Ontology highlight
ABSTRACT:
PROVIDER: PRJNA801609 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17804680_1.fastq.gz | Fastqsanger.gz | |||
| SRR17804680_2.fastq.gz | Fastqsanger.gz | |||
| SRR17804681_1.fastq.gz | Fastqsanger.gz | |||
| SRR17804681_2.fastq.gz | Fastqsanger.gz | |||
| SRR17804682_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
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Project description:Targetted metabolomics in U2OS PRDX1 WT and PRDX1-/- While cellular metabolism impacts the DNA damage response, a systematic understanding of the metabolic requirements that are crucial for DNA damage repair has yet to be achieved. Here, we investigate the metabolic enzymes and processes that are essential when cells are exposed to DNA damage. By integrating functional genomics with chromatin proteomics and metabolomics, we provide a detailed description of the interplay between cellular metabolism and the DNA damage response. Subsequent analysis identified Peroxiredoxin 1, PRDX1, as fundamental for DNA damage repair. During the DNA damage response, PRDX1 translocates to the nucleus where it is required to reduce DNA damage-induced nuclear reactive oxygen species levels. Moreover, PRDX1 controls aspartate availability, which is required for the DNA damage repair-induced upregulation of de novo nucleotide synthesis. Loss of PRDX1 leads to an impairment in the clearance of γΗ2ΑΧ nuclear foci, accumulation of replicative stress and cell proliferation defects, thus revealing a crucial role for PRDX1 as a DNA damage surveillance factor.
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Project description:Heldt2018 - Proliferation-quiescence decision
in response to DNA damage
This model is described in the article:
A comprehensive model for
the proliferation-quiescence decision in response to endogenous
DNA damage in human cells.
Heldt FS, Barr AR, Cooper S, Bakal
C, Novák B.
Proc. Natl. Acad. Sci. U.S.A. 2018 Feb;
:
Abstract:
Human cells that suffer mild DNA damage can enter a
reversible state of growth arrest known as quiescence. This
decision to temporarily exit the cell cycle is essential to
prevent the propagation of mutations, and most cancer cells
harbor defects in the underlying control system. Here we
present a mechanistic mathematical model to study the
proliferation-quiescence decision in nontransformed human
cells. We show that two bistable switches, the restriction
point (RP) and the G1/S transition, mediate this decision by
integrating DNA damage and mitogen signals. In particular, our
data suggest that the cyclin-dependent kinase inhibitor p21
(Cip1/Waf1), which is expressed in response to DNA damage,
promotes quiescence by blocking positive feedback loops that
facilitate G1 progression downstream of serum stimulation.
Intriguingly, cells exploit bistability in the RP to convert
graded p21 and mitogen signals into an all-or-nothing
cell-cycle response. The same mechanism creates a window of
opportunity where G1 cells that have passed the RP can revert
to quiescence if exposed to DNA damage. We present experimental
evidence that cells gradually lose this ability to revert to
quiescence as they progress through G1 and that the onset of
rapid p21 degradation at the G1/S transition prevents this
response altogether, insulating S phase from mild, endogenous
DNA damage. Thus, two bistable switches conspire in the early
cell cycle to provide both sensitivity and robustness to
external stimuli.
This model is hosted on
BioModels Database
and identified by:
MODEL1703030000.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000700 | BioModels
Project description:RBBP8 links DNA damage response and unfolded protein response
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Project description:Protein methylation plays important roles in DNA damage signaling. To date, there is still a lack of global profiling of whole-cell methylation changes during the DNA damage response and repair. In this study, using HILIC affinity enrichment combined with MS analysis, we conducted a quantitative analysis of the methylated proteins in HEK293T cells in response to IR-induced DNA damage. In total, 235 distinct methylation sites responding to IR treatment were identified, and 38% of them were previously unknown. Multiple RNA-binding proteins were differentially methylated upon DNA damage stress. Furthermore, we identified 14 novel methylations in DNA damage response-related proteins. Moreover, we validated the function of PARP1 K23 methylation in repairing IR-induced DNA lesions.
2022-02-14 | PXD031655 |
Project description:Proteome and PTMome changes in response to 5-FU mediated RNA and DNA damage
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