Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Bmal1 depletion on gene expression in poly(I:C)-stimulated myeloid peritoneal cells.

ABSTRACT: To investigate the effect of Bmal1 on poly(I:C) response, we isolate mRNA from PBS or poly(I:C)-injected WT and myeloid Bmal1 KO mice. We then compare the poly(I:C)-induced transcriptomic change between WT and Bmal1 KO peritoneal myeloid cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE222759 | GEO | 2024/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

TMT analysis of proteomic changes in the gastrocnemius skeletal muscles of WT and Bmal1-KO mice, and Bmal1-KO mice rescued with AAV-mediated muscle-specific expression of Bmal1.

Project description:TMT analysis of proteomic changes in the gastrocnemius skeletal muscles of WT and Bmal1-KO mice, and Bmal1-KO mice rescued with AAV-mediated muscle-specific expression of Bmal1.

2024-10-03 | PXD054406 | Pride

Genome-wide analysis of LPS or PBS challenged DUSP3-KO and WT female mice peritoneal macrophages gene expression

2015-03-11 | GSE66782 | GEO

Genome-wide analysis of LPS or PBS challenged DUSP3-KO and WT female mice peritoneal macrophages gene expression

Project description:Analysis of gene expression profile in peritoneal macrophage extracted from LPS or PBS challenged DUSP3-/- and WT mice. DUSP3 deletion protects mice from sepsis and endotoxemia. We performed a microarray analysis to get insights into the differentially regulated pathways between WT and KO under inflammatory conditions. Total RNA obtained from isolated peritoneal macrophages isolated from DUSP3-/- and WT mice 36 hours after challenging them in vivo with PBS or with 6mg/kg of LPS.

2015-03-11 | E-GEOD-66782 | biostudies-arrayexpress

Differential gene expression in mice with inducible loss of Bmal1 and HNF4α in the liver

Project description:Hepatocyte Nuclear Factor 4 alpha (HNF4α), a master regulator of hepatocyte differentiation, and circadian regulator Aryl Hydrocarbon-Like Receptor-Like 1 (ARNTL, or BMAL1) though robustly co-expressed in healthy liver, are incompatible within the context of HCC. Differential expression of Bmal1 and Hnf4α may control susceptibility to liver disease and ultimately, hepatocellular carcinoma. We compared gene expression profiles under conditions of inducible loss of hepatic Hnf4α and inducible loss of Hnf4a and Bmal1 in this RNA-seq experiment. Hepatic Hnf4a (H-KO) or Hnf4a and Bmal1 (BH-KO) were inducibly knocked out after 5 days tamoxifen treatment in eight week-old mice (H-KO) or (BH-KO) followed by vivarium chow or high fat feeding (BH-HF-KO). Littermate control mice (H-WT, BH-WT and BH-HF-WT ) were also treated with tamoxifen at eight weeks of age, but since they lacked the Cre transgene, Hnf4a and Bmal1 expression remained intact. Livers were harvested at 10 weeks of age (BH-WT/KO, H-WT/KO) or 45 weeks ( BH-HF-WT/KO) of age after high fat diet feeding, and liver tissue was flash frozen in liquid nitrogen.

2022-08-01 | GSE173968 | GEO

Microarray of hippocampus from 5mo wt, Bmal1 KO and Nr1d1 (Rev-Erb-alpha) KO mice at a single timepoint

Project description:Deletion of the circadian clock proteins Bmal1 or Nr1d1 (also known as Rev-Erb-alpha) can not only cause circadian dysfunction, but also neuroinflammation in the hippocampus. In this array, 3 wt, 2 Bmal1 KO, and 2 Nr1d1 KO mice, all 5mo, were kept in standard 12h:12h light:dark condition, then anesthetized and perfused with PBS+heparin. Mice were harvest in between noon and 3pm. Whole hippocampus was removed and flash frozen, then RNA was extracted using Trizol reagent and PureLink RNA columns, per manufacturers instructions. RNA microarray analysis was performed by the Washington Univ. Genome Technology Access Center using Agilent Mouse 4x44K mouse V2 array.

2019-02-11 | E-MTAB-7590 | biostudies-arrayexpress

BMAL1 Modulates Senescence Programming via AP-1 (WT and Bmal1 KO RNA-seq)

Project description:BMAL1 Modulates Senescence Programming via AP-1 (WT and Bmal1 KO RNA-seq)

| PRJNA952555 | ENA

Transcriptome analysis of the circadian clock gene BMAL1 deletion with opposite carcinogenic effects

Project description:We have previously reported that the deletion of BMAL1 gene has opposite effects in respect to its contribution to the pathways that are effective in the multistage carcinogenesis process. BMAL1 deletion sensitized nearly-normal breast epithelial (MCF10A) and invasive breast cancer cells (MDA-MB-231) to cisplatin and doxorubicin-induced apoptosis while this deletion also aggravated the invasive potential of MDA-MB-231 cells. However, the mechanistic relationship of the seemingly opposite contribution of BMAL1 deletion to carcinogenesis process is not known at genome-wide level. In this study, an RNA-seq approach was taken to uncover the differentially expressed genes (DEGs) and pathways after treating BMAL1 knockout (KO) or wild-type (WT) MDA-MB-231 cells with cisplatin and doxorubicin to initiate apoptosis. Gene Set Enrichment Analysis with the DEGs demonstrated enrichment in multiple genes/pathways contribute to sensitization to cisplatin or doxorubicin-induced apoptosis in BMAL1-dependent manner. Additionally, our DEG analysis suggested that non-coding transcripts RNA (such as lncRNA and processed pseudogenes) may have role in cisplatin or doxorubicin-induced apoptosis. Protein-protein interaction network obtained from common DEGs in cisplatin and doxorubicin treatments revealed that GSK3b, NACC1 and EGFR are the principal genes regulating the response of the KO cells. Moreover, the analysis of DEGs among untreated BMAL1 KO and WT cells revealed that epithelial-mesenchymal transition genes are upregulated in KO cells. As a negative control, we have also analyzed the DEGs following treatment with an endoplasmic reticulum (ER) stress-inducing agent, tunicamycin which was affected by BMAL1 deletion minimally. Collectively, the present study suggests BMAL1 regulates many genes/pathways of which the alteration in BMAL1 KO cells may shed light on pleotropic phenotype observed.

2020-08-29 | GSE157069 | GEO

Expression data from peritoneal macrophages stimulated with lipid A

Project description:Setdb1 is one of the H3K9 methyltransferases and represses gene expression by H3K9 methylation. In an attempt to elucidate the role of Setdb1 in the TLR4-mediated inflammatory responses, we performed DNA microarray analysis using lipid A (the active component of LPS)-stimulated peritoneal macrophages from macrophage specific Setdb1 KO (KO) and WT mice. The genes upregulated by lipid A treatment in WT macrophages and further increased in KO macrophages contain many genes associated with interleukins and chemokines. Peritoneal macrophages from WT and KO mice were stimulated with lipid A 10 ng/ml or vehicle for 4 h. Microarray analysis was performed using Affymetrix Mouse 430 2.0.

2016-06-27 | E-GEOD-78153 | biostudies-arrayexpress

Muscle-specific rescue of Bmal1 impacts survival and health span of the Bmal1-KO mouse

Project description:This dataset was generated to investigate the muscle and systemic effects of muscle-specific Bmal1 expression in the Bmal1-KO mouse model

2024-10-03 | GSE232957 | GEO

Bmal1 KO mouse lung versus WT under three ribosomal depletion methods

Project description:Embryonic Bmal1 knock-out (KO) mouse lungs were compared to wildtype (WT) mouse lungs. Three different library preparations were done on each sample in order to assess the impact of ribosomal depletion on differential expression.

2025-02-06 | GSE288461 | 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