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An Overview of Chromatin Remodeling

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Chromatin, the DNA-protein complex consisting of DNA tightly wound around histone proteins, is composed of numerous functional units termed nucleosomes. Each complex is comprised of 8 histones wrapping roughly 150 base pairs. Chromatin remodeling is the dynamic process of switching between “open” and “closed” chromatin states that permits or restricts access to DNA. Moreover, it is an essential activity of all cells1. By controlling the ability of transcription factors to bind to DNA, chromatin remodeling controls gene expression. It also regulates other critical DNA processes such as replication, repair, recombination, and apoptosis2.

Remodeling falls into two main categories: 1) activity of large ATP-dependent protein complexes termed chromatin remodelers that alter the structure and position of nucleosomes and 2) post-translational modification of the amino acid residues of histone tail domains, which affect DNA-nucleosome interactions and recruitment of chromatin remodeler complexes2. ATP-dependent chromatin remodeling complexes fall into four main families: SWI/SNF, ISWI, NuRD/Mi-2/CHD, and INO80. Each family contributes to both gene activation and repression3. At least eight different types of histone modifications have been identified (including acetylation, methylation, and phosphorylation), along with numerous enzymes that catalyze the addition or removal of the modifications2.

Alterations to the chromatin remodeling process have serious clinical implications. For example, mutations in the SWI/SNF complex are associated with a variety of intellectual disability syndromes and speech impairment4. Many ATP-dependent remodeler components (such as SMARCB1, SMARCA2, BRG1) as well as histone modification participants (including BMI1 and the HDAC family) are implicated in several different types of cancer3, 5, 6. Indeed, transcription activating HDAC inhibitors have long been used as mood-stabilizing and anti-epileptic drugs, and are currently being considered as possible cancer treatments.


Contributed by Allison A. Curley, Ph.D.


Detection of human BRD2 by WB of 293T, HeLa, SW620, SK-MEL-28 (SK), Jurkat, MCDF7, HERPG2, and A459 lysate.

Detection of human BRD2 by WB of 293T, HeLa, SW620, SK-MEL-28 (SK), Jurkat, MCDF7, HERPG2, and A459 lysate. Antibody: Rabbit anti-BRD2 recombinant monoclonal [BL-167-2A2] (A700-008). Secondary: HRP-conjugated goat anti-rabbit IgG (A120-101P).

Detection of human Phospho SMC1 (S957) by WB of lysate from etoposide treated 293T cells.

Detection of human Phospho SMC1 (S957) by WB of lysate from etoposide treated 293T cells.  Antibody: Rabbit anti-Phospho SMC1 (S957) (A300-045A). Secondary: HRP-conjugated goat anti-rabbit IgG (A120-101P).



Below is the current listing of Bethyl antibodies for studying chromatin remodeling:


Chromatin Remodeling


1. Phillips T, Shaw K. 2008. Chromatin remodeling in eukaryotes. Nat Ed. 1(1):209.

2. Bannister AJ, Kouzarides T. 2011. Regulation of chromatin by histone modifications. Cell Res. Mar; 21(3):381-395. 

3. Wang GG, Allis CD, Chi P. 2007.  Chromatin remodeling and cancer, Part II: ATP-dependent chromatin remodeling. Trends Mol Med. Sep;13(9):373-380.

4. Kosho T, Okamoto N, Ohashi H, Tsurusaki Y, Imai Y, Hibi-Ko Y, Kawame H, Homma T, Tanabe S, Kato M, et al. 2013. Clinical correlations of mutations affecting six components of the SWI/SNF complex: detailed description of 21 patients and a review of the literature. Am J Med Genet A. Jun; 161A(6):1221-1237.

5. Wang GG, Allis CD, Chi P. 2007. Chromatin remodeling and cancer, Part I: Covalent histone modifications. Trends Mol Med. Sep; 13(9):363-372.

6. Chi P, Allis CD, Wang GG. 2010. Covalent histone modifications--miswritten, misinterpreted and mis-erased in human cancers. Nat Rev Cancer. Jul;10(7):457-469.