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Gene expression data from differentiated myoblastic C2C12 cells expressing constitutively active estrogen receptor α

ABSTRACT: Gene expression data from differentiated myoblastic C2C12 cells expressing constitutively active estrogen receptor α

PROVIDER: PRJNA436727 | ENA |

REPOSITORIES: ENA

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Gene expression data from differentiated myoblastic C2C12 cells expressing constitutively active estrogen receptor α

Project description:To examine the role of estrogen in muscle, differentiated myoblastic C2C12 cells were transduced with adenoviruses expressing constitutively active estrogen receptor α mutant (Ad-caERα) or DsRed (Ad-DsRed) as a control. Microarray analysis showed that the mRNA level of nuclear receptor subfamily 4 group A member 1 (NR4A1) was upregulated by the Ad-caERα compared with the control Ad-DsRed.

2019-03-01 | GSE111367 | GEO

LaminB1 DamID in undifferentiated mouse C2C12 myoblasts (ATCC, Lot 59501261) and differentiated C2C12 myotubes

Project description:Maps of genomic regions in proximity to the nuclear lamina were determined in undifferentiated C2C12 myoblasts (MBs) and 6 day differentiated C2C12 myotubes (MTs) using DamID with a Dam-Lamin B1-encoding lentivirus.

2016-06-17 | GSE80328 | GEO

Transcription profiling of MCF-7 cell lines stably overexpressing constitutively active Raf-1, constitutively active MEK, constitutively active c-erbB-2, or ligand-activatable EGFR as models of overexpressed growth factor signaling

Project description:Profiling of MCF-7 cell lines stably overexpressing constitutively active Raf-1, constitutively active MEK, constitutively active c-erbB-2, or ligand-activatable EGFR as models of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2). Experiment Overall Design: Cell lines were profiled in biological triplicates, 18 arrays in all.

2007-10-02 | E-GEOD-3542 | biostudies-arrayexpress

Transcription profiling of mouse undifferentiated C2C12 myoblast to 4 day differentiated myotubes

Project description:Comparison of undifferentiated C2C12 myoblast to 4 day differentiated myotubes. Experiment Overall Design: this experiment include 2 samples and 6 replicates

2008-06-12 | E-GEOD-3243 | biostudies-arrayexpress

Emergence of constitutively active estrogen receptor-α mutations in pretreated advanced estrogen receptor-positive breast cancer.

Project description:PurposeWe undertook this study to determine the prevalence of estrogen receptor (ER) α (ESR1) mutations throughout the natural history of hormone-dependent breast cancer and to delineate the functional roles of the most commonly detected alterations.Experimental designWe studied a total of 249 tumor specimens from 208 patients. The specimens include 134 ER-positive (ER(+)/HER2(-)) and, as controls, 115 ER-negative (ER(-)) tumors. The ER(+) samples consist of 58 primary breast cancers and 76 metastatic samples. All tumors were sequenced to high unique coverage using next-generation sequencing targeting the coding sequence of the estrogen receptor and an additional 182 cancer-related genes.ResultsRecurring somatic mutations in codons 537 and 538 within the ligand-binding domain of ER were detected in ER(+) metastatic disease. Overall, the frequency of these mutations was 12% [9/76; 95% confidence interval (CI), 6%-21%] in metastatic tumors and in a subgroup of patients who received an average of 7 lines of treatment the frequency was 20% (5/25; 95% CI, 7%-41%). These mutations were not detected in primary or treatment-naïve ER(+) cancer or in any stage of ER(-) disease. Functional studies in cell line models demonstrate that these mutations render estrogen receptor constitutive activity and confer partial resistance to currently available endocrine treatments.ConclusionsIn this study, we show evidence for the temporal selection of functional ESR1 mutations as potential drivers of endocrine resistance during the progression of ER(+) breast cancer.

| S-EPMC3998833 | biostudies-literature

Effect of ATF4 overexpression on mRNA levels in differentiated C2C12 myotubes.

2012-09-15 | GSE39194 | GEO

Effect of ATF4 overexpression on mRNA levels in differentiated C2C12 myotubes.

Project description:ATF4 is a bZIP transcription factor that that promotes skeletal muscle atrophy. The goal of these studies was to determine the effects of ATF4 overexpression on mRNA levels in differentiated C2C12 myotubes. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12,2012 C2C12 myotubes were infected with adenovirus co-expressing eGFP and ATF4-FLAG. Control myotubes were infected with adenovirus co-expressing eGFP and a transcriptionally inactive ATF4 construct (ATF4∆bZIP).

2012-09-15 | E-GEOD-39194 | biostudies-arrayexpress

DeepCAGE and DeepSAGE with proliferating and differentiated C2C12 mouse myoblasts

Project description:We use tag-based next generation sequencing analysis to quantify gene expression levels during myogenic differentiation and focused on the identifcation of novel 3' ends with DeepSAGE and novel 5' ends with DeepCAGE. Illumina DeepCAGE and DeepSAGE with C2C12 cells at time points T0 (proliferating) and T9 (differentiated) days of differentiation.

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Constitutively Active YAP/TAZ Target Genes

Project description:Constitutively Active YAP/TAZ Target Genes

| PRJNA489431 | ENA

TEAD4 occupied genes in differentiated C2C12 myoblasts

Project description:The TEAD (1-4) transcription factors comprise the conserved TEA/ATTS DNA binding domain recognising the MCAT element in the promoters of muscle-specific genes. Despite extensive genetic analysis, the function of TEAD factors in muscle differentiation has proved elusive due to redundancy amongst the family members. Expression of the TEA/ATTS DNA binding domain that acts a dominant negative repressor of TEAD factors in C2C12 myoblasts inhibits their differentiation, while selective shRNA knockdown of TEAD4 results in abnormal differentiation characterised by the formation of shortened myotubes. Chromatin immunoprecipitation coupled to array hybridisation (ChIP-chip) shows that TEAD4 occupies 867 promoters including those of myogenic miRNAs. We show that TEAD factors cooperate with MYOD1 to directly induce Myogenin, CDKN1A and Caveolin 3 expression to promote myoblast differentiation and fusion. RNA-seq identifies a novel set of TEAD4 target genes encoding muscle structural and regulatory proteins and those required for the unfolded protein response. In contrast, TEAD4 represses expression of the growth factor CTGF and Cyclin D1 to promote differentiation. Together these results show that TEAD factor activity is essential for C2C12 cell differentiation and define a novel and nonredundant role for TEAD4 in regulating the unfolded protein response. C2C12 cells were infected with retrotiviral vector expressing Flag-HA-Tagged TEAD4 or with empty control vector and selected in the continouos presence of puromycin. Infected cell populations were then differentiated for 5 days in DMEM medium with 2% horse serum and fixed in 0.4% formaldehyde.

2011-08-21 | E-GEOD-29208 | biostudies-arrayexpress

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