Time-course inducible NOTCH3-IC expression in SH-SY5Y.
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ABSTRACT:
PROVIDER: PRJNA480495 | ENA |
REPOSITORIES: ENA
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Project description:Expression analysis of ADRN cell line SH-SY5Y with doxycycline-inducible NOTCH3-IC was used to study transcriptional reprogramming to a MES state. Overall design: Cells were induced with doxycycline for a time-course of 1-7-14-21 days to analyze mRNA.
2019-04-04 | GSE116890 | GEO
Project description:Expression analysis of xenograft tumors of ADRN cell line SH-SY5Y with doxycycline-inducible NOTCH3-IC was used to study transcriptional reprogramming to a MES state in vivo. Overall design: Mice with SH-SY5Y-NOTCH3IC tumors were administered doxycycline for 7 or 14 days to analyze mRNA.
2019-04-04 | GSE116892 | GEO
Project description:Expression analysis of ADRN cell line SH-SY5Y with transient- or permanent doxycycline-inducible NOTCH3-IC expression was used to study reversibility of transcriptional reprogramming. Overall design: Cells were induced with doxycycline for 7 or 14 days to analyze mRNA. Transient induction with doxycycline for 7 days was followed by 7 days off doxycycline to study reversibility of NOTCH3-IC-induced transcriptome.
2019-04-04 | GSE116891 | GEO
Project description:Reversible induction NOTCH3-IC in SH-SY5Y.
| PRJNA480494 | ENA
Project description:Xenograft SH-SY5Y tumors with inducible NOTCH3-IC expression.
| PRJNA480496 | ENA
Project description:BACKGROUND: Accumulation of amyloid ?-peptide (A?) in the plaques is one of the major pathological features in Alzheimer's disease (AD). Sequential cleavage of amyloid precursor protein (APP) by ?-site APP cleaving enzyme 1 (BACE-1) and ?-secretase results in the formation of A? peptides. Preventing A? formation is believed to attenuate AD progression and BACE-1 and ?-secretase are thus attractive targets for AD drug development. METHODS: Combining BACE-1 and ?-secretase inhibition on A? secretion from human neuroblastoma SH-SY5Y cells was evaluated in this study. Secreted A?40 and A?42 levels were measured from SH-SY5Y cells stably transfected with APPwt or APPswe genes. A selective BACE inhibitor and the ?-secretase inhibitor LY450139 (semagacestat) were used to inhibit respective secretase. RESULTS: LY450139 increased A?40 and A?42 secretion from SH-SY5Y APPwt cells at low concentrations (by 60% at 3 nM) followed by subsequent inhibition at higher concentrations (IC(50) 90 nM). Washout studies showed that the A? increase evoked by 3 nM LY450139 was not due to enhanced cleavage following substrate accumulation but rather to activation of A? formation. By contrast, LY450139 inhibited A? formation from SH-SY5Y APPswe in a monophasic manner (IC(50) 18 nM). The BACE inhibitor per se inhibited A? secretion from both SH-SY5Y APPwt and SH-SY5Y APPswe cells with IC(50)s ranging between 7 - 18 nM and also prevented the increased A? secretion evoked by 3 nM LY450139. Combining the BACE inhibitor with higher inhibitory concentrations of LY450139 failed to demonstrate any clear additive or synergistic effects. CONCLUSION: BACE-1 inhibition attenuates the A? increase evoked by LY450139 while not providing any obvious synergistic effects on LY450139-mediated inhibition.
2011-01-01 | S-EPMC3217850 | BioStudies
Project description:MicroRNA (miRNA) has been highlighted in pathogen-host interactions, however, little is known about roles of miRNAs in neurological pathogenesis of human enterovirus 71 (HEV71) infections. In this study, the comprehensive miRNA expression profiling in HEV71-infected human neuroblastoma SH-SY5Y cells were performed to identify cellular miRNAs response to HEV71. A total of 69 miRNAs were differentially expressed in HEV71-infected SH-SY5Y cells compared to non-infected cells. These findings provide new information on the miRNA and mRNA profiles in HEV71 infection, which may serve as a basis for further investigation into the biological functions of miRNAs in the neurological pathogenesis of HEV71 infections. Human neuroblastoma SH-SY5Y cells were infected with HEV71. After infection, the cells were harvested and extracted total RNA for miRNA profiling by hybridization on Affymetrix microarrays. A total of 69 miRNAs were differentially expressed inHEV71-infected SH-SY5Y cells compared to non-infected cells.
2014-07-31 | E-GEOD-45816 | BioStudies
Project description:SH-SY5Y neuroblastoma cells were examined to determine changes in protein expression following exposure to the organophosphate paraoxon (O,O-diethyl-p-nitrophenoxy phosphate). Exposure of SH-SY5Y cells to paraoxon (20 ?M) for 48 h showed no significant change in cell viability as established using an MTT assay. Protein expression changes from the paraoxon-treated SH-SY5Y cells were determined using a comparative, subproteome approach by fractionation into cytosolic, membrane, nuclear, and cytoskeletal fractions. The fractionated proteins were separated by 2D-PAGE, identified by MALDI-TOF mass spectrometry, and expression changes determined by densitometry. Over 400 proteins were separated from the four fractions, and 16 proteins were identified with altered expression ?1.3-fold including heat shock protein 90 (-1.3-fold), heterogeneous nuclear ribonucleoprotein C (+2.8-fold), and H(+) transporting ATP synthase beta chain (-3.1-fold). Western blot analysis conducted on total protein isolates confirmed the expression changes in these three proteins.
2010-01-01 | S-EPMC2981702 | BioStudies
Project description:To investigate the mechanisms of excitotoxic effects of glutamate on human neuroblastoma SH-SY5Y cells.SH-SY5Y cell viability was measured by MTT assay. Other damaged profile was detected by lactate dehydrogenase (LDH) release and by 4', 6-diamidino-2-phenylindole (DAPI) staining. The cytosolic calcium concentration was tested by calcium influx assay. The glutamate-induced oxidative stress was analyzed by cytosolic glutathione assay, superoxide dismutase (SOD) assay and extracellular malondialdehyde (MDA) assay.Glutamate treatment caused damage in SH-SY5Y cells, including the decrease of cell viability, the increase of LDH release and the alterations of morphological structures. Furthermore, the concentration of cytoplasmic calcium in SH-SY5Y cells was not changed within 20 min following glutamate treatment, while cytosolic calcium concentration significantly increased within 24 h after glutamate treatment, which could not be inhibited by MK801, an antagonist of NMDA receptors, or by LY341495, an antagonist of metabotropic glutamate receptors. On the other hand, oxidative damage was observed in SH-SY5Y cells treated with glutamate, including decreases in glutathione content and SOD activity, and elevation of MDA level, all of which could be alleviated by an antioxidant Tanshinone IIA (Tan IIA, a major active ingredient from a Chinese plant Salvia Miltiorrhiza Bge).Glutamate exerts toxicity in human neuroblastoma SH-SY5Y cells possibly through oxidative damage, not through calcium homeostasis destruction mediated by NMDA receptors.
2010-01-01 | S-EPMC5560379 | BioStudies