Transcript profiling of putative NF-kB activators in wild-type and NFKB1-null HeLa cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA643487 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12125200.fastq.gz | Fastqsanger.gz | |||
| SRR12125201.fastq.gz | Fastqsanger.gz | |||
| SRR12125202.fastq.gz | Fastqsanger.gz | |||
| SRR12125203.fastq.gz | Fastqsanger.gz | |||
| SRR12125204.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 30 |
Similar Datasets
Project description:In future high-throughput transcriptomic studies, we propose that the use of cell lines nullizygous for important target genes of environmental chemicals will greatly facilitate the interpretation of gene expression profiles. To provide support for this concept, we generated transcript profiles of known or putative NF-kB activators in wild-type and NFKB1-null HeLa cells. Both cell lines were treated with interleukin 1 (IL1beta), tumor necrosis alpha (TNFalpha) or one of two chemicals identified in high throughput assays for NF-kB activity (chlorhexidine diacetate and carbocyanine). The profiles were generated using TempO-Seq targeted sequencing of ~3000 human genes. Almost all of the genes regulated by IL1beta and TNFalpha in wild-type cells were no longer altered in the NFKB1-null cells and approximately half of the genes regulated by Chlorhexidine diacetate and carbocyanine were dependent on NFKB1 for expression changes. These studies demonstrate that many of the changes in gene expression after exposure to the putative NF-kB activators were NFKB1-dependent.
2021-07-01 | GSE153616 | GEO
Project description:Background: Ozone (O3) is the predominant oxidant air pollutant associated with respiratory inflammation, lung dysfunction, and worsening preexisting airway diseases. We previously determined that lack of NF-kB signlaing pathway suppressed lung injury and inflammation caused by O3 in mice. The current study was to determine transcriptome mechanisms orchestrated by NF-kB during the development of pulmonary O3 injury. Methods: To investigate the role of NF-kB1 pathway in lung gene expression changes, Nfkb1-deficient (Nfkb1-/-) and wild-type (Nfkb1+/+) mice were exposed to air or 0.3-ppm O3. Total RNAs were isolated from lung homogenates and cDNA microarray analyses were performed to elucidate NF-kB1-directed transcriptomics in basal lungs (air-exposed) as well as in the lung exposed to O3 (48 hr). Results: In air-exposed Nfkb1-/- lungs, leukocyte extravasation/adhesion and antigen presentation genes were overexpressed while immunity genes were suppressed, supporting the dual role of Nf-kB1 homodimer as a transcriptional repressor as well as transcriptional activator and the phenotype of Nfkb1-/- mice (defective response to infection and specific antibody production). After O3 exposure. Nfkb1-/- mice showed suppressed expression of lung cell cycle genes and enhanced expression of DNA damage checkpoint regulation pathway genes, compared to Nfkb1+/+ mice. Conclusion: Overall, deficiency of NF-kB1 in mouse lungs altered transcriptomes to protect lungs from O3-induced inflammation, cell proliferation, and DNA damages.
2021-09-29 | GSE166398 | GEO
Project description:The receptor-interacting protein kinase 3 (RIPK3) is a multi-functional protein best known for facilitating cellular necroptosis and inflammation. Recent evidence from our lab indicates that RIPK3 expression must be tightly regulated in endothelial cells to promote angiogenesis and maintain vascular integrity during embryogenesis and to provide protection from postnatal atherosclerosis. RIPK3 activity and stability are regulated by post-translational modifications and caspase-dependent cleavage. However, less is known about the transcriptional regulation of Ripk3. Here we utilized an unbiased CRISPR-based technology called genomic locus proteomics (GLoPro) to screen transcription factors and coregulatory proteins associated with the Ripk3 locus in a murine endothelial cell line. We found that 41 nuclear proteins are specifically enriched at the Ripk3 locus, including the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling pathway components NFkB1 and IKBKG. We further verified that NFkB1 and IKBKG directly bind the Ripk3 promoter and prevent TNFa-induced Ripk3 transcription in cultured human primary endothelial cells. Moreover, NFkB1 prevents RIPK3-mediated death of primary endothelial cells. These data provide new insights into NF-kB signaling and Ripk3 transcriptional regulation in endothelial cells.
2021-06-09 | PXD025675 | Pride
Project description:NF-kappaB Activation Model includes the activation of both NFKB1:RELA and NFKB2:RELB for Canonical and Non-Canonical Pathway respectively.
The model includes the pathway model integrated with post-translational modifications of NF-kB subunits that regulate the NFKB1:RELA and NFKB2:RELB activity. The processes that are regulated by NF-kB pathway can be monitored through following readouts NFKB1:RELA Activity, NFKB2:RELB Activity, Degraded RelA, Degraded RelB, Degraded IkB, Degraded NIK, Apoptosis, Tumour, Antiviral Activity, B Cell Growth and Cell Migration. However, last 5 processes above are also influenced by other pathways too, therefore while making predictions, caution has to be exercised.
2022-05-27 | MODEL2001290001 | BioModels
Project description:To investigate the effects of NFKB signaling, RNA-seq analysis was performed on both Jurkat and MT-2 cells. It was observed that either NFKB1 or NFKB2 knockout could alter the gene expression profile in MT-2 cells compared to Jurkat cells. Gene expression profiles of NFKB1/NFKB2 knockout Jurkat cells were compared to the mock edited Jurkat cells. On the other hand, it was hypothesized that the gene expression profile of MT-2 cells can be more drastically altered by NFKB1 or NFKB2 knockout. NFKB2 knockout MT-2 cells exhibited a unique gene expression profile compared to those of NFKB1 knockout MT-2 cells and mock edited MT-2 cells.
2023-11-01 | E-MTAB-13408 | biostudies-arrayexpress
Project description:Effect of NF-kappa B (NF-kB) p50 (Nfkb1) deletion on ozone-induced pulmonary transcriptome changes in mice
| PRJNA700686 | ENA
Project description:We report the application of ChIP-Seq for high-throughput profiling of NFKB1/p50 binding dynamics. The binding profiles were performed under three conditions/models. We first examine the p50 binding in HEK293T cells during G1 and S phase. HEK293T cells were synchronized with double thymidine block method. Before and after release to S phase, ChIP was performed, and chromatin immunoprecipitated DNA was converted to libraries for sequencing with HiSeq 4000. We find that these NFKB1/p50 binding peaks in G1 phase dramatically reduced at S phase. Then, we further examine the p50 binding in HEK293T/TopBP1 cells in response to tamoxifen treatment. These cells have stable expression of TopBP1 activation domain fusion with estrogen receptor. After treatment, chromatin immunoprecipitated DNA was converted to libraries for sequencing with HiSeq 4000. We find that these NFKB1/p50 binding peaks in vehicle control sample dramatically reduced after tamoxifen treatment. Final, we compare the genome wide binding behavior of wild type p50 and mutant p50 2KR (K354R and K356R). HEK293T cells was transfected with plasmids expression HA-tagged wild type or mutation p50. Chromatin immunoprecipitated DNA was converted to libraries for sequencing with HiSeq 4000. We find that both wild type and p50 2KR mutant share similar binding profile. However, in general, p50 mutant has less binding affinity to NFKB binding sites. This study provides a preliminary but solid basis to our understanding of NFKB1/p50 binding dynamics.
2020-08-13 | GSE129618 | GEO
Project description:In future high-throughput transcriptomic studies, we propose that the use of cell lines nullizygous for important targets of environmental chemicals will greatly facilitate the interpretation of regulated genes. To provide proof of this concept, we generated transcript profiles from wild-type and MTF-1-null cells exposed to zinc (Zn) and six putative activators of MTF-1 generated using TempO-Seq targeted sequencing of ~3000 human genes. In the absence of chemical exposure, knockout of MTF-1 resulted in expression changes in 44 genes indicating that MTF-1 has some effect on gene expression in the absence of overt activation. Almost all of the genes regulated by Zn and phenoxybenzamine were no longer regulated in the MTF-1-null cells. For the rest of the chemicals, more than half of the genes regulated in the wild-type cells were no longer regulated in the MTF-1-null cells. These studies demonstrate that many of the changes in gene expression after exposure to the putative MTF-1 activators were MTF-1-dependent.
2020-06-17 | GSE152703 | GEO
Project description:As the master regulator of X-chromosome inactivation (XCI), the Xist RNA is expressed nearly ubiquitously in female mice. Xist is only absent in the germ line and at the pluripotent state. Xist is generally assumed to be expressed “by default” in females, while being actively repressed in the few tissues where it is silent. Whether activating mechanisms also contribute remained largely unknown. Through a pooled CRISPR screen we identify the GATA family of transcription factors as potent direct activators of Xist. We describe a GATA-responsive regulatory element (RE79), located ~100 kb upstream of the Xist promoter. In cell lines derived from the two extraembryonic lineages, XEN and TS cells, where imprinted Xist expression is maintained, RE79 is bound by different sets of GATA factors expressed in those tissues. Here we use a CRISPR activation screen targeting X-chromosomal genes on differentiating XO mouse embryonic stem cells to identify putative Xist activators.
2022-01-26 | GSE194013 | GEO
Project description:Genome-wide maps of NFKB1/p50 binding dynamics
| PRJNA531961 | ENA