Chromatin remodelling allows cells to dynamically alter the structure of chromatin to regulate gene expression. It involves molecular machines that can physically reposition, remove, or modify nucleosomes, the building blocks of chromatin, to make DNA accessible or not to transcription factors and RNA polymerase. Nucleosomes consist of around 147 base pairs of DNA wrapped around an octamer of histone proteins, containing two copies each of histones H2A, H2B, H3, and H4. Histones have N-terminal tails that extend from the nucleosome core. These tails are the areas subject to various post-translational modifications, including acetylation, methylation, phosphorylation, and ubiquitylation. ATP-dependent chromatin remodelling complexes are central to the process of modifying nucleosome structures, using the energy from ATP hydrolysis. Examples of these complexes include the SWI/SNF (switch/sucrose non-fermentable), ISWI (imitation SWI), and NuRD (nucleosome remodelling and deacetylase) complexes. Chromatin remodelling complexes utilize specialized ATPases or helicases that can physically disrupt histone-DNA interactions, leading to nucleosome sliding, removal, or reorganization. For example, SWI/SNF complexes use the BRG1/BRM ATPase to disrupt histone-DNA contacts, enabling DNA accessibility. One common remodelling mechanism is nucleosome sliding, whereby a nucleosome is moved along the DNA without being disassembled. This movement can expose or conceal transcription factor binding sites, thereby regulating gene expression. In some cases, however, chromatin remodellers remove entire nucleosomes from DNA. This results in a more open chromatin structure, promoting gene activation. The ejection of nucleosomes may also be facilitated by histone acetylation, which weakens histone-DNA interactions. Chromatin remodelling and histone modifications often work together to regulate gene expression. For example, acetylation of histone tails by histone acetyltransferases (HATs) can subsequently facilitate nucleosome sliding by chromatin remodellers. Conversely, chromatin remodellers can expose or bury histone modification sites, influencing the recruitment of effector proteins. Chromatin remodelling can lead to diverse functional outcomes, including: 1) Activation or repression of gene transcription by making gene promoters accessible or inaccessible to transcription factors and RNA polymerase; 2) Facilitation of DNA repair processes by exposing damaged DNA sites; 3) Maintenance of genomic stability by suppressing the expression of transposable elements; 4) Control of chromatin structure during mitosis and meiosis. The various modes of chromatin remodelling are highly regulated processes. Factors such as DNA sequence, covalent histone modifications, non-coding RNAs, and specific DNA-binding proteins can each influence the recruitment and activity of chromatin remodelling complexes, with the balance between chromatin remodellers with opposing functions, such as activators and repressors, determining the outcome upon gene expression. Dysregulation of chromatin remodelling is associated with various diseases, including cancer, with mutations in chromatin remodeller genes leading to aberrant gene expression patterns that can contribute to tumour development. For example, clear cell renal cell carcinoma (ccRCC) often features mutations in PBRM1, a subunit of the PBAF chromatin remodelling complex. Chromatin remodelling complex dysregulation is also common in lung cancer, particularly non-small cell lung cancer (NSCLC), with mutations in genes encoding SWI/SNF complex subunits, such as ARID1A and SMARCA4, reported in NSCLC. We offer a comprehensive product catalogue of research tools for investigating chromatin remodeling, including Daxx antibodies, Bmi1 antibodies, BRG1 antibodies, ATRX antibodies, and ASF1A antibodies. Explore our full chromatin remodeling product range below and discover more, for less. Alternatively, you can explore our Polycomb Silencing, SWI & SNF, and Histone Chaperones product ranges.