MiRNA expression in oxygen-stable HIF1 transgenic mice
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PROVIDER: PRJNA489479 | ENA |
REPOSITORIES: ENA
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Project description:Oxygen-stable HIF1 was inducibly expressed in cardiomyocytes of double transgenic mice. Specifically, tetracycline-inducible HIF-PPN mice (Pro402, Pro564 and Asn803 of HIF1a were mutated to Ala residues to limit degradation, termed HIF-PPN) were crossed to a-MHC-tTA expressing mice. HIF-PPN expression was induced by removal of doxycycline for 3 days and compared to control hearts that remained on doxycycline (uninduced).
2019-01-09 | GSE119535 | GEO
Project description:Ischemic heart disease is a leading cause of heart failure and hypoxia inducible factor 1 (HIF1) has been shown to be a key transcription factor in the early response to hypoxic injury. We previously developed an inducble model of cardiomyopathy using cardiomyocyte-specific expression of a mutated, oxygen-stable form of HIF-1⍺ (HIF-PPN). In this study, we used high throughput sequencing to explore HIF1-mediated transcriptional changes in the heart.
2021-06-15 | GSE148351 | GEO
Project description:RNA-Seq of silenced MYB123 stable transgenic plants
| PRJNA635423 | ENA
Project description:DNA binding profiling of endogenous HIF1A on proximal promoters in human HeLa cells exposed to 1% oxygen (hypoxia), using normoxic cells (21% oxygen) as reference.<br><br>Biological background: The Hypoxia Inducible Factor Family of transcription factors is proposed as the main orchestrator of the cellular response to hypoxia. HIFs are heterodimers of a HIF alpha and a HIF beta subunit. HIF alpha protein stability is regulated by oxygen-dependent proteasomal degradation, and hence HIFs are strongly stabilized in hypoxia.<br><br>Purpose of the study: a number of HIF1 ChIP-chip studies have been reported, employing various cell types, array platforms and HIF antibodies, and the overlap of HIF binding locations in these studies is relatively small. The aim of this study was to characterize HIF1 binding in an additional cell line (HeLa), and employing a different HIFalpha antibody.<br><br>Experimental design: We conducted a total of six hybridizations employing four biological replicates. For two biological replicates, we performed dye-swap technical replicate experiments.<br><br>Results summary: We identified 55 HIF binding locations in HeLa cells (FDR<2%). While this number is relatively low compared to previous studies, presumably due to limiting antibody sensitivity, the overlap with data from other cell lines is comparable to our HeLa data.
2012-05-20 | E-MEXP-3499 | biostudies-arrayexpress
Project description:Report of an RNA-Seq analysis done with strawberries taken from MYB123 RNAi silenced and stable transgenic plants vs control plants transformed with the pFRN empty vector
2021-05-25 | GSE151308 | GEO
Project description:Background In mammalian ovaries, the majorities of developing follicles (up to 95% in human) undergo atresia. A considerable part of follicle atresia is initiated by granulosa cell (GCs) apoptosis. Our previous work identified hypoxia-inducible factors 1 (HIF1) pathway induced by follicle-stimulating hormone as a protective factor against atresia, yet the molecular mechanism of follicles’ “norm” death, and how HIF1 pathway protect follicles has not been fully delineated. Methods We employed a single-follicle, multi-dimensional profiling strategy based on serial sectioning, to dissect the signaling logic underlying physiological follicle fate decisions. Results HIF1 and forkhead box protein O1 (FOXO1) pathway show complementary activation patterns in GCs of healthy versus atretic mouse follicles. In growing mouse follicles, HIF1 pathway activity is associated with increased reactive oxygen species (ROS)-related signals, likely through enhanced granulosa-cell metabolic activity. Under the physiological conditions, ROS-related signals appear to help maintain HIF1 pathway activity in mouse granulosa cells during follicle growth, and are not by themselves associated with follicle atresia. HIF1 pathway appears to promote Bcl-XL expression, which may counterbalance FOXO1-associated atretic pressure. Conclusion In mouse ovaries, follicular fate appears to be associated with the dynamic balance between the pro-survival HIF1/Bcl-XL axis and the pro-apoptotic FOXO1/Bim axis.
2026-06-11 | GSE335191 | GEO
Project description:Background In mammalian ovaries, the majorities of developing follicles (up to 95% in human) undergo atresia. A considerable part of follicle atresia is initiated by granulosa cell (GCs) apoptosis. Our previous work identified hypoxia-inducible factors 1 (HIF1) pathway induced by follicle-stimulating hormone as a protective factor against atresia, yet the molecular mechanism of follicles’ “norm” death, and how HIF1 pathway protect follicles has not been fully delineated. Methods We employed a single-follicle, multi-dimensional profiling strategy based on serial sectioning, to dissect the signaling logic underlying physiological follicle fate decisions. Results HIF1 and forkhead box protein O1 (FOXO1) pathway show complementary activation patterns in GCs of healthy versus atretic mouse follicles. In growing mouse follicles, HIF1 pathway activity is associated with increased reactive oxygen species (ROS)-related signals, likely through enhanced granulosa-cell metabolic activity. Under the physiological conditions, ROS-related signals appear to help maintain HIF1 pathway activity in mouse granulosa cells during follicle growth, and are not by themselves associated with follicle atresia. HIF1 pathway appears to promote Bcl-XL expression, which may counterbalance FOXO1-associated atretic pressure. Conclusion In mouse ovaries, follicular fate appears to be associated with the dynamic balance between the pro-survival HIF1/Bcl-XL axis and the pro-apoptotic FOXO1/Bim axis.
2026-06-11 | GSE304305 | GEO
Project description:An oxygen stable form of HIF-1alpha was overexpressed in the hearts of mice, under tet-off control. Bi-allelic transgenic mice were created by crossing alpha-MHC promoter/tet transactivating protein expressing mice with tet responsive element promter/stable HIF-1alpha protein expressing mice. Mice were either, maintained on Doxycycline (inhibiting the expression of the HIF-1alpha transgene) or removed from doxycycline (inducing expression) for one or three days.
2010-05-15 | E-GEOD-12673 | biostudies-arrayexpress
Project description:Hypoxia inducible factors (HIF)1 and 2 are transcription factors which regulate the homeostatic response to low oxygen conditions. Since data related to the importance of HIF1 and 2 in haematopoietic stem and progenitors is conflicting, we investigated the chromatin binding profiles of HIF1 and HIF2 and linked that to transcriptional networks and the cellular metabolic state. Genome-wide ChIP-seq and transcriptome studies revealed that overlapping HIF1- and HIF2-controlled loci were highly enriched for various processes like including metabolism, particularly those involved in glucose metabolism, but also for chromatin organization, cellular response to stress and G protein-coupled receptor signaling. ChIP-qPCR validation studies confirmed that glycolysis-related genes - but not genes related to the TCA cycle or glutaminolysis - were controlled by both HIF1 and HIF2 in leukemic cell lines and primary AMLs, while in healthy human CD34+ cells these loci were predominantly controlled by HIF1 but not HIF2. However, and in contrast to our initial hypotheses, CRISPR/Cas9-mediated knockout of HIF signaling did not affect growth, internal metabolite concentrations, glucose consumption or lactate production under hypoxia. These data indicate that, while HIFs exert control over glycolysis but not OxPHOS gene expression in human leukemic cells, this is not critically important for their metabolic state.
2020-02-04 | GSE123461 | GEO
Project description:Migroglia cells were exposed to oxygen-glucose deprivation (OGD) for 3 h. The miRNA was isolated and the expression profiles of OGD-activated cells were compared with the profiles of resting cells.
2015-11-23 | GSE63504 | GEO