Cell differentiation is a fundamental process in multicellular organisms, whereby undifferentiated cells (stem cells) iteratively give rise to specialized cell types within an organism. Epigenetic mechanisms play various roles in controlling cell differentiation by regulating gene expression patterns without altering the underlying DNA sequence. DNA methylation, for example, is a key player in controlling the differentiation of embryonic stem cells (ESCs) into various cell lineages. During early development, ESCs have a relatively low level of DNA methylation, allowing pluripotency and self-renewal. As cells differentiate however, DNA methylation patterns change, leading to lineage-specific gene expression. For example, genes associated with pluripotency, such as the transcription factors OCT4 and NANOG, are hypomethylated in ESCs but become hypermethylated upon differentiation. Hematopoietic stem cells (HSCs) give rise to various blood cell types. Epigenetic modifications, including histone acetylation and methylation, play roles in HSC differentiation. For example, promoter histone acetylation of hematopoietic transcription factors like GATA1 and PU.1 are essential for lineage-specific differentiation and dysregulation of such histone modifications can lead to blood disorders. MicroRNAs (miRNAs) are the small non-coding RNAs that can post-transcriptionally regulate gene expression. They are thought to play an important role in neural stem cell (NSC) differentiation. For example, miR-124 is highly expressed in differentiated neurons and represses genes associated with stemness, thereby promoting neuronal differentiation. Epigenetic mechanisms control the expression of miRNAs during NSC differentiation. For example, trimethylation of histone H3 at lysine 27 (H3K27me3) by Polycomb group proteins can lead to gene silencing. In some cases, miRNA genes are marked with H3K27me3 in undifferentiated NSCs, and removal of this mark is necessary for their activation during differentiation. Myogenic transcription factors like MyoD and Myogenin are known regulators that drive the differentiation of muscle cells. Epigenetic mechanisms, including histone acetylation and methylation, play roles in regulating the accessibility of these genes. For example, histone acetylation at the MyoD promoter region is required for its activation during myoblast differentiation. Epigenetic reprogramming is also thought to be crucial during gametogenesis and early embryonic development. Imprinted genes, which are mono-allelically expressed depending on their parental origin, are regulated by DNA methylation. For example, the imprinted gene Insulin-like Growth Factor 2 (IGF2) is methylated and silenced on the maternal allele, whilst the paternal allele is active. Epigenetic changes in such imprinted genes can lead to developmental disorders. Cancer stem cells (CSCs) - a subpopulation of tumour cells with stem-like properties - are thought to be important mediators of tumour recurrence after therapy. Epigenetic changes, such as DNA hypermethylation of tumour suppressor genes and histone modifications, can block differentiation in CSCs, promoting their self-renewal and contributing to cancer progression. Epigenetic therapies, including DNA demethylating agents and histone deacetylase inhibitors, are being explored to restore normal differentiation processes in various types of disorders. For example, in acute promyelocytic leukaemia (APL), treatment with all-trans retinoic acid (ATRA) and arsenic trioxide can induce differentiation of leukemic cells into mature granulocytes and does so by altering epigenetic marks on the retinoic acid receptor (RAR) and promyelocytic leukaemia (PML) genes. We offer a wide product catalogue of research tools for studying cell differentiation, including S100 beta antibodies, Tal1 antibodies, KLF4 antibodies, NOTCH3 antibodies, and DLL4 ELISA Kits. Explore our full cell differentiation product range below and discover more, for less.