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Hypoxic regulation of hypoxia inducible factor 1 alpha via antisense transcription

ABSTRACT: Hypoxic regulation of hypoxia inducible factor 1 alpha via antisense transcription

PROVIDER: PRJNA914233 | ENA |

REPOSITORIES: ENA

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Hypoxic regulation of hypoxia inducible factor 1 alpha via antisense transcription

Project description:Impaired oxygen homeostasis is a frequently encountered pathophysiological factor in multiple complex diseases, including cardiovascular disease and cancer. While the canonical hypoxia response pathway is well characterised, less is known about the role of non-coding RNAs in this process. Here, we investigated the nascent and steady-state non-coding transcriptional responses in endothelial cells and their potential roles in regulating the hypoxic response. Notably, we identify a novel antisense long non-coding RNA that convergently overlaps the majority of the HIF1A locus, which is expressed across several cell types and elevated in atherosclerotic lesions. The antisense (HIF1A-AS) is produced as a stable, unspliced and polyadenylated nuclear retained transcript. HIF1A-AS is highly induced in hypoxia by both HIF1A and HIF2A and exhibits anticorrelation with the coding HIF1a transcript. We further characterized this functional relationship by CRISPR-mediated bimodal perturbation of the HIF1A-AS promoter. We provide evidence that HIF1A-AS represses the expression of HIF1a in cis by repressing transcriptional elongation and deposition of H3K4me3, and that this mechanism is dependent on the act of antisense transcription.

2023-09-29 | GSE221387 | GEO

Attenuating Hypoxia Driven Malignant Behavior in Glioblastoma with a Novel Hypoxia-Inducible Factor 2 Alpha Inhibitor

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Influences of chronic hypoxia and hypoxic-inducible factor 2A on mouse myoblasts

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Influences of chronic hypoxia and hypoxic-inducible factor 2A on mouse myoblasts

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Project description:We performed gene expression profiling for designed oligooxopiperazines targeting the hypoxia-inducible transcription factor complex, which resulted in an effective inhibition of hypoxia-inducible genes with relatively minimal perturbation of non-targeted signaling pathways. Hypoxic A549 cells were treated with transcriptional inhibitors BB2-162, BB2-125, BB2-282 or vehicle and their expression profiles were compared to normoxic A549 cells treated with vehicle.

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Hypoxia-inducible PRMT2 addiction in cancers

Project description:Hypoxia-inducible transcription factors (HIFs) are crucial transcription factors for cellular response to low oxygen levels, but the key mediators for their downstream transcription activation are not well characterized. We previously found that PRMT2 activates target gene expression through its methyltransferase activity on histone H3R8. Here we find that PRMT2 expression is activated by HIF1 at hypoxic conditions. And PRMT2 activity is widely required for hypoxia-induced transcription activation. Accordingly, PRMT2 inactivation alleviates hypoxia-induced glioblastoma progression and chemotherapeutic resistance. And PRMT2 expression is associated with hypoxia signature

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Attenuating Hypoxia Driven Malignant Behavior in Glioblastoma with a Novel Hypoxia-Inducible Factor 2 Alpha Inhibitor

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Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes

Project description:Gene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing the hypoxia inducible factor-2 alpha (HIF-2α) protein. In this study, we have attempted to explore the effects of HIF-2α overexpression on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis.

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Protein Domain Mimetics as In Vivo Modulators of Hypoxia-Inducible Factor Signaling

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Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes

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