Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

46 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data in inguinal adipose tissue at different circadian times

ABSTRACT: Peripheral circadian clocks regulate many aspects of physiology. In this study we deleted the core circadian clock component Bmal1 specifically in mouse adipocytes in order to study the role of the adipocyte clock in energy homeostasis and body weight. We used microarrays to indentify changes in gene expression in the adipose tissue of mice lacking a functional adipocyte circadian clock and identified a small number of up- and down- regulated genes. Adipose tissues were isolated from inguinal adipose fat pads at four different times of the diurnal cycle under constant darkness (circadian time, CT) for RNA extraction and hybridization on Affymetrix microarrays. Adipocyte-specific Bmal1 KO (Ad-Bmal1-/-) and control mice were used for isolation of tissues at CT0, CT6, CT12, CT18 where CT0 the beginning of the subjective day.

ORGANISM(S): Mus musculus

SUBMITTER: Georgios Paschos

PROVIDER: E-GEOD-35026 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome changes in mouse livers upon Bmal1 or Nr1d1 knock out and interactome of lnc-Crot by 4C-seq

Project description:To explore the circadian regulations of Bmal1, we examined the transcriptome changes in mouse livers upon Bmal1 knock out at two circadian time points, CT0 and CT12. To explore the circadian regulations of Nr1d1, we examined the transcriptome changes in mouse livers upon Nr1d1 knock out at two circadian time points, CT0 and CT12. To explore interactome of lnc-Crot, 4C-seq was performed with lnc-Crot as bait region at CT6 and CT18.

2017-04-12 | GSE87299 | GEO

Transcriptome changes in mouse livers upon Bmal1 knock out

Project description:To explore the circadian regulations of Bmal1, we examined the transcriptome changes in mouse livers upon Bmal1 knock out at two circadian time points, CT0 and CT12.

2016-09-21 | GSE73271 | GEO

Microarray analysis of mouse cerebral cortex from brain-specific Bmal1 knockout and Per1;Per2 double mutant mice at 2 timepoints

Project description:The aim of this study was to examine the effect of genetic disruption of the circadian clock on gene expression in the cortex across timepoints. Circadian clock protein regulate many critical aspects of cellular function, and Bmal1 knockout mice develop severe neuroinflammation, suggesting a role for circadian clock gene in brain homeostatic function. We compared brain-specific Bmal1 KO mice (Nestin-Cre;Bmal1(flox/flox) with Per1/2 double mutant mice, in order to assess the effects of deletion of the positive and negative limbs of the core clock. 11mo Cre-, NestinCre+/-;Bmal1(fx/fx), or Per1brdm,Per2brdm mice were entrained to 12h light:dark conditions with lights on at 6am for one month, then placed in constant darkness for 24 hours, after which mice were harvested at 6am (CT6) or 6pm (CT18), still in the dark. Mice were anesthetized in the dark, then perfused briefly with PBS+heparin. The brain was then quickly dissected on a cold surface, and the cerebral cortex flash frozen in liquid nitrogen. Cortex samples were mechanically dissociated with a Qiashredder device, then extracted with chloroform and diluted in 70% ethanol. RNA was extracted using Qiagen RNEasy kit according to manufacturers specifications. cDNAs were chemically labeled with Kreatech ULS RNA labeling kit (Kreatech Diagnostics) and Cy5-labeled cDNAs were hybridized to Agilent Mouse v2 4x44K microarrays (G4846A-026655).

2018-09-11 | E-MTAB-7151 | biostudies-arrayexpress

Expression data in inguinal adipose tissue at different circadian times

Project description:Peripheral circadian clocks regulate many aspects of physiology. In this study we deleted the core circadian clock component Bmal1 specifically in mouse adipocytes in order to study the role of the adipocyte clock in energy homeostasis and body weight. We used microarrays to indentify changes in gene expression in the adipose tissue of mice lacking a functional adipocyte circadian clock and identified a small number of up- and down- regulated genes.

2012-10-21 | GSE35026 | GEO

Identification of the circadian ubiquitylated proteome of Drosophila melanogaster.

Project description:Circadian clocks have evolved as time-measuring molecular devices to help organisms adapt their physiology to daily changes in light and temperature. Cycling transcription has been long hypothesized to account for the wealth of rhythmic protein abundance. However, cyclic degradation signals such as ubiquitylation could shape the rhythmic protein landscape as well. In order to document the circadian ubiquitylated proteome of Drosophila melanogaster, we took advantage of a new means of Ub purification based on in vivo biotinylation of AviTag-tagged ubiquitin by the BirA protein, the bioUb system. NeutrAvidin-bound fractions of head lysates were collected at four circadian times six hours apart and proteins were identified and quantified using a proteomic-based approach.

2018-05-22 | PXD005015 | Pride

Transcriptional Repressor Gm129 Modulates the Circadian Gene Expression by Inhibiting CLOCK:BMAL1 Activity

Project description:The mammalian circadian clock is a molecular oscillator composed of a feedback loop that involves transcriptional activators CLOCK and BMAL1, and repressors Cryptochrome (CRY) and Period (PER). Here we show that a direct CLOCK-BMAL1 target gene, Gm129, is a novel regulator of the feedback loop. ChIP analysis revealed that the CLOCK:BMAL1:CRY1 complex strongly occupies the promoter region of Gm129. Both mRNA and protein levels of GM129 exhibit high amplitude circadian oscillations in mouse liver, and Gm129 gene encodes a nuclear-localized protein that directly interacts with BMAL1 and represses CLOCK:BMAL1 activity. In vitro and in vivo protein-DNA interaction results demonstrate that, like CRY1, GM129 functions as a repressor by binding to the CLOCK:BMAL1 complex on DNA. Although Gm129-/- or Cry1-/- Gm129-/- mice retain a robust circadian rhythm, the peaks of Nr1d1 and Dbp mRNAs in liver exhibit significant phase delay compared to control. Our results suggest that, in addition to CRYs and PERs, GM129 protein contributes to the transcriptional feedback loop by modulating CLOCK:BMAL1 activity as a transcriptional repressor. Examination of 3 transcriptional regulators in mouse liver

2014-01-07 | E-GEOD-53828 | biostudies-arrayexpress

The clock gene BMAL1 inhibits macrophage motility, phagocytosis, and impairs defence against pneumonia

Project description:The circadian clock regulates many aspects of immunity. Bacterial infections are affected by time of day, but the mechanisms involved remain undefined. Here we show that loss of the core clock protein BMAL1 in macrophages confers protection against pneumococcal pneumonia. RNAseq was performed on peritoneal macrophages from wild type and BMAL1 knock out mice.

2019-12-20 | E-MTAB-8411 | biostudies-arrayexpress

Mouse white adipose tissue HaloREVERBα ChIP-seq

Project description:The circadian clock component REVERBα is considered a dominant regulator of lipid metabolism, with global Reverbα deletion driving dysregulation of white adipose tissue (WAT) lipogenesis and obesity. However, a similar phenotype is not observed under adipocyte-selective deletion (ReverbαFlox2-6AdipoCre), and transcriptional profiling demonstrates that, under basal conditions, direct targets of REVERBα regulation are limited, and include the circadian clock and collagen dynamics. Under high-fat diet (HFD) feeding, ReverbαFlox2-6AdipoCre mice do manifest profound obesity, yet without the accompanying WAT inflammation and fibrosis exhibited by controls. Integration of the WAT REVERBα cistrome with differential gene expression reveals broad control of metabolic processes by REVERBα which is unmasked in the obese state.

2021-07-31 | E-MTAB-10573 | biostudies-arrayexpress

BMAL1 associates with NOP58 in the nucleolus and contributes to pre-rRNA processing

Project description:The transcription factor BMAL1 is a core element of the circadian clock that contributes to cyclic control of genes transcribed by RNA polymerase II. By using biochemical cellular fractionation and immunofluorescence analyses we reveal a previously uncharacterized nucleolar localization for BMAL1. We used an unbiased approach to determine the BMAL1 interactome by mass spectrometry and identified NOP58 as a prominent nucleolar interactor. NOP58, a core component of the box C/D small nucleolar ribonucleoprotein complex, associates with Snord118 to control specific pre-ribosomal RNA (rRNA) processing steps. These results suggest a non-canonical role of BMAL1 in rRNA regulation. Indeed, we show that BMAL1 controls NOP58-associated Snord118 nucleolar levels and cleavage of unique pre-rRNA intermediates. Our findings identify an unsuspected function of BMAL1 in the nucleolus that appears distinct from its canonical role in the circadian clock system

2020-08-25 | PXD018946 | Pride

Time Restricted Feeding Mitigates Obesity Through Adipocyte Thermogenesis

Project description:In obesity, misalignment of feeding time with the light/dark environment results in disruption of peripheral circadian clocks. Conversely, restricting feeding to the active period mitigates metabolic syndrome through mechanisms that remain unknown. Here we show that adipocyte thermogenesis is essential for the healthful metabolic response to time restricted feeding. Genetic enhancement of adipocyte thermogenesis through ablation of Zfp423 attenuates obesity caused by circadian mistimed high fat diet feeding through a mechanism involving creatine metabolism. Circadian control of adipocyte creatine metabolism underlies timing of diet-induced thermogenesis, and enhancement of adipocyte circadian rhythms through overexpression of the clock activator Bmal1 ameliorates metabolic complications during diet induced obesity. These findings establish creatine mediated diet-induced thermogenesis as a bioenergetic mechanism driving metabolic benefits during time-restricted feeding.

2022-10-24 | GSE181443 | 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