 KO mice displayed a deficit in hippocampus-dependent spatial learning and memory. At the cellular level, this was accompanied by impaired hippocampal long-term potentiation, but normal long-term depression, suggesting a severe functional imbalance in NMDA-dependent synaptic plasticity. In conclusion, the present findings indicate that NXF5, and its murine ortholog Nxf7, play a crucial role in neurocognitive (memory) functions, and explain why its deletion leads to intellectual disability. Two male wild type (WT1 and WT2) and two Nxf7 knockout (KO1 and KO2) mice were used in each hybridization experiment (hippocampus or cortex). A loop-design hybridization scheme (WT1/KO1, KO1/WT2, WT2/KO2 and KO2/WT1) was performed for each experiment so as to have each sample labeled once with Cy5 and once with Cy3, and hybridised to both samples of the other genotype (WT or KO). Hybridization was done on Agilent Mouse Whole Genome arrays according to the manufacturerM-bM-^@M-^Ys procedures.