Project description:Growth differentiation factor 11 (GDF11), is one of the members of transforming growth factor β (TGFβ) superfamily. We set out to unequivocally reveal the effect of endogenous GDF11 on biological process by adopting CRISPR/Cas9 gene knockout strategy to specifically delete GDF11 gene in Neuro-2a cells. We analyze mRNA profiles of differentially genes in wild type (WT) and GDF11 knockout (GDF11-/-) Neuro-2a cells by using RNA-seq technology. The RNA-seq data reported here provide a fundamental materials and evidence for investigations of biological function of GDF11.
Project description:These ChIP-seq analyses identified binding DNAs of ONEUCT2 in Neuro-2a (mouse neuroblastoma)cells. We overexpressed OC2ΔHOX (a gain-of-function mutant) in Neuro-2a cells, and infected the cells with HSV-1 at 40 hours post transfection. Samples infected for 5 hours were sequenced by ChIP for binding DNAs of the OC2 mutant in Neuro-2a cells.
Project description:This is a part of the study that shows that a host gene,ONECUT2 (OC2), promote herpes simplex virus 1 (HSV-1) transcription. These RNA-seq analyses viral genes transcription in Neuro-2a cells. Neuro-2a cells were transfected with pOC2△HOX2 and pcDNA plasmids for 42 hours then infected with herpes simple virus1 for 5 hours.
Project description:This is a part of the study that shows that a host gene,ONECUT2( OC2), promotes herpes simplex virus 1 (HSV-1) genome accessibility. These ATAC analyses are for viral and host genome accessibility in Neuro-2a cells. Neuro-2a cells were transfected with pOC2△HOX2 and pcDNA plasmids for 42 hours then infected with herpes simple virus1 for 2 hours.
Project description:Our fingdings suggested that Pax3 not only inhibited the cell viability and proliferation, but also affected the cell cycle and the neurite outgrowth of Neuro-2a cells.RNA sequencing analysis showed upregulated genes in Pax3 overexpressed group were involved in cell cycle machinery, which may reveal the potential mechanism of proliferation.
Project description:This is a part of the study that shows that a host microRNA, miR-138, represses herpes simplex virus 1 (HSV-1) gene expression through both viral and host targets. These PAR-CLIP analyses identified viral and host targets of miR-138 in Neuro-2a (mouse neuroblastoma) and 293T (human embryonic kidney) cells. We constructed two cell lines derived from Neuro-2a cells, one overexpressing miR-138 (N2A138) and one antagonizing miR-138 (N2Aanti138). We also constructed two cell lines derived from 293T cells, one overexpressing miR-138 (293T138) and one control cells (293Tcontrol). Uninfected N2A138 and N2Aanti138 were compared by PAR-CLIP for host targets in Neuro-2A cells. 293T138 and 293Tcontrol cells infected for 4 and 8 hours were compared by PAR-CLIP for HSV-1 targets in 293T cells. 293T138 and 293Tcontrol cells infected for 4 hours were also compared for host targets in 293T cells.
Project description:Alzheimer's disease (AD) is a progressive and irreversible neurological disorder which impairs the living quality of old people and even life spans. New compounds have shown potential inneuroprotective effects in AD, such as GFKP-19, which is a 2-pyrrolidone derivative, which has been proved to enhance the memory of dysmnesia mouse. The molecular mechanisms remains to be established for these drug candidates. Large-scale phosphoproteomic approach has been evolved rapidly in the last several years, which should provide useful toolkit to understand cellular signaling underlying drug effects. To establish and test such a method framework, we accurately analyzed the deep quantitative phosphoproteome of the neuro-2a cells treated with or without GFKP-19 using triple SILAC labeling. A total of 14,761 class I phosphosites were quantified between control, damaged, and protected conditions using the high resolution mass spectrometry, with a high inter-mass spectrometer reproducibility for even subtle regulation events. Our data suggests that GFKP-19 can reverse Aβ25-35 caused phosphorylation change in neuro-2a cells, and might perform the neuronal protective effect by decreasing tau protein phosphorylation through down-regulating the phosphorylation level of MAPK14 at T180.
Project description:This project studies a compound, which induces potent neuronal differentiation, by using iTRAQ-based proteomic analysis in Neuro-2a progenitor cells.