Response of C2C12-hN1∆ECD to DAPT washout
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE72847 | GEO | 2016/09/04
SECONDARY ACCESSION(S): PRJNA295185
REPOSITORIES: GEO
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Project description:C2C12 cells expressing constitutively active hN1âECD were activated by complete DAPT washout for 1h or 6h, or left in 10 uM DAPT 2 Samples and 1 Control
2016-09-04 | E-GEOD-72847 | biostudies-arrayexpress
Project description:The Notch signaling pathway regulates several processes including development and differentiation and its aberrant regulation leads to several diseases. Here, we analyzed the gene expression profile upon washout of the Notch inhibitor DAPT in mouse pre-T (Beko) cells.
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Project description:Purpose: To study the expression and function of a novel cell cycle regulatory protein, human ecdysoneless (Ecd), during pancreatic cancer (PC) pathogenesis. Experimental Design: Immunohistochemical expression profiling of Ecd was done in non-neoplastic normal pancreatic tissues and pancreatic ductal adenocarcinoma lesions (from tissue microarray and Rapid Autopsy program) as well as precancerous PanIN lesions and metastatic organs. To analyze the biological significance of Ecd in PC progression, Ecd was stably knocked down in PC cell line followed by in vitro and in vivo functional assays. Results: Normal pancreatic ducts show very weak to no Ecd expression compared to significant positive expression in PC tissues (mean±SE composite score: 0.3±0.2 and 3.8±0.2 respectively, p<0.0001) as well as in PanIN precursor lesions with a progressive increase in Ecd expression with increasing dysplasia (PanIN-1 to PanIN-3). Analysis of matched primary tumors and metastases from PC patients revealed that Ecd is highly expressed in both primary pancreatic tumor and in distant metastatic sites. Further, knockdown of Ecd suppressed cell proliferation in vitro and tumorigenicity of PC cells in mice orthotopic tumors. Microarray study revealed that Ecd regulates expression of glucose transporter GLUT4 in PC cells and was subsequently shown to modulate glucose uptake, lactate production and ATP generation by PC cells. Finally, knockdown of Ecd also reduced level of pAkt, key signaling molecule known to regulate aerobic glycolysis in cancer cells. Conclusion: Ecd is a novel tumor promoting factor that is differentially expressed in pancreatic cancer and potentially regulates glucose metabolism within cancer cells. Two-condition experiment, Ecd knockdown vs Scrambled cells. Biological replicates: 3 Ecd knockdownl, 3 Scrambled, independently grown and harvested. One replicate per array
2012-08-09 | E-GEOD-39988 | biostudies-arrayexpress
Project description:Purpose: To study the expression and function of a novel cell cycle regulatory protein, human ecdysoneless (Ecd), during pancreatic cancer (PC) pathogenesis. Experimental Design: Immunohistochemical expression profiling of Ecd was done in non-neoplastic normal pancreatic tissues and pancreatic ductal adenocarcinoma lesions (from tissue microarray and Rapid Autopsy program) as well as precancerous PanIN lesions and metastatic organs. To analyze the biological significance of Ecd in PC progression, Ecd was stably knocked down in PC cell line followed by in vitro and in vivo functional assays. Results: Normal pancreatic ducts show very weak to no Ecd expression compared to significant positive expression in PC tissues (mean±SE composite score: 0.3±0.2 and 3.8±0.2 respectively, p<0.0001) as well as in PanIN precursor lesions with a progressive increase in Ecd expression with increasing dysplasia (PanIN-1 to PanIN-3). Analysis of matched primary tumors and metastases from PC patients revealed that Ecd is highly expressed in both primary pancreatic tumor and in distant metastatic sites. Further, knockdown of Ecd suppressed cell proliferation in vitro and tumorigenicity of PC cells in mice orthotopic tumors. Microarray study revealed that Ecd regulates expression of glucose transporter GLUT4 in PC cells and was subsequently shown to modulate glucose uptake, lactate production and ATP generation by PC cells. Finally, knockdown of Ecd also reduced level of pAkt, key signaling molecule known to regulate aerobic glycolysis in cancer cells. Conclusion: Ecd is a novel tumor promoting factor that is differentially expressed in pancreatic cancer and potentially regulates glucose metabolism within cancer cells.
2012-08-10 | GSE39988 | GEO
Project description:Overexpression of ECD in mammary gland promotes mammary tumorigenesis. To determine the plausible mechanism of how ECD contributes the oncogenesis, we performed RNAseq analysis of three independent control mice mammary glands (6 months old) and four independent ECD transgenic mammary tumors. Out of these four tumors, T1a and T1b were adenosquamous carcinoma type, T3 was Spindle cell carcinoma type and T4 was papillary carcinoma. RNA was isolated from the respective samples and RNAseq was performed.
2022-05-18 | GSE200838 | GEO
Project description:Identification of the interaction partners of the protein ecdysoneless (Ecd) in Drosophila melanogaster S2 cells as well as profiling of the changes in binding for mutant, truncated Ecd del34 protein.
2021-09-09 | PXD019838 | Pride
Project description:In this work we identify changes in Muller glial cell chromatin accessibility in response to DAPT-treatment
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Project description:Analysis of gene expression changes that occur in keratinocytes during reprogramming when they are treated with DAPT, a small molecule gamma-secretase inhibitor. The hypothesis tested in the present study was that Notch inhibition by DAPT treatment would promote reprogramming by inhibiting p21 activity while leaving p53 expression intact. Results provide important information of the gene expression changes in response to DAPT treatment, such as changes in the expression of p21, p21-responsive genes, p53, p53-responsive genes involved in apoptosis, and Notch-responsive genes.
2014-05-25 | GSE35090 | GEO
Project description:In this work we identify genes differentially expressed in Muller glia from uninjured retina in zebrafish treated with and without DAPT for 1 day.
2021-07-31 | GSE160047 | GEO