Ontology highlight
ABSTRACT:
PROVIDER: PRJNA448166 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We aimed to decipher APOBEC3A driven mutational differences in human PDX_PDAC tissues. 40 human PDX_PDAC tissues were grouped based on their APOBEC3A expression levels into APOBEC3A High and Low groups. Illumina whole exome sequencing (WES) was performed and downstream variant analysis was applied.
2021-09-06 | E-MTAB-10115 | biostudies-arrayexpress
Project description:We aimed to decipher human APOBEC3A driven genomic differences in pancreatic tumors in vivo using a genetically engineered mouse model for pancreatic cancer. Murine pancreatic tumor formation was driven by p53fl/+;KrasLSL-G12D/+;Pdx1-Cre;Rosa26LSL-YFP (PKCY) and p53fl/+;KrasLSL-G12D/+;Pdx1-Cre; Rosa26LSL-YFP; A3A+/- (A3A PKCY).
2021-09-06 | E-MTAB-9843 | biostudies-arrayexpress
Project description:We aimed to decipher human APOBEC3A driven mutational differences in pancreatic tumor in vivo using a genetically engineered mouse model of pancreatic cancer. Murine pancreatic tumor formation was driven by p53fl/+;KrasLSL-G12D/+;Pdx1-Cre;Rosa26LSL-YFP (PKCY) and p53fl/+;KrasLSL-G12D/+;Pdx1-Cre; Rosa26LSL-YFP; A3A+/- (A3A PKCY).
2021-09-06 | E-MTAB-9972 | biostudies-arrayexpress
Project description:APOBEC3s-related somatic mutations are the predominant burden in biliary tract cancers (BTCs). Here, we reveal the effects and mechanisms of APOBEC3A/3B functional polymorphisms on cholangiocarcinoma and gallbladder cancer (GBC). rs2267401-G at the APOBEC3B promoter decreases cholangiocarcinoma risk but increased GBC risk. rs2267401-G confers a decreased APOBEC3B promoter activity in cholangiocarcinoma cells but an increased activity in GBC cells. rs12157810-C at the APOBEC3A promoter decreases the risk of BTCs. rs12157810-C up-regulated the promoter activity in both cells. APOBEC3A overexpression attenuates cancer evolution via causing apoptosis, in contrast to APOBEC3B. Inflammatory factors promote cancer evolution via interacting with transcriptional repressors regulating the APOBEC3A/3B promoters. ATAC-seq was used to identify the difference between transcriptional networks of cholangiocarcinoma and GBC.
2022-01-07 | GSE166372 | GEO
Project description:APOBEC3A mutagenesis
| PRJEB50626 | ENA
Project description:We aimed to decipher human APOBEC3A driven transcriptomic differences in pancreatic tumors in vivo using a genetically engineered mouse model for pancreatic cancer. Murine pancreatic tumor formation was driven by p53fl/+;KrasLSL-G12D/+;Pdx1-Cre;Rosa26LSL-YFP (PKCY) and p53fl/+;KrasLSL-G12D/+;Pdx1-Cre; Rosa26LSL-YFP; A3A+/- (A3A PKCY).
2021-09-06 | E-MTAB-9966 | biostudies-arrayexpress
Project description:Recombinant inbred lines were created by crossing the alpha-synuclein containing Caenorhabditis elegans strains NL5901 and SCH4856. These strains contain the human alpha-synuclein gene fused to YFP and under the control of an unc-54 promotor (unc-54p::alpha-synnuclein::YFP) in an N2 and CB4856 genetic background, respectively. These two strains were used to generate a total of 212 recombinant inbred lines, of which 88 were genotyped by whole-genome sequencing using a MiSeq. These recombinant inbred lines can be used for mapping genetic modifiers affecting protein accumulation.
2023-06-30 | E-MTAB-12575 | biostudies-arrayexpress
Project description:To assess the impact of the proteasome inhibitor MG132 on nascent transcription inMDA-MB-453 cells, csRNA-seq was conducted to compare transcript abundances between treated and DMSO control cells. Analysis of transcripts following MG132 treatment showed that APOBEC3A is one of the most differentially expressed genes. Comparison to other APOBEC family genes, revealed APOBEC3A is unique in its transcriptional upregulation by MG132. Analysis of transcription factor binding sites enriched in the promoter regions of genes changed greater than 2-fold in expression highlighted potential transcription factors driving increased APOBEC3A transcription.
2023-12-05 | GSE248016 | GEO
Project description:N 4-methylcytosine (4mC) is a natural DNA modification occurring in thermophiles and plays important roles in restriction-modification (R-M) systems in bacterial genomes. However, the precise location and sequence context of 4mC in the whole genome are limited. In this study, we developed an APOBEC3A-mediated deamination sequencing (4mC-AMD-seq) method for genome-wide mapping of 4mC at single-base resolution. In the 4mC-AMD-seq method, cytosine and 5-methylcytosine (5mC) are deaminated by APOBEC3A (A3A) protein to generate uracil and thymine, both of which are read as thymine in sequencing, while 4mC is resistant to deamination and therefore read as cytosine. Thus, the readouts of cytosines from sequencing could manifest the original 4mC sites in genomes. With the 4mC-AMD-seq method, we achieved the genome-wide mapping of 4mC in Deinococcus radiodurans (D. radiodurans). In addition, we confirmed that 4mC, but not 5mC, was the major modification in the D. radiodurans genome. We identified 1586 4mC sites in the genome of D. radiodurans, among which 564 sites were located in the CCGCGG motif. The average methylation levels in the CCGCGG motif and non-CCGCGG sequence were 70.0% and 22.8%, respectively. We envision that the 4mC-AMD-seq method will facilitate the investigation of 4mC functions, including the 4mC-involved R-M systems, in uncharacterized but potentially useful strains.
2021-12-15 | GSE189965 | GEO
Project description:Macrophages acquire a pro-inflammatory M1 phenotype in response to microbial products or pro-inflammatory cytokines through incompletely understood molecular mechanisms. We recently described the induction of APOBEC3A-mediated cellular site-specific cytosine-to-uracil (C>U) RNA editing during M1 macrophage polarization. However, the functional significance of this RNA editing is unknown. Here, we find that cellular RNA editing by APOBEC3A can also be induced by influenza or Maraba virus infections in normal macrophages, and by interferons in tumor-associated macrophages. Gene knockdown and RNA Seq analyses show that APOBEC3A induces C>U RNA editing (range 7%-88%) of 209 exonic or UTR sites in 203 genes during M1 polarization of monocyte-derived macrophages. The highest level of deleterious protein-recoding C>U RNA editing is observed in THOC5, which encodes a key nuclear protein implicated in the export of mRNAs during M-CSF driven macrophage differentiation. Knockdown of APOBEC3A in M1 macrophages reduces pro-inflammatory IL6, IL23A, and IL12B gene expression, CD80 and CD86 surface protein expression, and TNF-α, IL-1β and IL-6 cytokine secretion, and increases glycolysis and glycolytic capacity. These results demonstrate that APOBEC3A cytidine deaminase plays an important role in transcriptomic and functional polarization of pro-inflammatory M1 macrophages.
2020-03-13 | GSE146867 | GEO