ABSTRACT: Differential gene expression profiles between SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid).
Project description:To dissect the molecular mechanisms of PEA-15-mediated paclitaxel sensitization in ovarian cancer cells, we performed cDNA microarray analysis using SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid). cDNA microarray data analysis showed that SCLIP (SCG10-like protein), also known as STMN3, was highly expressed in SKOV3.ip1-S116D cells and was involved in pPEA-15-mediated paclitaxel sensitization in ovarian cancer cells.
Project description:To dissect the molecular mechanisms of PEA-15-mediated paclitaxel sensitization in ovarian cancer cells, we performed cDNA microarray analysis using SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid). cDNA microarray data analysis showed that SCLIP (SCG10-like protein), also known as STMN3, was highly expressed in SKOV3.ip1-S116D cells and was involved in pPEA-15-mediated paclitaxel sensitization in ovarian cancer cells. SKOV3.ip1-S116A cells (Ser116 of PEA-15 substituted with alanine) and SKOV3.ip1-S116D cells (Ser116 of PEA-15 substituted with aspartic acid) were used. Total RNA was extracted and purified using RNeasy mini kit (Qiagen, Inc.) according to the manufacturerM-bM-^@M-^Ys instructions. The integrity of the obtained RNA was assessed using an Agilent 2100 BioAnalyzer (Agilent Technologies). The Affymetrix HGU133 plus platform was used for hybridization, staining, and imaging of the arrays by following the manufacturerM-bM-^@M-^Ys instructions. Gene expression analysis was performed in triplicate.
Project description:Sensitivity to cisplatin is increased in SKOV-3 cells after transfecting the cells with unphosphorylatable PEA-15 (PEA-15AA) but not in cells transfected with the empty vector and phosphomimetic PEA-15 (PEA-15DD). In order to investigate the regulation of the underlying genes that increased the sensitivity to cisplatin after transfection with PEA-15AA, a small and well-annotated Clariom S gene microarray was performed.
Project description:Purpose: Identify differentially expressed genes between 5 pea aphid morphs Methods: Collected whole bodies of 30 adult aphids of each of the five pea morphs and three clones (total of 15 samples)
Project description:ChIP-seq experiment for histone H3 and H3K4me3 from wild-type Saccharomyces cerevisiae (WT) and strains in which H3K14 has been substituted for alanine (K14A) or H3P16 has been substituted with valine (P16V).
Project description:Purpose: Identify differentially expressed genes between 5 pea aphid morphs Methods: Collected whole bodies of 30 adult aphids of each of the five pea morphs and three clones (total of 15 samples) 5 pea aphid morphs * 3 genotypes = 15 samples
Project description:To investigate the downstream effects of a polymorphism in the pyk1 gene of Schizosaccharomyces pombe (A343T) we generated a strain that differed from the lab strain (JB50) only in the amino acid at position 343 of pyk1 where a threonine was substituted with an alanine. Five replicates were grown for each strain and harvested in log phase. From each of these cultures RNA was isolated and underwent polyA-enrichment. Reads were sequenced and mapped against the strain-specific genomes.
Project description:To define the function of FOXA1-S331 phosphorylation, we substituted S331 in both FOXA1 alleles for alanine in C4-2 cells via CRISPR/Cas9-based gene editing, thereby generating phosphorylation incompetent FOXA1S331A cells. We directly assessed the consequences of phospho-incompetent FOXA1S331A mutation on the transcription profile, chromatin deposition of FOXA1, AR, H3K27ac and chromatin accessibility.
Project description:To define the function of FOXA1-S331 phosphorylation, we substituted S331 in both FOXA1 alleles for alanine in C4-2 cells via CRISPR/Cas9-based gene editing, thereby generating phosphorylation incompetent FOXA1S331A cells. We directly assessed the consequences of phospho-incompetent FOXA1S331A mutation on the transcription profile, chromatin deposition of FOXA1, AR, H3K27ac and chromatin accessibility.
Project description:To define the function of FOXA1-S331 phosphorylation, we substituted S331 in both FOXA1 alleles for alanine in C4-2 cells via CRISPR/Cas9-based gene editing, thereby generating phosphorylation incompetent FOXA1S331A cells. We directly assessed the consequences of phospho-incompetent FOXA1S331A mutation on the transcription profile, chromatin deposition of FOXA1, AR, H3K27ac and chromatin accessibility.
