Function: +wl
Okumaya devam et...
← Previous revision | Revision as of 03:24, 4 May 2024 |
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| [[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 G1.]] | [[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 G1.]] |
| 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 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" /> | 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 G1 and G0, and plays a key role in phosphorylation of 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> | 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 G1 and G0, and plays a key role in phosphorylation of 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> |
Okumaya devam et...