Related references
Note: Only part of the references are listed.Mad2 and Mad3 Cooperate to Arrest Budding Yeast in Mitosis
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Substrate binding on the APC/C occurs between the coactivator Cdh1 and the processivity factor Doc1
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p31comet promotes disassembly of the mitotic checkpoint complex in an ATP-dependent process
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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2011)
How cyclin A destruction escapes the spindle assembly checkpoint
Barbara Di Fiore et al.
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Mps1 directs the assembly of Cdc20 inhibitory complexes during interphase and mitosis to control M phase timing and spindle checkpoint signaling
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JOURNAL OF CELL BIOLOGY (2010)
Dissecting the role of MPS1 in chromosome biorientation and the spindle checkpoint through the small molecule inhibitor reversine
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Uncoupling of the spindle-checkpoint and chromosome-congression functions of BubR1
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APC16 is a conserved subunit of the anaphase-promoting complex/cyclosome
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Centromere tension: a divisive issue
Alexey Khodjakov et al.
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APC/C- and Mad2-mediated degradation of Cdc20 during spindle checkpoint activation
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Unattached Kinetochores Catalyze Production of an Anaphase Inhibitor that Requires a Mad2 Template to Prime Cdc20 for BubR1 Binding
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Separating the spindle, checkpoint, and timer functions of BubR1
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JOURNAL OF CELL BIOLOGY (2009)
Analysis of Activator-Binding Sites on the APC/C Supports a Cooperative Substrate-Binding Mechanism
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UBE2S elongates ubiquitin chains on APC/C substrates to promote mitotic exit
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The spindle checkpoint functions of Mad3 and Mad2 depend on a Mad3 KEN box-mediated interaction with Cdc20-anaphase-promoting complex (APC/C)
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JOURNAL OF BIOLOGICAL CHEMISTRY (2008)
Cdc20 and Cks direct the spindle checkpoint-independent destruction of cyclin A
Rob Wolthuis et al.
MOLECULAR CELL (2008)
A Role for the Fizzy/Cdc20 Family of Proteins in Activation of the APC/C Distinct from Substrate Recruitment
Yuu Kimata et al.
MOLECULAR CELL (2008)
The APC/C maintains the spindle assembly checkpoint by targeting Cdc20 for destruction
Jakob Nilsson et al.
NATURE CELL BIOLOGY (2008)
Insights into Mad2 regulation in the spindle checkpoint revealed by the crystal structure of the symmetric Mad2 dimer
Maojun Yang et al.
PLOS BIOLOGY (2008)
The spindle-assembly checkpoint in space and time
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NATURE REVIEWS MOLECULAR CELL BIOLOGY (2007)
Mad3p, a pseudosubstrate inhibitor of APCCdc20 in the spindle assembly checkpoint
Janet L. Burton et al.
GENES & DEVELOPMENT (2007)
Spindle checkpoint function requires Mad2-dependent Cdc20 binding to the Mad3 homology domain of BubR1
James Davenport et al.
EXPERIMENTAL CELL RESEARCH (2006)
An architectural map of the anaphase-promoting complex
BR Thornton et al.
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Bub1 and aurora B cooperate to maintain BubR1-mediated inhibition of APC/CCdc20
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The WD40 propeller domain of Cdh1 functions as a destruction box receptor for APC/C substrates
C Kraft et al.
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Timing and checkpoints in the regulation of mitotic progression
P Meraldi et al.
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TPR subunits of the anaphase-promoting complex mediate binding to the activator protein CDH1
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CURRENT BIOLOGY (2003)
Crystal structure of the tetrameric Mad1-Mad2 core complex: implications of 'safety belt' binding mechanism for the spindle checkpoint
L Sironi et al.
EMBO JOURNAL (2002)
The Mad2 spindle checkpoint protein undergoes similar major conformational changes upon binding to either Mad1 or Cdc20
XL Luo et al.
MOLECULAR CELL (2002)
Checkpoint protein BubR1 acts synergistically with Mad2 to inhibit anaphase-promoting complex
GW Fang
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Yeast Hct1 recognizes the mitotic cyclin Clb2 and other substrates of the ubiquitin ligase APC
M Schwab et al.
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Checkpoint inhibition of the APC/C in HeLa cells is mediated by a complex of BUBR1, BUB3, CDC20, and MAD2
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Identification of an overlapping binding domain on Cdc20 for Mad2 and anaphase-promoting complex: Model for spindle checkpoint regulation
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MOLECULAR AND CELLULAR BIOLOGY (2001)
Mad2-independent inhibition of APCCdc20 by the mitotic checkpoint protein BubR1
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Chromosome missegregation and apoptosis in mice lacking the mitotic checkpoint protein Mad2
M Dobles et al.
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