Hypoxia, the reduced supply of oxygen to tissues, leads to significant changes in gene expression allowing cells to adapt to low oxygen levels, some of which are mediated or maintained by epigenetic modifications, the heritable changes in chromatin not involving the underlying DNA sequence. One of the most studied epigenetic modifications is DNA methylation. DNA methylation involves the addition of a methyl group to cytosine residues, often resulting in gene silencing. Hypoxia-induced changes in DNA methylation patterns can influence gene expression. For example, HIFs are the transcription factors that play a central role in the cellular response to hypoxia. Epigenetic modifications, such as DNA methylation and histone acetylation, can modulate the expression of HIF or HIF target genes. For example, DNA hypomethylation of HIF-1α promoter regions can increase HIF-1α expression under hypoxic conditions, whilst the promoter region of the E-cadherin gene, a critical regulator of cell adhesion, can become hypermethylated in response to hypoxia, leading to reduced E-cadherin expression and promoting the epithelial-mesenchymal transition (EMT) typical of tumour progression. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), also play roles in the epigenetic regulation of hypoxia-related genes. MicroRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally regulate gene expression. Several miRNAs are known to be upregulated or downregulated in response to hypoxia. For example, miR-210, miR-21, miR-155, miR-424 (322) and miR-23a are upregulated during hypoxia, with miR-210 for example, playing a role in regulating mitochondrial function and cell survival. Additionally, lncRNA H19 can be epigenetically silenced by DNA methylation in hypoxic conditions, contributing to altered gene expression patterns in cancer cells. Hypoxia also affects histone modifications, which play key roles in chromatin remodelling and regulation of gene expression. One important histone modification is acetylation, catalysed by histone acetyltransferases (HATs) and histone deacetylases (HDACs). In hypoxic conditions, HDAC activity often increases, resulting in histone deacetylation and gene repression. In glioblastoma cells exposed to hypoxia, increased HDAC activity for example leads to the repression of pro-apoptotic genes, contributing to cell survival. Hypoxia-inducible factors (HIFs) are transcription factors central to the cellular response to low oxygen levels. Importantly, HIFs can also interact with epigenetic modifiers to control gene expression. HIF-1α can recruit histone demethylases like Jumonji domain-containing protein 1A (JMJD1A) to target gene promoters, resulting in the removal of repressive histone marks, and facilitating transcription of HIF target genes. Hypoxia can induce epigenetic memory, whereby cells retain altered epigenetic marks even after returning to normoxic conditions. This phenomenon can have long-lasting consequences for gene expression and cellular behaviour. For example, in cancer cells exposed to hypoxia, the promoter regions of tumour suppressor genes like p16INK4a and VHL often become hypermethylated, silencing their expression. These methylation changes can persist even after the cells return to normal oxygen levels, contributing to long-term alterations in gene expression patterns. Other studies have shown that exposure to hypoxia during development can similarly lead to persistent changes in DNA methylation patterns, potentially increasing the risk of chronic diseases later in life. We provide a large product catalogue of research tools for studying hypoxia, including HIF-1 alpha antibodies, ORP150 antibodies, HIF1 beta antibodies, Adenosine A2b Receptor antibodies, and HIF-1 alpha ELISA Kits. Explore our full hypoxia product range below and discover more, for less. Alternatively, you can explore our HIF, Hypoxia Regulated, and Prolyl Hydroxylase product ranges.