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Links from GEO DataSets

Items: 20

1.

NFIA in adipocytes reciprocally regulates mitochondrial and inflammatory gene program to improve glucose homeostasis [RNA-seq]

(Submitter supplied) Adipose tissue is central to regulation of systemic energy homeostasis. Adaptive thermogenesis in brown and beige adipocytes, which relies on mitochondrial oxidative phosphorylation, dissipates energy to counteract obesity. On the other hand, chronic inflammation in adipose tissue is linked to insulin resistance, type 2 diabetes and obesity. Here we show that nuclear factor I-A (NFIA), a transcriptional regulator of brown and beige adipocytes, improves systemic glucose homeostasis via up-regulation of oxidative phosphorylation and reciprocal down-regulation of inflammation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
18 Samples
Download data: TXT
Series
Accession:
GSE200193
ID:
200200193
2.

NFIA in adipocytes reciprocally regulates mitochondrial and inflammatory gene program to improve glucose homeostasis [flox RNA-Seq]

(Submitter supplied) Adipose tissue is central to regulation of systemic energy homeostasis. Adaptive thermogenesis in brown and beige adipocytes, which relies on mitochondrial oxidative phosphorylation, dissipates energy to counteract obesity. On the other hand, chronic inflammation in adipose tissue is linked to insulin resistance, type 2 diabetes and obesity. Here we show that nuclear factor I-A (NFIA), a transcriptional regulator of brown and beige adipocytes, improves systemic glucose homeostasis via up-regulation of oxidative phosphorylation and reciprocal down-regulation of inflammation. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
18 Samples
Download data: TXT
Series
Accession:
GSE228492
ID:
200228492
3.

NFIA in adipocytes reciprocally regulates mitochondrial and inflammatory gene program to improve glucose homeostasis [flox ChIP-Seq]

(Submitter supplied) Adipose tissue is central to regulation of systemic energy homeostasis. Adaptive thermogenesis in brown and beige adipocytes, which relies on mitochondrial oxidative phosphorylation, dissipates energy to counteract obesity. On the other hand, chronic inflammation in adipose tissue is linked to insulin resistance, type 2 diabetes and obesity. Here we show that nuclear factor I-A (NFIA), a transcriptional regulator of brown and beige adipocytes, improves systemic glucose homeostasis via up-regulation of oxidative phosphorylation and reciprocal down-regulation of inflammation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: BIGWIG
Series
Accession:
GSE228490
ID:
200228490
4.

NFIA in adipocytes reciprocally regulates mitochondrial and inflammatory gene program to improve glucose homeostasis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL16417
54 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE200194
ID:
200200194
5.

NFIA in adipocytes reciprocally regulates mitochondrial and inflammatory gene program to improve glucose homeostasis [ChIP-seq]

(Submitter supplied) Adipose tissue is central to regulation of systemic energy homeostasis. Adaptive thermogenesis in brown and beige adipocytes, which relies on mitochondrial oxidative phosphorylation, dissipates energy to counteract obesity. On the other hand, chronic inflammation in adipose tissue is linked to insulin resistance, type 2 diabetes and obesity. Here we show that nuclear factor I-A (NFIA), a transcriptional regulator of brown and beige adipocytes, improves systemic glucose homeostasis via up-regulation of oxidative phosphorylation and reciprocal down-regulation of inflammation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16417
6 Samples
Download data: BIGWIG
Series
Accession:
GSE200192
ID:
200200192
6.

NFIA Controls the Brown Fat Gene Program by Co-Localizing with PPARgamma at Cell-Type-Specific Enhancers

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL16417 GPL11002
48 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE83764
ID:
200083764
7.

NFIA Controls the Brown Fat Gene Program by Co-Localizing with PPARgamma at Cell-Type-Specific Enhancers (RNA)

(Submitter supplied) Brown fat dissipates energy as heat and protects against obesity. Here, we identified nuclear factor I-A (NFIA) as a novel transcriptional regulator of brown fat by a genome-wide open chromatin analysis of murine brown and white fat followed by motif analysis of brown-fat-specific open chromatin regions. NFIA and the adipogenic master regulator, PPARγ, co-localize at the brown-fat-specific enhancers. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
24 Samples
Download data: TXT
Series
Accession:
GSE83762
ID:
200083762
8.

NFIA Controls the Brown Fat Gene Program by Co-Localizing with PPARgamma at Cell-Type-Specific Enhancers (chromatin)

(Submitter supplied) Brown fat dissipates energy as heat and protects against obesity. Here, we identified nuclear factor I-A (NFIA) as a novel transcriptional regulator of brown fat by a genome-wide open chromatin analysis of murine brown and white fat followed by motif analysis of brown-fat-specific open chromatin regions. NFIA and the adipogenic master regulator, PPARgamma, co-localize at the brown-fat-specific enhancers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16417 GPL17021 GPL11002
24 Samples
Download data: BEDGRAPH, BIGWIG
Series
Accession:
GSE83757
ID:
200083757
9.

NFIA differentially controls adipogenic and myogenic gene program through distinct pathways to ensure adipocyte differentiation [ingSVF RNA-seq]

(Submitter supplied) The transcription factor nuclear factor I-A (NFIA) is a regulator of brown adipocyte differentiation. Here we show that the C-terminal 17 amino acid residues of NFIA (which we named pro#3 domain) is required for transcriptional activity of NFIA. Full-length NFIA, but not deletion mutant lacking pro#3 domain rescued impaired Pparg expression and adipogenesis in NFIA-knockout cells. Mechanistically, the ability of NFIA to increase chromatin accessibility is mediated through pro#3 domain. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
24 Samples
Download data: TXT
Series
Accession:
GSE142609
ID:
200142609
10.

NFIA differentially controls adipogenic and myogenic gene program through distinct pathways to ensure adipocyte differentiation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11002 GPL16417 GPL17021
57 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE130390
ID:
200130390
11.

NFIA differentially controls adipogenic and myogenic gene program through distinct pathways to ensure adipocyte differentiation [RNA-seq]

(Submitter supplied) The transcription factor nuclear factor I-A (NFIA) is a regulator of brown adipocyte differentiation. Here we show that the most C-terminal 17 amino acid residues of NFIA (which we named pro#3 domain) is required for transcriptional activity of NFIA. Full-length NFIA, but not deletion mutant lacking pro#3 domain rescued impaired Pparg expression and adipogenesis in NFIA-knockout cells. Mechanistically, the ability of NFIA to increase chromatin accessibility is mediated through pro#3 domain. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
27 Samples
Download data: TXT
Series
Accession:
GSE130389
ID:
200130389
12.

NFIA differentially controls adipogenic and myogenic gene program through distinct pathways to ensure adipocyte differentiation [chromatin]

(Submitter supplied) The transcription factor nuclear factor I-A (NFIA) is a regulator of brown adipocyte differentiation. Here we show that the C-terminal 17 amino acid residues of NFIA (which we named pro#3 domain) is required for transcriptional activity of NFIA. Full-length NFIA, but not deletion mutant lacking pro#3 domain rescued impaired Pparg expression and adipogenesis in NFIA-knockout cells. Mechanistically, the ability of NFIA to increase chromatin accessibility is mediated through pro#3 domain. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11002 GPL16417
6 Samples
Download data: BIGWIG
Series
Accession:
GSE130388
ID:
200130388
13.

mouse 3T3L1 adipocytes transduced with Lmo3- or LacZ-Adenovirus

(Submitter supplied) Background. Obesity and body fat distribution are important risk factors for the development of type 2 diabetes and metabolic syndrome. Evidence has accumulated that this risk is related to intrinsic differences in behavior of adipocytes in different fat depots. LIM Domain Only 3 (LMO3) plays a crucial role in adipogenesis modulating the key adipogenic master switch PPARγ in human, but not mouse, visceral adipose progenitors; however, despite high expression in mature adipocytes, its function in these cells is currently unknown. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: TXT
Series
Accession:
GSE155781
ID:
200155781
14.

LMO3 reprogramms viseral adipocyte metabolism during obesity

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL19057 GPL6246 GPL6244
16 Samples
Download data: CEL, TXT
Series
Accession:
GSE139163
ID:
200139163
15.

LMO3 reprogramms viseral adipocyte metabolism during obesity [Mouse]

(Submitter supplied) Aims/Hypothesis. The aim of this study was to determine the potential involvement of LMO3-dependent pathways in the modulation of key functions of mature adipocytes during obesity. Methods. Based on a recently engineered hybrid rAAV serotype Rec2 shown to efficiently transduce both brown adipose tissue (BAT) and white adipose tissue (WAT), we delivered YFP  or Lmo3 to epididymal WAT (eWAT) of C57Bl6/J mice on a high fat diet (HFD). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
6 Samples
Download data: CEL
Series
Accession:
GSE139162
ID:
200139162
16.

LMO3 reprogramms viseral adipocyte metabolism during obesity [Human]

(Submitter supplied) Aims/Hypothesis. The aim of this study was to determine the potential involvement of LMO3-dependent pathways in the modulation of key functions of mature adipocytes during obesity. Methods. Based on a recently engineered hybrid rAAV serotype Rec2 shown to efficiently transduce both brown adipose tissue (BAT) and white adipose tissue (WAT), we delivered YFP  or Lmo3 to epididymal WAT (eWAT) of C57Bl6/J mice on a high fat diet (HFD). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
4 Samples
Download data: CEL
Series
Accession:
GSE139155
ID:
200139155
17.

Expression data from human adipose tissue using an expanded patient cohort

(Submitter supplied) Obesity is a risk factor for numerous metabolic disorders; however, not all obese individuals are prone to insulin resistance. The central aim of this study was to identify molecular pathways directly related to insulin resistance independent of BMI in obesity. We sought to determine the gene expression signature of adipose tissue in a body mass index (BMI)-matched obese cohort of patients that are either insulin sensitive or insulin resistant.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3781
Platform:
GPL570
39 Samples
Download data: CEL
Series
Accession:
GSE20950
ID:
200020950
18.
Full record GDS3781

Morbidly obese insulin-resistant patients: omental and subcutaneous adipose tissue

Analysis of subcutaneous and visceral adipose tissue from body mass index (BMI)-matched, obese patients who were insulin-sensitive versus insulin-resistant, thereby eliminating obesity as a variable. Results provide insight into molecular mechanisms mediating obesity-related insulin resistance.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 disease state, 2 gender, 2 tissue sets
Platform:
GPL570
Series:
GSE20950
39 Samples
Download data: CEL
19.

Gene expression Analysis of wild type (WT) and Blnc1 adipose specific transgenic mice (Tg) epididymal WAT (eWAT) Transcriptomes after 21 weeks high fat diet (HFD) feeding

(Submitter supplied) Long noncoding RNAs (lncRNAs) are emerging as powerful regulators of adipocyte differentiation and gene expression. However, their physiological role in adipose tissue biology and systemic energy metabolism has not been established. Here we show that adipose tissue expression of Blnc1, a conserved lncRNA regulator of thermogenic genes, is highly induced in obese mice. Fat-specific inactivation of Blnc1 impairs cold-induced thermogenesis and browning, exacerbates obesity-associated brown fat whitening, and worsens adipose tissue inflammation and fibrosis, leading to more severe insulin resistance and hepatic steatosis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17400
6 Samples
Download data: CEL
Series
Accession:
GSE111865
ID:
200111865
20.

Sex-dependent effects of Siah2 on brown adipose tissue whitening and inflammation with a high fat diet

(Submitter supplied) The goal of this experiment was to examine the sex-dependent effect of Siah2 in brown adipose tissue
Organism:
Mus musculus
Type:
Expression profiling by array
Platforms:
GPL6887 GPL6885
18 Samples
Download data: TXT
Series
Accession:
GSE123990
ID:
200123990
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