Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1305037 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Klebsiella pneumoniae strains carrying both blaKPC-2 and blaNDM-1
| PRJNA534178 | ENA
Project description:Klebsiella quasipneumoniae strains carrying both blaKPC-2 and blaNDM-1
| PRJNA547702 | ENA
Project description:Megakaryocytes isolated from Gfi1b flox/flox mice carrying PF4-Cre or not, and from Gfi1b flox/flox mice carrying ROSA-Cre-ERT with or without tamoxifen injection were analyzed for differential expression by RNA-Seq
2017-01-21 | GSE71310 | GEO
Project description:pBIC-1a is a IncFIIk-IncFI blaKPC-2-producing plasmid. Transcriptomic analysis was performed to dive deeper into the biology of this prototypical successful plasmid. The transcriptional landscape of pBIC-1a was assessed without antibiotic, and differential analysis after imipenem exposure was performed on E. coli TOP10(pBIC-1a) whole transcriptome.
2018-09-15 | E-MTAB-7190 | biostudies-arrayexpress
Project description:We have generated mice that carry Cre-dependent "knock-in" alleles (MGS34F and IES34F) of U2af1(S34F), a mutation commonly encountered in human myelodysplastic syndromes and acute myeloid leukemia (AML). MEFs were generated from the progenies of these mice with those carrying a UBC-CreERT2 transgene, and were treated with 4-Hydroxytamoxifen (4OHT) to induce Cre-mediated recombination and subsequent U2af1(S34F) expression. Mice carrying the MGS34F allele were further crossed with those carrying a floxed Runx1 allele and Mx1-Cre. U2af1(S34F) expression and Runx1 deletion caused changes in gene expression and RNA splicing. Mice with a conditional "knock-in" U2af1(S34F) allele and conditional "knockout" alleles of Runx1 were mutagenized with low-dose N-Ethyl-N-Nitrosourea (ENU). Within 1.5 year, one of fourteen ENU-treated mice with U2af1(S34F) and Runx1 deletion developed AML, as did recipients of allografted splenic cells from two other such mice, but AML did not arise from cells with other genotypes or mice without ENU treatment.
2018-07-26 | GSE112174 | GEO
Project description:While histone H3 lysine 27 trimethylation (H3K27Me3) is associated with gene silencing, whether H3K27Me3 demethylation affects transcription and cell differentiation in vivo has remained elusive. To investigate this, we conditionally inactivated the two H3K27Me3 demethylases, Jmjd3 and Utx, in non-dividing intrathymic CD4+ T cell precursors. We show that both enzymes redundantly promote H3K27Me3 removal at, and expression of, a specific subset of genes involved in terminal thymocyte differentiation, especially S1pr1, encoding a sphingosine-phosphate receptor required for thymocyte egress. Floxed alleles of the genes encoding Utx and Jmjd3 (Kdm6a and Kdm6b, respectively) were deleted in double positive (DP) thymocytes carrying a CD4 Cre transgene. Genome-wide H3K27Me3 ChipSeq was performed on (i) pre-selection (CD69lo) DP thymocytes from wild-type mice carrying an endogenous polyclonal TCR repertoire, (ii) mature (TCRhi CD24lo) CD4 SP thymocytes from wild type (Wt), Jmjd3KO, UtxKO and dKO mice carrying an endogenous polyclonal TCR repertoire and (iii) mature (Va2hi CD24lo) CD4 SP thymocytes from wild type and dKO mice carrying the OTII TCR transgene.
2015-09-02 | E-GEOD-70795 | biostudies-arrayexpress