Author: Wenbin Ji; Yibo Luo; Ejaz Ahmad; Song-Tao Liu
Title: Coordination between discrete Mitotic Arrest Deficient 1 (MAD1) domains is required for efficient mitotic checkpoint signaling Document date: 2017_11_1
ID: i4yquw4k_3
Snippet: Moreover, even the MAD1 fragment encompassing (485-718) residues only exhibits low catalytic activity for MAD2 O-C conversion in vitro (12, 13, 19) . The N-terminal domain of MAD1 (1-485 residues, MAD1 NTD ) was thought to target the protein to nuclear envelope or kinetochores but may also interact with other proteins (20) (21) (22) (23) . Whether and how MAD1 domains outside MIM contribute to the checkpoint signaling warrants re-visit and carefu.....
Document: Moreover, even the MAD1 fragment encompassing (485-718) residues only exhibits low catalytic activity for MAD2 O-C conversion in vitro (12, 13, 19) . The N-terminal domain of MAD1 (1-485 residues, MAD1 NTD ) was thought to target the protein to nuclear envelope or kinetochores but may also interact with other proteins (20) (21) (22) (23) . Whether and how MAD1 domains outside MIM contribute to the checkpoint signaling warrants re-visit and careful investigation. Second, MAD1 forms a cell cycle independent complex with C-MAD2; how the complex only becomes an effective catalyst during prometaphase needs to be better defined (18, 24) . Several kinetochore-localized mitotic kinases including MPS1 kinase were known to elevate C-MAD2 production but direct biochemical evidence is still incomplete despite exciting recent progress (25) (26) (27) (28) (29) (30) (31) .
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