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FWD-AMR

ABSTRACT: sequences for the project FWD-AMR

PROVIDER: PRJEB57330 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	ERR10466124_1.fastq.gz	Fastqsanger.gz
	ERR10466124_2.fastq.gz	Fastqsanger.gz
	ERR10466125_1.fastq.gz	Fastqsanger.gz
	ERR10466125_2.fastq.gz	Fastqsanger.gz
	ERR10466126_1.fastq.gz	Fastqsanger.gz

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AMR-SURPRISE

Project description:AMR-SURPRISE

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HEK293T cells were transfected with the Rbp1-amr or slow (R729H-amr) Î±-amanitin resistant subunit of RNA Pol II and selected with Î±-amanitin 24 hours after transfection for additional 24 hours

Project description:HEK293T cells were transfected with the Rbp1-amr or slow (R729H-amr) Î±-amanitin resistant subunit of RNA Pol II and selected with Î±-amanitin 24 hours after transfection for additional 24 hours. Total RNA was extracted and global changes in gene expression were determined using microarray chips. MiRNAs are transcribed by RNA pol II but the transcriptional features influencing their synthesis are poorly defined. Here we report that a TATA-box in miRNA and a subset of protein-coding genes is associated with increased sensitivity to a slow rate of transcription elongation. We also show that promoters driven by TATA-box or NF-ÎºB elicit high transcription re-initiation rate, but paradoxically lower levels of miRNA. Interestingly, miRNA synthesis was converted to a more productive mode by decreasing initiation rate, but less productive when the re-initiation rate increased. This phenomenon was found to be associated with a delay in miR-146a induction by NF-ÎºB. We also demonstrate that miRNAs are remarkably strong pause sites. Our findings suggest that lower efficiency of miRNA synthesis directed by the TATA-box or NF-ÎºB is a consequence of frequent transcription initiation that lead to Pol II crowding at pause sites, thereby increasing the chance of collision and premature termination. These findings highlight the importance of the transcription initiation mechanism for miRNA synthesis, and have implications for TATA-box promoters in general. HEK293T cells were transfected with plasmids directing the expression of Î±-amanitin-resistant variants of Pol II (Rpb1-amr and R749H-amr). Î±-amanitin was added and RNA was prepared 24 and 48 h later, respectively. The data provided is from 3 Rpb1-amr vs 3 R749H-amr (6 samples).

2013-07-01 | E-GEOD-48163 | biostudies-arrayexpress

AMR in AD

Project description:AMR in AD

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VTEC-AMR

Project description:Verotoxin-producing E.coli genomes with AMR data

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HEK293T cells were transfected with the Rbp1-amr or slow (R729H-amr) α-amanitin resistant subunit of RNA Pol II and selected with α-amanitin 24 hours after transfection for additional 24 hours

Project description:HEK293T cells were transfected with the Rbp1-amr or slow (R729H-amr) α-amanitin resistant subunit of RNA Pol II and selected with α-amanitin 24 hours after transfection for additional 24 hours. Total RNA was extracted and global changes in gene expression were determined using microarray chips. MiRNAs are transcribed by RNA pol II but the transcriptional features influencing their synthesis are poorly defined. Here we report that a TATA-box in miRNA and a subset of protein-coding genes is associated with increased sensitivity to a slow rate of transcription elongation. We also show that promoters driven by TATA-box or NF-κB elicit high transcription re-initiation rate, but paradoxically lower levels of miRNA. Interestingly, miRNA synthesis was converted to a more productive mode by decreasing initiation rate, but less productive when the re-initiation rate increased. This phenomenon was found to be associated with a delay in miR-146a induction by NF-κB. We also demonstrate that miRNAs are remarkably strong pause sites. Our findings suggest that lower efficiency of miRNA synthesis directed by the TATA-box or NF-κB is a consequence of frequent transcription initiation that lead to Pol II crowding at pause sites, thereby increasing the chance of collision and premature termination. These findings highlight the importance of the transcription initiation mechanism for miRNA synthesis, and have implications for TATA-box promoters in general.

2013-07-01 | GSE48163 | GEO

Enrichment Culture AMR-1

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Case study- Neonatal infection & AMR & phage therapy

Project description:Case study- Neonatal infection & AMR & phage therapy

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Phenotypic and genotypic AMR of Streptococcus uberis

Project description:Phenotypic and genotypic AMR of Streptococcus uberis

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Ample glycosylation in membrane and cell envelope protein explains phenotypic diversity, virulence and AMR in the Mycobacterium tuberculosis complex

Project description:Glycoproteomics is likely to identify Mtb virulence factors because glycoproteins on the bacterial cell envelope are used by mycobacteria to enter the primary human host cell, the macrophage. It has been proposed that Mtb interacts with mannose receptors on host cells via mannosylated proteins to enter the macrophages. Despite the vital importance of these proteins in Mtb pathogenesis, our current knowledge of Mtb glycoproteins is still limited, and only a few secreted and cell wall-associated glycoproteins have to date been described. Previous studies have used laboratory strains as model systems to study glycosylation in Mtb. However, only a few sub-groups within the genetically conserved MTBC appear to cause extensive outbreaks with different clinical presentation and AMR. In this study, we employed qualitative and quantitative mass spectrometry and bioinformatics to explore the glycoproteomic patterns of clinical isolates from four lineages of the MTBC, lineages 3, 4, 5 and 7, to investigate the role of protein glycosylation in Mtb adaptation, survival and AMR.

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Expression data from blood and biopsies of Donor-Specific Antibody positive patients

Project description:The presence of Donor-Specific anti-HLA Antibodies (DSA) is associated with an increased risk of both acute and chronic antibody-mediated rejection (AMR) in kidney allografts. AMR has remained challenging in kidney transplantation and is the major cause of late allograft loss. However, not all patients with DSA develop AMR, leading to the question of whether this represents accommodation, if other protective mechanisms exist or if this is actually a state of pre-rejection. Clinical and histological features, and gene expression profiles of kidney biopsy and blood samples of donor-specific antibody (DSA)+ patients without rejection were compared to antibody-mediated rejection (AMR) patients to elucidate the mechanisms involved in prevention of AMR. Of the 71 DSA+ patients, 46 had diagnosis of AMR and 25 did not show rejection. 50 DSA- patients without rejection were used as control. A subgroup of patients with available biopsy (n=61) and blood samples (n=54) were analyzed by microarrays. Both, DSA+/AMR+ and DSA+/AMR- biopsies showed increased expression of gene transcripts associated with cytotoxic T, natural killer cells, macrophages, interferon-gamma and rejection compared to DSA- biopsies. Regulatory T cell transcripts were up-regulated in DSA+/AMR+ and B cell transcripts in DSA+/AMR- biopsies. Whole blood gene expression analysis showed increased immune activity in only DSA+/AMR+ patients. There were no differentially expressed tolerant genes studied (n=14) in the blood or biopsy specimens of DSA+/AMR- patients. During a median 36 months follow-up, 4 DSA+/AMR- patients developed AMR, 12 continued to have DSAs but 9 lost DSAs. Gene expression profiles did not predict the development of AMR or persistence of DSAs. These results indicate increased immune activity in DSA+/AMR- biopsies despite lack of histologic findings of rejection.

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