This SuperSeries is composed of the SubSeries listed below.
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesResponse of A549 cells treated with Aspergillus fumigatus wild type germinating conidia (WT_GC) or PrtT protease deficient mutant conidia (PrtT-GC) or inert acrylic 2-4 micron beads (Beads) for 8h
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesResponse of A549 cells treated with Aspergillus fumigatus wild type culture filtrate (WT-CF) or PrtT protease deficient mutant culture filtrate (PrtT-CF) for 8h
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesResponse of A549 cells treated with Aspergillus fumigatus germinating conidia (WT-GC) or culture filtrate (WT-CF) for 8h
PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.
Specimen part, Cell line, Treatment
View SamplesCategorisation of LGGs related to their lesion site (infratentorial vs. supratentorial)
Molecular fingerprinting reflects different histotypes and brain region in low grade gliomas.
No sample metadata fields
View SamplesThe glycopeptide antibiotic vancomycin (VCM) represents one of the last lines of defense against methicillin-resistant Staphylococcus aureus infections. However, vancomycin is nephrotoxic, but the mechanism of toxicity is still unclear.
Gene expression analysis reveals new possible mechanisms of vancomycin-induced nephrotoxicity and identifies gene markers candidates.
Specimen part
View SamplesWe used microarrays to detail the global programme of gene expression after knockdown of Ecdysoneless in hMECs
The cell cycle regulator ecdysoneless cooperates with H-Ras to promote oncogenic transformation of human mammary epithelial cells.
Specimen part, Cell line
View SamplesBreast cancers with HER2 overexpression are sensitive to drugs targeting the receptor or its kinase activity. HER2-targeting drugs are initially effective against HER2- positive breast cancer, but resistance inevitably occurs. We previously found that nuclear factor kappa B is hyper-activated in the subset of HER-2 positive breast cancer cells and tissue specimens. In this study, we report that constitutively active NF-B rendered HER2-positive cancer cells resistant to anti-HER2 drugs, and cells selected for Lapatinib resistance up-regulated NF-B. In both circumstances, cells were anti-apoptotic and grew rapidly as xenografts. Lapatinib-resistant cells were refractory to HER2 and NF-B inhibitors alone but were sensitive to their combination, suggesting a novel therapeutic strategy. A subset of NF-B-responsive genes was overexpressed in HER2-positive and triple-negative breast cancers, and patients with this NF-B signature had poor clinical outcome. Anti-HER2 drug resistance may be a consequence of NF-B activation, and selection for resistance results in NF-B activation, suggesting this transcription factor is central to oncogenesis and drug resistance. Clinically, the combined targeting of HER2 and NF-B suggests a potential treatment paradigm for patients who relapse after anti-HER2 therapy. Patients with these cancers may be treated by simultaneously suppressing HER2 signaling and NF-B activation.
NF-κB activation-induced anti-apoptosis renders HER2-positive cells drug resistant and accelerates tumor growth.
Specimen part
View SamplesPreparation of Synaptosomes by density gradient and compare synaptically enriched mRNA to total homogenate transcriptome Overall design: In brief, mouse brains were homogenized in 5 ml homogenization buffer (0.32 M sucrose, 1 mM EDTA pH 7.4, 1 mM dithiothreitol, phenylmethanesulfonyl fluoride solution (Sigma, 93482-50ML-F), complete mini-protease inhibitor (Roche Diagnostics) for 10 sec using a polytron. The homogenate was centrifuged at 1,000g for 10 min at 4 °C yielding the nuclear fraction (Nuc) and the supernatant (Sup). The supernatant was centrifuged at 31,000g for 5 min at 4°C using a discontinuous Percoll gradient. The layer between 3% and 10% of Percoll were collected, washed in 30 ml of homogenization buffer and further centrifuged at 22,000 × g for 15 min at 4°CT. The pellet was resuspended in in EBC buffer (50 mM Tris-HCl pH 8.0, 120 mM NaCl and 0.5% NP-40) containing complete mini-protease inhibitor (Roche Diagnostics) and phosphatase inhibitor cocktail 1 and 2 (Sigma–Aldrich)) for Western blot analysis or lysis buffer for RNA extraction (GenElute Mammalian Total RNA Miniprep Kit, Sigma).
Mutations in NONO lead to syndromic intellectual disability and inhibitory synaptic defects.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Molecular signatures of cardiac defects in Down syndrome lymphoblastoid cell lines suggest altered ciliome and Hedgehog pathways.
Sex, Specimen part
View Samples