Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: 2018 Arctic 0.2-3 um Imitervirales polB

PROVIDER: PRJNA674422 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12981759_1.fastq.gz	Fastqsanger.gz
	SRR12981759_2.fastq.gz	Fastqsanger.gz
	SRR12981760_1.fastq.gz	Fastqsanger.gz
	SRR12981760_2.fastq.gz	Fastqsanger.gz
	SRR12981761_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 44

Similar Datasets

Project description:2018 Arctic 0.2-3 um eukaryotic 18S

| PRJNA674418 | ENA

Project description:2018 Arctic 3-144 um eukaryotic 18S

| PRJNA674408 | ENA

LMO J.Pinhassi_19_01

Project description:LMO 2018 (0.2, 3-0.2, 3)

| PRJEB52837 | ENA

water microbes

Project description:Water sample filtered through 3 um and 0.2 um

| PRJEB25897 | ENA

Project description:Metaranscriptomes of the Lake Baikal (fraction 0.2-5 um)

| PRJNA1043873 | ENA

Comparative toxicogenomic response in developing zebrafish to the flame retardant, mono-substituted isopropylated triaryl phosphate

Project description:mITP-induced transcriptional changes were measured in 48 hpf wild-type or ahr2hu3335 embryos exposed to 0 or 0.2 uM mITP from 6-48 hpf.

2016-12-24 | GSE86834 | GEO

bulk sample

Project description:Arctic BIOSCAN 2018-2023

| PRJNA1022048 | ENA

Gene expression profiles of Herceptin-resistant breast cancer cells

Project description:Herceptin (trastuzumab) is a humanized monoclonal antibody targeted to the Her2 receptor tyrosine kinase. Despite a robust response rate to Herceptin-based therapies in Her2-positive patients, resistance frequently arises within one year of the initial response. To address the mechanism of Herceptin resistance, we selected clonal variants of Her2-positive BT474 human breast cancer cells (BT/HerR) that are highly resistant to the anti-proliferative effects of Herceptin in the presence of 0.2 uM or 1.0 uM Herceptin. Our original report on these cell lines demonstrated sustained PI3K/Akt signaling and sensitivity to PI3K inhibitors in BT/HerR cells in the presence of Herceptin, suggesting dysregulation of that pathway as an essential component of Herceptin-resistant proliferation. To address the mechanism by which BT/HerR cells and their PI3K/Akt signaling pathway became resistant to Herceptin, we analyzed gene expression profiles of two clones (BT/HerR1.0C and BT/HerR 1.0E) that were selected in 1.0 uM Herceptin and two clones (BT/HerR0.2D and BT/HerR 0.2J) that were selected in 0.2 uM Herceptin, in comparison to the Herceptin sensitive BT474 parent cells.

2009-08-21 | GSE15043 | GEO

NAD+ supplementation normalizes key Alzheimer’s features and DNA damage in a new AD mouse model with introduced DNA repair deficiency

Project description:Emerging findings suggest that compromised cellular bioenergetics and DNA repair contribute to the pathogenesis of Alzheimer's disease (AD), but their role in disease-defining pathology is unclear. We developed a DNA repair-deficient 3xTgAD/Polb+/- mouse that exacerbates major features of human AD including pTau pathologies, synaptic dysfunction, neuronal death and cognitive impairment. Here we report that 3xTgAD/Polb+/- mice have reduced cerebral NAD+/NADH ratio indicating impaired cerebral energy metabolism, which is normalized by nicotinamide riboside (NR) treatment. NR lessened pTau pathology in both 3xTgAD and 3xTgAD/Polb+/- mice, but had no impact on Abeta accumulation. NR-treated 3xTgAD/Polb+/- mice exhibited reduced DNA damage, neuroinflammation, apoptosis of hippocampal neurons, and increased activity of SIRT3 in the brain. NR improves cognitive function in multiple behavioral tests, and restored hippocampal synaptic plasticity in 3xTgAD mice and 3xTgAD/Polb+/- mice. In general, the deficits and the benefits of NR were greater in 3xTgAD/Polb+/- mice than in 3xTgAD mice. Our findings suggest a pivotal role for cellular NAD+ depletion upstream of neuroinflammation, pTau, DNA damage, synaptic dysfunction and neuronal degeneration in AD. Interventions that bolster neuronal NAD+ levels therefore have potential in AD.

2018-02-26 | GSE109055 | GEO

Homo sapiens

Project description:Expression data from JQ1 (0.2 uM) treated tamoxifen-resistant MCF7 cells

| PRJNA213138 | ENA