Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1062389 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27759624.fastq.gz | Fastqsanger.gz | |||
| SRR27759625.fastq.gz | Fastqsanger.gz |
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Project description:Lion-head goose is the only large goose species in China, and it was one of the largest goose species in the world. Our previous study firstly reported a chromosome-level genome assembly of Lion-head goose (Anser cygnoides), a native breed in South China, through the combination of PacBio, Bionano, and Hi-C technologies. The fat content of foie gras is augmented during its preparation due to the special feeding regimen. Lion-head geese have a strong tolerance of massive energy intake and show a priority of fat accumulation in liver tissue. In this study, we studied for the first time the important differential genes that regulate fatty liver in Lion-head goose. After high-intake feeding, the fatty livers of Lion-head geese were distinctly characterized. The revelation of gene regulation is an important basis for the study of liver development and molecular characteristics for the Lion-head goose. To analyze the excellent fatty liver performance of Lion-head goose at the molecular level, we performed whole transcriptome analysis by high-throughput RNA sequencing to analyze the key regulatory genes that determine the fatty livers in high-intake feeding group compared with the normal livers in normally-fed Lion-head geese. We identified 716 differentially expressed mRNAs, 145 differentially expressed circRNAs, and 39 differentially expressed lncRNAs in the fatty livers in high-intake feeding group compared with the normal livers in normally-fed Lion-head geese, including upregulated and downregulated genes, respectively. GO enrichment analysis showed that these genes were significantly enriched in molecular function, involved in extracellular regions, DNA-binding transcription factor activity, extracellular matrix, heme binding and other life activities. We chose differentially expressed genes involved in either upregulation or downregulation, and we additionally confirmed the accuracy of sequencing at the RNA level. In summary, our research suggested that these differentially expressed genes may play important roles in fatty liver development in Lion-head goose. However, the functions and mechanisms of these significantly differentially expressed genes should be investigated in future studies.
2023-11-16 | GSE243829 | GEO
Project description:This mathematical model of T cell-tumour interactions considering the roles of T cell competition and stochastic extinction events in CAR T cell therapy is described by the publication:
Kimmel GJ, Locke FL, Altrock PM. "The roles of T cell competition and stochastic extinction events in chimeric antigen receptor T cell therapy." Proc Biol Sci. 2021 Mar 31;288(1947):20210229.
doi: 10.1098/rspb.2021.0229
Comment:
Reproduction of Fig. 2(a) and (b) was simulated by using the fitted model parameter set given in Table 1 of the manuscript's Supplementary Material, however substituting the values of r_N and rho_C for those stated in Table 1 of the publication manuscript, i.e. r_N = 0.17 and rho_C = 0.0251.
Abstract:
Chimeric antigen receptor (CAR) T cell therapy is a remarkably effective immunotherapy that relies on in vivo expansion of engineered CAR T cells, after lymphodepletion (LD) by chemotherapy. The quantitative laws underlying this expansion and subsequent tumour eradication remain unknown. We develop a mathematical model of T cell–tumour cell interactions and demonstrate that expansion can be explained by immune reconstitution dynamics after LD and competition among T cells. CAR T cells rapidly grow and engage tumour cells but experience an emerging growth rate disadvantage compared to normal T cells. Since tumour eradication is deterministically unstable in our model, we define cure as a stochastic event, which, even when likely, can occur at variable times. However, we show that variability in timing is largely determined by patient variability. While cure events impacted by these fluctuations occur early and are narrowly distributed, progression events occur late and are more widely distributed in time. We parameterized our model using population-level CAR T cell and tumour data over time and compare our predictions with progression-free survival rates. We find that therapy could be improved by optimizing the tumour-killing rate and the CAR T cells' ability to adapt, as quantified by their carrying capacity. Our tumour extinction model can be leveraged to examine why therapy works in some patients but not others, and to better understand the interplay of deterministic and stochastic effects on outcomes. For example, our model implies that LD before a second CAR T injection is necessary.
2024-09-02 | BIOMD0000001041 | BioModels
Project description:Ngorongoro Crater Lion population genomics
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Project description:Pocillopora population genomic connectivity in the southwestern Indian Ocean
| PRJNA909966 | ENA
Project description:Small-cell lung cancer H446 cells were treated with CAPE. The regulation mediated by miR-3960 after CAPE treatment was explored and the altered signaling pathways were predicted in a bioinformatics analysis.CAPE decreased the expression of yes-associated protein 1 (YAP1) and cellular myelocytomatosis oncogene (c-MYC) protein. Moreover, the upregulation of miR-3960 by CAPE contributed to CAPE-induced apoptosis. The knockdown of miR-3960 decreased the CAPE-induced apoptosis.
2020-06-11 | GSE152167 | GEO
Project description:The neural crest is a dynamic progenitor cell population that arises at the border of neural and non-neural ectoderm. The inductive roles of FGF, Wnt, and BMP at the neural plate border are well established, but the signals required for subsequent neural crest development remain poorly characterized. Here, we conducted a screen in primary zebrafish embryo cultures for chemicals that decrease neural crest formation, as read out by crestin:EGFP expression. We found that the natural product caffeic acid phenethyl ester (CAPE) disrupts neural crest gene expression, migration, and melanocytic differentiation by reducing Sox10 activity. CAPE inhibits PI3K/Akt signaling specifically in FGF-stimulated cells, and neural crest defects in CAPE-treated embryos are suppressed by constitutively active Akt1. Inhibition of Akt activity by constitutively active PTEN similarly decreases crestin expression and Sox10 activity. Our study has identified Akt as a novel intracellular pathway required for neural crest development.
2017-08-17 | GSE95814 | GEO
Project description:The neural crest is a dynamic progenitor cell population that arises at the border of neural and non-neural ectoderm. The inductive roles of FGF, Wnt, and BMP at the neural plate border are well established, but the signals required for subsequent neural crest development remain poorly characterized. Here, we conducted a screen in primary zebrafish embryo cultures for chemicals that decrease neural crest formation, as read out by crestin:EGFP expression. We found that the natural product caffeic acid phenethyl ester (CAPE) disrupts neural crest gene expression, migration, and melanocytic differentiation by reducing Sox10 activity. CAPE inhibits PI3K/Akt signaling specifically in FGF-stimulated cells, and neural crest defects in CAPE-treated embryos are suppressed by constitutively active Akt1. Inhibition of Akt activity by constitutively active PTEN similarly decreases crestin expression and Sox10 activity. Our study has identified Akt as a novel intracellular pathway required for neural crest development.
2017-08-17 | GSE95813 | GEO
Project description:Caffeic acid phenethyl ester (CAPE), derived from various plant sources, has been shown to ameliorate ischemia/reperfusion (I/R) injury in vivo, and this has been attributed to its ability to reduce the oxidative stress. Here we investigated the cytoprotection of CAPE against menadione (MD)-induced oxidative stress in human umbilical vein endothelial cells (HUVEC) to evaluate potential gene expression involvement. CAPE exhibited dose-dependent cytoprotection of HUVEC that required preincubation. A gene screen with microarrays was performed to identify the potential cytoprotective gene(s) induced by CAPE. Heme oxygenase-1 (HO-1) was highly upregulated by CAPE and this was confirmed with reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting. Keywords: gene expression in HUVEC, CAPE cytoprotective dose response
2008-02-12 | GSE10429 | GEO