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The double-strand-break repair protein rad21 homolog (RAD21) is a core structural subunit of the cohesin complex, a highly conserved multi-protein assembly required for holding sister chromatids together during cell division and ensuring accurate chromosome segregation[1][2][3][4]. As a member of the cohesin complex (with SMC1, SMC3, and STAG1/2), RAD21 mediates not only chromatid cohesion and chromosome architecture but also DNA repair, regulation of gene expression via chromatin looping, and genome stability[1][2][3][4][5]. RAD21 interacts with numerous cellular proteins and is necessary for proper mitosis, DNA double-strand break repair, and developmental gene regulation. Germline or somatic mutations in RAD21 cause cohesinopathies, including Cornelia de Lange syndrome, and are recurrent in various cancers[2][3]. RAD21 deregulation leads to defects in chromosome segregation, developmental disorders, and tumorigenesis[2][3]. Note: - There are currently no approved or well-known drugs directly targeting RAD21 or the cohesin complex in the clinic, and it is not classified as an enzyme, receptor, or transporter but as a chromatin and cohesin complex-associated protein[1][2][5]. If further drug development or clinical trials emerge for this target, these fields should be updated accordingly.
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