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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE68429 | GEO | 2015/11/10

SECONDARY ACCESSION(S): PRJNA282723

REPOSITORIES: GEO

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

Project description: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

2015-11-10 | E-GEOD-68382 | biostudies-arrayexpress

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

2015-11-10 | GSE68382 | GEO

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.

2015-11-10 | GSE70562 | GEO

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

Differentially expressed genes between YY1 knockdown and control cells, transfected in colorectal cancer cell line SW48

Project description:Yin Yang 1 (YY1) is a multifunctional transcription factor with critical roles in carcinogenesis and metastasis. However, its biological role and clinical impact in colorectal cancer (CRC) remain unclear. This study aimed to elucidate the oncological role of YY1 in CRC. To indentify the target genes of YY1, microarray analysis was performed on siYY1 and siControl transfected cells.

2022-01-19 | GSE193949 | GEO

Differentially expressed genes between YY1 knockdown and control cells, transfected in colorectal cancer cell line DLD-1

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Transcriptome Analysis Identifies Linc-Yy1, A Novel Functional LincRNA During Myogenesis

Project description:Little is known how lincRNAs are involved in skeletal myogenesis. Here we describe the discovery of a novel lincRNA, Linc-YY1 from the promoter of transcription factor (TF) Yin Yang 1 (YY1) gene. We demonstrate that Linc-YY1 is dynamically regulated during myogenesis in vitro and in vivo. Gain or loss of function of Linc-YY1 in C2C12 myoblast cells or satellite cells alters myogenic differentiation and in injured muscles impacts the course of regeneration. Further studies suggest LincYY1 may interact with YY1 through its middle domain to evict YY1

2015-10-16 | GSE74049 | GEO

A novel YY1-miR-1 regulatory circuit in skeletal myogenesis revealed by genome-wide prediction of YY1-miRNA network

Project description:microRNAs (miRNAs) are non-coding RNAs that regulate gene expression post-transcriptionally, and mounting evidences support the prevalence and functional significance of their interplay with transcription factors (TFs). Here we describe the identification of a regulatory circuit between muscle miRNAs (miR-1, miR-133 and miR-206) and Yin Yang 1 (YY1), an epigenetic repressor of skeletal myogenesis. Genome-wide identification of potential YY1 down-stream targets by combining computational prediction with expression profiling data reveals a large number of putative miRNA targets of YY1 during skeletal myoblasts differentiation into myotubes with muscle miRs rank on top of the list. Murine skeletal muscle cells (C2C12 cells) were differentiated for 0, 1 or 3 days. Total RNAs were isolated from the cells and used for array profiling of miRNA expression.

2011-12-31 | E-GEOD-32238 | biostudies-arrayexpress

Steap4 controls adipocyte thermogenesis and energy expenditure by modulating mitochondrial function

Project description:Steap4, a highly expressed protein in adipose tissue, has been implicated in metabolic homeostasis. In this study, we generated adipocyte-specific Steap4-deficient mice and observed that Steap4 deficiency led to increased fat mass and severe insulin resistance in a high-fat diet model. Mass spectrometry analysis revealed two classes of Steap4 interactomes: mitochondrial proteins and proteins involved in spliceosome. RNA-seq analysis of white adipose tissue demonstrated that Steap4 deficiency altered RNA splicing patterns with enriched functions in mitochondria. While interactome and transcriptome data implicate a role of Steap4 in mitochondria, Steap4 deficiency indeed impaired mitochondrial respiratory chain complex activity resulting in mitochondrial dysfunction in white adipose tissue. Consistently, brown adipocyte-specific Steap4-deficient mice also showed impaired mitochondrial function, increased whitening of brown adipose tissue, reduced energy expenditure, and exacerbated insulin resistance under HFD conditions. Overall, our findings elucidate the critical role of Steap4 in regulating adipocyte thermogenesis and energy expenditure by modulating mitochondrial function.

2025-02-03 | PXD046997 | Pride

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