Open ValWood opened 6 years ago
also he Mad3(BubR1) family proteins contain two lysine, gluta- mic acid, glutamine (KEN) boxes that are both required for inhi- bition of APC/C in response to unattached kinetochores. The N-terminal KEN-20 box interacts directly with MCCCdc20 and is required for MCC assembly, whereas the second KEN-271 box is dispensable for MCC assembly (Chao et al., 2012; Sczaniecka et al., 2008) but, instead, is required for interaction of MCCCdc20
with a second Cdc20 molecule bound to APC/C (Izawa and Pines, 2015; Lara- Gonzalez et al., 2011).
(this doesn't currently model ver well)
A reminder:
Given the role of PP2A-B56Par1 in the silencing of the spindle assembly checkpoint (SAC) (reviewed in Saurin, 2018; Hayward et al., 2019),
might be in. PMID: 11514436
This review looks really useful for the KML network https://www.frontiersin.org/articles/10.3389/fcell.2018.00062/full
Spindle checkpoint model: Mph1 phosphorylates spc7 (at unattached kinetochores) Spc7-P. (NEED ACTIVE FORM T453/T507) recruits bub1(and bub3) to kinetochore Mph1 Phosphorylates mpc7 involved in Bub1-bub3 complex localisation during mitotic metaphase phosphorylated bub1 recruits mad1
redo? PMID:27618268 (Heinrich et al., 2014; Mora-Santos et al., 2016).
It is well known that APC/C activation is inhibited when microtubule-kinetochore interaction is perturbed, such as in cells lacking Dam1 (Dam1, Ask1, Spc34, Hsk3 [DASH] complex) or Klp5/Klp6 (kinesin-8) (Sanchez-Perez et al., 2005).