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 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.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE136827 | GEO | 2020/08/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

H3K4me2 regulates the recovery of protein biosynthesis and homeostasis from UV-induced DNA damage during development and aging

Project description:DNA damage causes cancer, impairs development and accelerates aging. UV irradiation induces transcription-blocking lesions and defects in transcription-coupled nucleotide excision repair lead to developmental failure and premature aging in humans. Following DNA repair, the homeostatic processes need to be reestablished to ensure development and maintain tissue functionality. Here, we report that in C. elegans removal of the MLL/COMPASS H3K4 methyltransferase exacerbates the developmental growth retardation and accelerates aging, while depletion of the H3K4 demethylase, SPR-5, promotes developmental growth and extends lifespan amid UV-induced damage. We demonstrate that specifically the DDR-induced H3K4me2 is associated with the activation of genes regulating RNA transport, splicing, ribosome biogenesis, and protein homeostasis and regulates the recovery of protein biosynthesis that is essential for survival of UV-induced DNA damage. Our study uncovers a role of H3K4me2 in coordinating the recovery of protein biosynthesis and homeostasis that is required for developmental growth and longevity after DNA damage.

2020-10-13 | PXD015354 | Pride

UV irradiated C. elegans

Project description:UV irradiated C. elegans

| PRJNA563824 | ENA

ChIP-seq for UV-irradiated C. elegans

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

| PRJNA563831 | ENA

RNA-seq for C.elegans lin-52 vs N2 (UV & non-UV)

Project description:RNA-seq for C.elegans lin-52 vs N2 (UV & non-UV)

| PRJNA638670 | ENA

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

2012-05-01 | GSE37063 | GEO

RNA-seq for UV irradiated C. elegans

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

| PRJNA563830 | ENA

Studying Gene Expression Profiles of UV-Irradiated Human Keratinocytes by cDNA Microarray

Project description:The goal of this thesis is to study the response of a human keratinocyte cell line (HaCaT cells) after UVB irradiation. In order to develop a system for UV irradiation, we firtstly studied the UV illumination system to find out a stable and reliable condition for UV irradiation experiments. Further, we found out the proper dose of UVB radiation and time points after UVB irradiation by performing MTT assay and trypan blue viability test. According to the results of MTT assay and trypan blue viability test, the cellular activity as well as survival rate of UVB-irradiated cells were in proportion to the radiation doses within a lower UVB dose range. We wanted to find out the possible reasons for this phenomenon by using cDNA microarray. We hope the thesis could be a guide for the following researches, and be useful in the clinical studies about the UV damage. Keywords: dose response and time course

2008-11-18 | GSE4223 | GEO

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 ›

Tweets

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