Project description:Microarray analysis revealed MCP-1 treatment altered protein folding processes in RCC CRL1932 cells. In response to MCP-1 treatment, CRL1932 cells and xenograft tumors expressed MCP-1-induced protein (MCPIP) which was reported to cause endoplasmic reticulum (ER) stress-induced apoptosis in human cardiomyocytes. In line with MCPIP induction, the expression of ER stress mediators, such as GRP78, PERK, IRE1α, and PDI, as well as molecules involved in ER stress-induced apoptosis, CHOP, calnexin, and Ero1α, presented in MCP-1 treated RCC cell line and xenograft tumors whereas absent or downregulated in untreated controls. TUNEL assay confirmed apoptosis of MCP-1 treated CRL1932 cells. MCPIP ectopically expressed in HEK293 cell resulted in apoptosis. Meta-analysis showed low level of MCP-1 associated with lower one year-survival rate after nephrectomy in RCC. In this dataset, we include the expression array data from human kidney cancer CRL-1932 cell line with or without the treatment of MCP-1. These data were used to obtain genes upregulated in MCP-1-treated CRL-1932 cells.
Project description:au13-04_cdtbis; cdt1_bis crl mutants and CDT1-RNAi lines have very similar macroscopic phenotypes as well as identical defects in plastid division and biogenesis. Our goal wwas to determine how much of these similarities originated from similar alterations of gene expression. Plantlets of crl mutant and CDT1-RNAi lines were grown in vitro on MS1/2 medium for 14 days. CDT1-RNAi lines were compared to the corresponding wild-type (Ws), whereas crl mutants were compared to their wild-type siblings and are in the Col0 ecotype.
Project description:We identified a recurrent gene fusion TRA2B-DNAH5 in human lung squamous cell carcinoma. This gene fusion can promote tumor growth in CRL-5889 xenograft tumors. Microarary was performed to identify these differential genes which may mediate the tumor promotive function of TRA2B-DNAH5 fusion.
Project description:au13-04_cdtbis; cdt1_bis crl mutants and CDT1-RNAi lines have very similar macroscopic phenotypes as well as identical defects in plastid division and biogenesis. Our goal wwas to determine how much of these similarities originated from similar alterations of gene expression. Plantlets of crl mutant and CDT1-RNAi lines were grown in vitro on MS1/2 medium for 14 days. CDT1-RNAi lines were compared to the corresponding wild-type (Ws), whereas crl mutants were compared to their wild-type siblings and are in the Col0 ecotype. 4 dye-swap - normal vs rnai mutant comparaison, normal vs transgenic comparaison
Project description:Purpose: we conducted a froward genetic screen to isolate suppressors of the chloroplast-deficient crl mutant, and isolated a mutation affecting the OEP80 protein. Methods: We used EMS mutagenesis to find supressors of the crl mutant. Suppressors were phenotyped at the cellular and molecular (transcriptome) level, and OEP80 complex formation was investigated in the WT and crl mutant background. Results: a mutation in OEP80 fully restores the phenotype of the crl mutant, at the whole plant level, as well as at the cellular or transcriptome level
Project description:The objective of the study was to discover new functions of chemokine CXCL9/MIG, a cationic chemokine that has antimicrobial properties. Human monocytic cell line, THP-1 cells were stimulated 4 hours with chemokine MIG or CCL2/MCP-1 (a chemokine that is not positively charged and has no antimicrobial activity). By using a 21,000 oligo-based DNA human microarray we analyzed gene expression profiles induced by MIG and by MCP-1. The gene expression profile induced by MIG was >85% different from that induced by MCP-1. MIG increased transcription of genes encoding various chemokines (including CCL3/MIP-1alpha, CCL4/MIP-1beta, CCL2/MCP-1 and CXCL8/IL-8), cytokines (TNF-alpha), indicating that MIG has an immunomodulatory effect on THP-1 cells. Additionally, MIG strongly up-regulated a set of genes identified as having tumor suppressor functions, including BTG2, BTG1, P21, IGFBP3, DSCR1 and genes encoding markers for mature leukocyte differentiation (PLAU, LPL, PLAUR etc). In parallel, MIG down-regulated the expression of oncogenes (MYC), and genes related to cell proliferation and cell cycle progression. This gene profile strongly suggested that the chemokine MIG had anti-proliferative activity and might induce THP-1 cells to undergo terminal differentiation.
Project description:In this study, we used quantitative proteomics mass spectrometry with 16-plex TMT labeling to compare individual protein levels of DMSO and 1 μM CSN5i-3-treated K562 cells for 2, 8, and 24 hours. CSN5i-3 is a selective and potent inhibitor of Cop9 Signalosome (CSN), which regulates the activity of Cullin-RING E3 ubiquitin ligases (CRLs). CSN5i-3 treatment resulted in reduced CSN activity, and consequently increased cullin neddylation and constitutively active CRL. Gene Ontology analysis of the changed proteins between DMSO- and CSN5i-3-treated samples showed the enrichment of CSN subunits, cell cycle and chromosome-related components, and phosphatase complex, which include multiple CSN subunits (e.g., CSN7B and CSN5), components of CRLs, especially CRL SRs (e.g., SKP2, ELOA and DCAF1/VPRBP), and known substrates of CRLs (e.g., MAGEA6, GLUL, and RHOB). Indeed, eight out of the top 20 most decreased proteins were CRL adaptor and substrate receptors, two out of the top 20 were E2 proteins (CDC34/UBE2R1 and UBE2R2), and two were CSN subunits. Eight out of the top 20 most increased proteins were reported CRL substrates.
Project description:We wished to identify Crl-regulated genes in stationary phase in E.coli, and whether those overlap with the previously identified regulon of RpoS. Therefore wildtype E.coli (MC4100) and its isogenic crl::cat mutant were grown at 30oC. Total RNA was extracted at on OD (578nm) of 4 (during entry into stationary phase) and then the analysis proceeded as described in detail in the protocoles. The experiment was repeated three times and the results from those experiments are presented here.