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Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [IWAT]

ABSTRACT: Analysis of subcutaneous adipose tissue (IWAT) from Yin Yang 1 brown fat specific knockout mice fed a high fat diet for 2 weeks. The goal was to identify a gene signature of IWAT browning in YY1 mutant mice. Control mice YY1flox/flox versus YY1flox/flox; Ucp1Cre were fed a high fat diet for 2 weeks

ORGANISM(S): Mus musculus

SUBMITTER: Francisco Verdeguer

PROVIDER: E-GEOD-68382 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.

Verdeguer Francisco F Soustek Meghan S MS Hatting Maximilian M Blättler Sharon M SM McDonald Devin D Barrow Joeva J JJ Puigserver Pere P

Molecular and cellular biology 20151026 1

Mitochondrial oxidative and thermogenic functions in brown and beige adipose tissues modulate rates of energy expenditure. It is unclear, however, how beige or white adipose tissue contributes to brown fat thermogenic function or compensates for partial deficiencies in this tissue and protects against obesity. Here, we show that the transcription factor Yin Yang 1 (YY1) in brown adipose tissue activates the canonical thermogenic and uncoupling gene expression program. In contrast, YY1 represses ...[more]

PMID: 26503783

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Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity [BAT]

Project description:Analysis of brown adipose tissue from Yin Yang 1 (YY1) brown fat specific knockout mice fed a high fat diet for 3 months. YY1 deficiency in brown adipose tissue leads to strong thermogenic deficiency. The goal was to identify the genes controlled by YY1 responsible of brown fat defective function. Control mice YY1flox/flox versus YY1flox/flox; Ucp1Cre were fed a high fat diet for 3 months

2015-11-10 | E-GEOD-68429 | biostudies-arrayexpress

Brown fat-specific YY1 deficiency effect on subcutaneous white adipose tissue

Project description:Analysis of visceral white adipose tissue (EWAT) from Yin Yang 1 adipose-specific knockout mice exposed to cold (4ºC) for 4 days. Control mice YY1flox/flox versus YY1flox/flox; Adiponectin Cre were cold exposed for 4 days.

2015-11-10 | E-GEOD-70562 | biostudies-arrayexpress

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-11-10 | E-GEOD-68443 | biostudies-arrayexpress

Expression data from mouse skeletal muscle

Project description:We generated skeletal muscle-specific knockout mice lacking the transcription factor Yin Yang 1 (YY1) and analyzed expression patterns in the skeletal muscle these mice. We used microarrays to detail the global programme of gene expression regulated by YY1. Wild type or knockout mice at 6 months were sacrificed and the soleus was isolated for RNA extraction.

2012-06-29 | E-GEOD-39009 | biostudies-arrayexpress

Identification of genes characteristic of primary inguinal or epididymal preadipocyte fibroblasts

Project description:Committed preadipocyte fibroblasts were genetically labelled in transgenic mice by expressing GFP under the control of the locus for Zfp423, a gene controlling preadipocyte determination. These mice are herein referred to as Zfp423-GFP mice. The overall goal was to identify genes differentially expressed between adipogenic GFP+ firboblasts and non-adipogenic GFP- fibroblasts from either inguinal or epididymal fat stromal vascular cultures obtained from Zfp423-GFP mice. Adipose stromal vascular cultures were obtained from inguinal or epididymal fat of 6-8 week-old male Zfp423-GFP mice. GFP+ and GFP- fibroblasts were sorted from fat stromal vascular cultures and then returned to culture. Subconfluent cultures of GFP+ and GFP- cells were compared in triplicate for Affymetrix analysis.

2011-12-31 | E-GEOD-34775 | biostudies-arrayexpress

Identification of genes characteristic of committed preadipocyte fibroblasts

Project description:In order to identify the molecular mechanisms controlling preadipocyte commitment we derived new sublines of Swiss 3T3 fibroblasts with varying potential for adipogenesis. Swiss 2, Swiss 8, Swiss 9, and Swiss 19 differentiate into fat cells while Swiss 3, Swiss 5, and Swiss 22 have a lower propensity to differentiate into fat cells. The overall goal was to identify genes whose expression in the fibroblast state correlates with the ultimate potential of the cells to undergo adipogenesis 4 preadipose fibroblast cell lines (Swiss 2, Swiss 8, Swiss 9, and Swiss 19 in triplicate or duplicate) were compared to 3 non-adipogenic fibroblast cell lines (Swiss 3, Swiss 5, Swiss 22 in triplicate)

2010-02-21 | E-GEOD-19732 | biostudies-arrayexpress

Adiponectin-cre FTO flox/flox and FTO flox/flox mouse white fat tissues

Project description:Single nucleotide polymorphisms in intron 1 of the fat mass and obesity-associated (FTO) gene were found to be associated with an increased risk of adult obesity. Enhanced FTO expression in mice leads to hyperphagia, increased fat mass, and higher body weight. Neuronal-specific FTOâ??deleted mice have an identical lean body weight phenotype to global FTO-deleted mice. The physiological role of adipose FTO in the homeostasis of energy regulation remains to be elucidated. We used microarrays to elucidate the metabolic pathways that are regulated by FTO in the white fat. FTO flox/flox and Adiponectin-cre FTO flox/flox (AFO) mice were fed with chow diet. White fat tissues from epididymal adipose pad were harvested under ad lib condition for RNA isolation. Three independent pools of FTO flox/flox and AFO mouse white fat RNA were included in the study.

2016-07-03 | E-GEOD-65098 | biostudies-arrayexpress

Transcription profiling of mouse LckCre, CD4Cre-Ctnnbex3 mutants before and after T-cell transformation reveals stabilization of b-catenin induces lymphomas

Project description:Activation of b-catenin has been causatively linked to the etiology of colon cancer. Conditional stabilization of this molecule in pro-T-cells promotes thymocyte development without the requirement for preTCR signaling. We show here that activated b-catenin stalls the developmental transition from the double-positive (DP) to the single-positive (SP) thymocyte stage and predisposes DP thymocytes to transformation. b-Catenin induced thymic lymphomas have a leukemic arrest at the early DP stage. Lymphomagenesis requires Rag activity, which peaks at this developmental stage, as well as additional secondary genetic events. A consistent secondary event is the transcriptional upregulation of c-Myc, whose activity is required for transformation since its conditional ablation abrogates lymphomagenesis. In contrast, the expression of Notch receptors as well as targets is reduced in DP thymocytes with stabilized b-catenin and remains low in the lymphomas indicating that Notch activation is not required or selected for in b-catenin induced lymphomas. Thus, b-catenin activation may provide a mechanism for the induction of T-ALL that does not depend on Notch activation. Experiment Overall Design: This study was used to compare gene expression patterns of LckCre mice, CD4Cre-Ctnnbex3 mice before and after T-cell transformation. 5 independent Lckcre (control), 5 independent CD4Cre-Ctnnbex3 mice and 8 independent mice with lymphomas were used. Thymocytes or tumor masses were collected from Lckcre, CD4Cre-Ctnnbex3 mice. Total RNA isolation and purification followed by synthesis of dscDNA, Biotinylated cRNA and purification of Biotinylated cRNA. Then the hybridization to Affymetrix âMouse Expression Array 430 Genechipsâ was done. Data was analysed by dchip.

2008-06-15 | E-GEOD-7050 | biostudies-arrayexpress

Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors

Project description:The goal of this study is to derive a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the hematopoietic transcription factor, GATA1 (called GATA1s mutation). We achieved this through transduction of Gata1s mutant fetal progenitors by MSCV-based retrovirus expressing a GFP marker, followed by in vitro selection (for immortalized cell lines), and then in vivo selection (for transformed cell lines) through transplantation. Here we report one such cell line [T6(6)] that gives rise to megakaryocytic leukemia (M7 leukemia) upon transplantation. Since the leukemic cells were retrovirally tagged with a GFP reporter, we sorted GFP+ leukemic blasts and generated their expression profiles by microarray.

2010-08-01 | E-GEOD-16682 | biostudies-arrayexpress

Developmental stage-specific interplay between GATA1 and IGF signaling in fetal hematopoiesis and leukemogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE16676: Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1 GSE16677: Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples GSE16679: Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia GSE16682: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors GSE16684: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors depends on IGF signaling Refer to individual Series

2010-08-01 | E-GEOD-16655 | biostudies-arrayexpress

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