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: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 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:Chromogranin A (CHGA) is elevated in plasma of patients with renal failure and several CHGA polymorphisms are associated with hypertensive renal disease. Therefore, we investigated the role of CHGA in kidney disease using the partial nephrectomy model of kidney failure. Mice under surgery to remove 2/3rds of the left kidney and the entire right kidney. Control mice received the sham surgery. Wild-type and CHGA-/- mice used. To model the changes in vitro, CRL-1927 kidney cells were treated with or without CHGA in vitro.
Project description:The mouse melanoma cell line B16-F10 provided by American Type Culture Collection (ATCC® CRL-6475™) were treated with DMSO, G007-LK, WNT or G007-LK+WNT, done in triplicates for a total of 12 samples.
Project description:The kidney, similar to non-renal tissue, is adversely affected by increased Hedgehog signaling. We treated human kidney organoids with the Hedgehog activator SAG in order to study the effects of constitutive active Hedghog signaling on human kidney development. We used microarrays to identify gene expression changes in human kidney tissue following Hedgehog activation.