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created	[InstanceEdit:2470937] Orlic-Milacic, M, 2012-09-20
dbId	2470933
displayName	In mitotic telophase, as chromosomes decondense, cohesin com...
literatureReference	[LiteratureReference:2470265] Releasing cohesin from chromosome arms in early mitosis: opposing actions of Wapl-Pds5 and Sgo1 [LiteratureReference:2470251] Wapl controls the dynamic association of cohesin with chromatin [LiteratureReference:2470256] Human Wapl is a cohesin-binding protein that promotes sister-chromatid resolution in mitotic prophase [LiteratureReference:2470257] Cohesin's DNA Exit Gate Is Distinct from Its Entrance Gate and Is Regulated by Acetylation [LiteratureReference:2470942] Human Scc4 is required for cohesin binding to chromatin, sister-chromatid cohesion, and mitotic progression [LiteratureReference:2470932] NIPBL, encoding a homolog of fungal Scc2-type sister chromatid cohesion proteins and fly Nipped-B, is mutated in Cornelia de Lange syndrome [LiteratureReference:2537594] X-linked Cornelia de Lange syndrome owing to SMC1L1 mutations [LiteratureReference:2537602] Incidence and clinical features of X-linked Cornelia de Lange syndrome due to SMC1L1 mutations [LiteratureReference:2537585] Mutations in cohesin complex members SMC3 and SMC1A cause a mild variant of cornelia de Lange syndrome with predominant mental retardation [LiteratureReference:2537599] Mutations and variants in the cohesion factor genes NIPBL, SMC1A, and SMC3 in a cohort of 30 unrelated patients with Cornelia de Lange syndrome
modified	[InstanceEdit:2550410] Orlic-Milacic, M, 2012-11-01
schemaClass	Summation
text	In mitotic telophase, as chromosomes decondense, cohesin complex associated with PDS5 (PDS5A and PDS5B) and WAPAL (WAPL) proteins is loaded onto chromatin (Shintomi and Hirano, 2009, Kueng et al. 2006, Gandhi et al. 2006, Chan et al. 2012). Cohesin loading is facilitated by the complex of NIPBL (SCC2) and MAU2 (SCC4) proteins, which constitute an evolutionarily conserved cohesin loading complex. MAU2 depletion in HeLa cells results in 2-3-fold reduction in the amount of cohesin in the chromatin fraction (Watrin et al. 2006). NIPBL mutations are the cause of the Cornelia de Lange syndrome, a dominantly inherited disorder characterized by facial malformations, limb defects, and growth and cognitive retardation (Tonkin et al. 2004). Cornelia de Lange syndrome can also be caused by mutations in cohesin subunits SMC1A (Musio et al. 2006, Borck et al. 2007, Deardorff et al. 2007, Pie et al. 2010) and SMC3 (Deardorff et al. 2007).

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[Pathway:R-HSA-2470946] Cohesin Loading onto Chromatin

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