Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq for UV-irradiated C. elegans

ABSTRACT: ChIP-seq for UV-irradiated C. elegans

PROVIDER: PRJNA563831 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

UV irradiated C. elegans

Project description:UV irradiated C. elegans

| PRJNA563824 | ENA

RNA-seq for UV irradiated C. elegans

Project description:RNA-seq for UV irradiated C. elegans

| PRJNA563830 | ENA

ChIP-seq for UV-irradiated C. elegans

Project description:ChIP-seq was applied for identifying the deposition of H3K4me2 on genome of UV-treated C. elegans. C.elegans larvae are sensitive to UV treatment, and it may due to the deposition of various histone modification during DNA damage response (DDR). In our study, we identified one of the histone marks, H3K4me2, as a positive regulator of DDR related transcription. This ChIP-seq experiment was used to identify the genes that have H3K4me2 deposition.

2020-08-27 | GSE136827 | GEO

RNA-seq for UV irradiated C. elegans

Project description:RNA-seq was applied for identifying the change of transcriptome 6h and 24h post UV irradiation.

2020-08-27 | GSE136826 | GEO

Identification of intermediate-sized non-coding RNAs involved in the UV-induced DNA damage response in C. elegans

Project description:We utilized high-throughput RNA-seq to uncover the intermediate-sized noncoding RNAs invovled in UV-DNA Damage Responses in C. elegans. 450 novel transfrags were discovered, some of which show dramatic expression change between the UV irradiation and control. This study should lead to a better understanding of the role of is-ncRNAs invovled in UV-DDR. Examination of intermediate-sized transcripts (70-500nt) in L4 larvae of C. elegans strains, including wild-type (N2), UV-irradiated (N2-UV100J/m2) and NER-deficient mutant (xpa-1) strains.

2012-05-01 | E-GEOD-37063 | biostudies-arrayexpress

GLI1 ChIP-Seq in non-irradiated versus irradiated SUM1315 cells

Project description:GLI1 ChIP-Seq in non-irradiated versus irradiated SUM1315 cells

| PRJNA609752 | ENA

CPD-capture-seq map of CPD formation in UV-irradiated primary melanocytes, normal human skin fibroblasts and UV-irradiated genomic DNA

Project description:UV-induced CPDs were mapped in primary skin melanocytes or normal human skin fibroblasts following either UVC or UVB irradiation and in isolated human genomic DNA (naked DNA control) that was UVB or UVC irradiated. CPDs were mapped across the human genome using the CPD-capture-seq method and the resulting libraries were captured for ~4000 genomic regions of interest (~3 Mbp) of the human genome by the company Rapid Genomics prior to Illumina sequencing

2023-04-12 | GSE225362 | GEO

C. elegans development (ChIP-Seq)

Project description:C. elegans development (ChIP-Seq)

| PRJNA591185 | ENA

p53 Chip-Seq in U2OS treated with UV

Project description:p53 Chip-Seq in U2OS treated with UV

| PRJEB4851 | ENA

Reticulon-1 and reduced migration towards chemoattractants by macrophages differentiated from the bone marrow of UV-irradiated and UV-chimeric mice

Project description:The ability of macrophages to respond to chemoattractants and inflammatory signals is important for their migration to sites of inflammation and immune activity and for host responses to infection. Macrophages differentiated from the bone marrow of UV-irradiated mice, even after activation with LPS, migrated inefficiently towards CSF-1 and CCL2. When bone marrow cells were harvested from UV-irradiated mice, and transplanted into naïve mice, the recipient mice (UV-chimeric) had reduced accumulation of elicited macrophages in the peritoneal cavity in response to inflammatory thioglycollate or alum. Macrophages differentiating from the bone marrow of UV-chimeric mice also had an inherent reduced ability to migrate towards chemoattractants in vitro, even after LPS activation. Microarray analysis identified reduced reticulon-1 mRNA in macrophages differentiated from the bone marrow of UV-chimeric mice. By using an anti-reticulon-1 antibody, a role for reticulon-1 in macrophage migration was confirmed. The proposal that reduced reticulon-1 is responsible for the poor inherent ability of macrophages to respond to chemokine gradients was supported by Western blotting. In summary, skin exposure to erythemal UV radiation can modulate macrophage progenitors in the bone marrow such that the properties of their differentiated progeny respond inefficiently to signals to accumulate at sites of inflammation and immunity.

2017-05-12 | GSE98840 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data