Similar Datasets
Project description:H3k27ac assessment by ChIPseq was performed on 16h-activated naïve CD4+ T cells with variables of RARα expression and RA concentration.
2022-10-05 | GSE201728 | GEO
Project description:ChIPseq to detect binding of Nup98, SET1A to chromatin and to observe H3K4me3 on chromatin under various conditions
2018-04-11 | GSE112928 | GEO
Project description:There is increasing evidence that microRNA and transcription factors interact in an instructive fashion in normal and malignant hematopoiesis. We explored the impact of TEL-AML1 (ETV6-RUNX1), the most common fusion protein in childhood leukemia, on miRNA expression and the leukemic phenotype. Using RNA interference, miRNA expression arrays, and quantitative PCR, we identified miRNA-494 and miRNA-320a to be upregulated upon TEL-AML1 silencing independently of TEL expression. Chromatin immunoprecipitation analysis identified miRNA-494 as a direct miRNA target of the fusion protein TEL-AML1. Using bioinformatic analysis as well as functional luciferase experiments we demonstrate that survivin is a target of the two miRNAs. MiRNA-494 and -320a were introduced to the cells by transfection and survivin expression determined by western blot analysis. These miRNAs blocked survivin expression and resulted in apoptosis in a similar manner as TEL-AML1 silencing by itself; this silencing was also shown to be DICER-dependent. MiRNAs-494 and -320a are expressed at lower levels in TEL-AML1+ leukemias compared to immunophenotype-matched non-TEL-AML1 ALL subtypes, and within TEL-AML1+ leukemias their expression is correlated to survivin levels. In summary our data suggest that TEL-AML1 might exert its anti-apoptotic action at least in part by suppressing miRNA-494 and miRNA-320a, lowering their expression causing enhanced survivin expression.
2010-08-28 | GSE23842 | GEO
Project description:Background: Survivin was described as strongly expressed in human cancer. To date, little is known about the association between Survivin splice variants and the other apoptosis-related genes. In this study, we analyzed the apoptosis gene signature of Survivin and its variant expression in breast cancer. Methods: Expression of the 5 transcripts was measured by RT-PCR in 135 breast carcinomas. Human Apoptosis Gene Arrays were used to screen the genes that could be associated with Survivin variants. Cox survival analysis was analyzed according to the breast cancer patient outcome. Results: Significant associations between Survivin transcript and the apoptotic gene array were found. Interestingly, Survivin-3B variant showed major inverse correlations with the pro-apoptotic gene array. Overexpression of Survivin-3B strongly inhibits 5-fluorouracil/epirubicin/Cyclophosphamide induced-apoptosis in breast tumor cell lines. In breast carcinomas, uni- and multivariate analysis showed patients with high level of survivin-3B expression had a shorter overall (p=0.030 and p=0.042, respectively) and disease-free (p=0.024 and p=0.009) survival. Conclusion: Our data indicate Survivin-3B could have an anti-apoptotic activity and its expression level might be used as a prognostic marker in breast carcinoma.
2010-10-06 | GSE24556 | GEO
Project description:The liver possesses remarkable regenerative capacity in response to injury. Upon partial hepatectomy (PHx), terminally differentiated hepatocytes in the remaining liver enter the cell cycle and restore the liver mass and function within weeks. However, liver regeneration is often impaired in livers with chronic diseases. Survivin, an inhibitor of apoptosis protein (IAP) and member of chromosome passenger complex (CPC), plays versatile roles in cell mitosis and apoptosis. We and others found that the expression of Survivin was highly increased in liver during PHx-induced liver regeneration, which indicated that Survivin played important roles in this process. However, the function of Survivin in liver regeneration remains largely undefined. Here, using mice with genetic deletion of Survivin, we found that during PHx-induced liver regeneration Survivin regulated both hepatocyte G1/S phase transition by inhibiting the expression of p21 and G2/M phase transition by regulating the localization of CPC. Moreover, restoration of Survivin expression in Survivin-deficient hepatocytes inhibited p21 expression and promote both hepatocyte G1/S and G2/M transition during PHx-induced liver regeneration.
2017-01-01 | GSE83598 | GEO
Project description:There is increasing evidence that microRNA and transcription factors interact in an instructive fashion in normal and malignant hematopoiesis. We explored the impact of TEL-AML1 (ETV6-RUNX1), the most common fusion protein in childhood leukemia, on miRNA expression and the leukemic phenotype. Using RNA interference, miRNA expression arrays, and quantitative PCR, we identified miRNA-494 and miRNA-320a to be upregulated upon TEL-AML1 silencing independently of TEL expression. Chromatin immunoprecipitation analysis identified miRNA-494 as a direct miRNA target of the fusion protein TEL-AML1. Using bioinformatic analysis as well as functional luciferase experiments we demonstrate that survivin is a target of the two miRNAs. MiRNA-494 and -320a were introduced to the cells by transfection and survivin expression determined by western blot analysis. These miRNAs blocked survivin expression and resulted in apoptosis in a similar manner as TEL-AML1 silencing by itself; this silencing was also shown to be DICER-dependent. MiRNAs-494 and -320a are expressed at lower levels in TEL-AML1+ leukemias compared to immunophenotype-matched non-TEL-AML1 ALL subtypes, and within TEL-AML1+ leukemias their expression is correlated to survivin levels. In summary our data suggest that TEL-AML1 might exert its anti-apoptotic action at least in part by suppressing miRNA-494 and miRNA-320a, lowering their expression causing enhanced survivin expression. DNAs from REH cells were pulled down using ChIP antibodies to TEL and hybridized to microRNA promoter tiling arrays.
2010-08-28 | E-GEOD-23842 | biostudies-arrayexpress
Project description:As a part of a modelling experiment for transcriptional control of mouse primordial germ cell specification, the transcription factor BLIMP1 was transiently expressed in the mouse p19 embryonal carcinoma cell line and its genome wide binding sites were defined using ChIPseq.
2013-07-17 | E-MTAB-1599 | biostudies-arrayexpress
Project description:As a part of a modelling experiment for transcriptional control of mouse primordial germ cell specification, the transcription factor AP2gamma was stably expressed in the mouse p19 embryonal carcinoma cell line and its genome wide binding sites were defined using ChIPseq.
2013-07-17 | E-MTAB-1600 | biostudies-arrayexpress
Project description:Background: Survivin was described as strongly expressed in human cancer. To date, little is known about the association between Survivin splice variants and the other apoptosis-related genes. In this study, we analyzed the apoptosis gene signature of Survivin and its variant expression in breast cancer. Methods: Expression of the 5 transcripts was measured by RT-PCR in 135 breast carcinomas. Human Apoptosis Gene Arrays were used to screen the genes that could be associated with Survivin variants. Cox survival analysis was analyzed according to the breast cancer patient outcome. Results: Significant associations between Survivin transcript and the apoptotic gene array were found. Interestingly, Survivin-3B variant showed major inverse correlations with the pro-apoptotic gene array. Overexpression of Survivin-3B strongly inhibits 5-fluorouracil/epirubicin/Cyclophosphamide induced-apoptosis in breast tumor cell lines. In breast carcinomas, uni- and multivariate analysis showed patients with high level of survivin-3B expression had a shorter overall (p=0.030 and p=0.042, respectively) and disease-free (p=0.024 and p=0.009) survival. Conclusion: Our data indicate Survivin-3B could have an anti-apoptotic activity and its expression level might be used as a prognostic marker in breast carcinoma. The expression of 96 apoptosis genes and was analyzed in 41 breast carcinomas and 1 pool of normal mammary tissues. In parallel, every survivin isoform expression was quantified by real-time quantitative PCR. Data obtained with the macro-array were correlated with survivin isoform levels detected by RT-PCR.
2010-10-06 | E-GEOD-24556 | biostudies-arrayexpress
Project description:Purpose: The purpose of this study is to find the binding partner of IRF4 in the context of Th17- cell differentiation. To this end, we have used ChIPseq analysis followed by de novo motif search around genome-wide binding sites to identify BATF as the binding partner for IRF4 in the context of not only Th17 cells but other immune cell types as well. Naïve T-cells isolated from the spleen of C57BL/6J mice are cultured under Th17, Th2 or Th0 polarizing conditions for 42 hrs and subject to ChIP using IRF4 and/or BATF antibodies followed by high-throughput sequencing. Bone marrow derived dendritic cells (BMDCs) were stimulated with LPS for 6hrs and similrly subjected to ChIPseq analysis with IRF4.
2012-09-13 | E-GEOD-40727 | biostudies-arrayexpress