Editing Anaphase-promoting complex (section)

== Function ==
[[File:Control of late mitotic events by the APC.pdf|thumb|M–Cdk activity promotes the events of early mitosis, resulting in the metaphase alignment of sister chromatids on the spindle. M–Cdk activity also promotes the activation of APCCdc20, which triggers anaphase and mitotic exit by stimulating the destruction of regulatory proteins, such as securin and cyclins, that govern these events. By promoting cyclin destruction and thus Cdk inactivation, APCCdc20 also triggers activation of APCCdh1, thereby ensuring continued APC activity in G<sub>1</sub>.]]

The APC/C's main function is to trigger the transition from [[metaphase]] to [[anaphase]] by tagging specific proteins for degradation.  The three major targets for degradation by the APC/C are [[securin]] and S and M [[cyclin]]s. Securin releases [[separase]], a protease, when degraded. Separase then triggers the cleavage of [[cohesin]], the protein complex that binds sister [[chromatid]]s together.  During [[metaphase]], sister chromatids are linked by intact cohesin complexes.  When securin undergoes ubiquitination by the APC/C and releases separase, which degrades cohesin, sister chromatids become free to move to opposite [[Spindle pole|poles]] for anaphase.  The APC/C also targets the [[mitotic cyclin]]s for degradation, resulting in the inactivation of M-CDK (mitotic [[cyclin-dependent kinase]]) complexes, promoting exit from [[mitosis]] and [[cytokinesis]].<ref name= "Morgan_2007" />

Unlike the SCF, activator subunits control the APC/C.  [[Cdc20]] and [[APC/C activator protein CDH1|Cdh1]] are the two activators of particular importance to the cell cycle.  These proteins target the APC/C to specific sets of substrates at different times in the cell cycle, thus driving it forward.  The APC/C also plays an integral role in the maintenance of chromatin metabolism, particularly in G<sub>1</sub> and G<sub>0</sub>, and plays a key role in phosphorylation of [[Histone H3|H3]] through destruction of the [[aurora A kinase]].<ref name=MBoC>{{cite book | year = 2002 | title = Molecular Biology of the Cell | veditors = Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P | publisher = Garland Science | url = https://www.ncbi.nlm.nih.gov/books/NBK21054/ | isbn = 0-8153-3218-1 | chapter = Chapter 17. The Cell Cycle and Programmed Cell Death | chapter-url = https://www.ncbi.nlm.nih.gov/books/NBK21056/ | edition = 4th }}</ref>

The critical substrates of the APC/C appear to be securin and the B type cyclins. This is conserved between mammals and yeast. In fact, yeast are viable in the absence of the APC/C if the requirement for targeting these two substrates is eliminated.<ref name=Thornton>{{cite journal | vauthors = Thornton BR, Toczyski DP | s2cid = 30582585 | title = Securin and B-cyclin/CDK are the only essential targets of the APC | journal = Nature Cell Biology | volume = 5 | issue = 12 | pages = 1090–4 | date = December 2003 | pmid = 14634663 | doi = 10.1038/ncb1066 }}</ref>