C. Lindon

Development of D-box peptides to inhibit the Anaphase Promoting Complex/Cyclosome

This study develops D-box peptides that inhibit APC/C by binding Cdc20, showing they are more potent than Apcin and can drive protein degradation.

Post-transcriptional control drives Aurora kinase A expression in human cancers

This study identifies post-transcriptional mechanisms, including APA and miRNA regulation, that influence AURKA expression in cancer.

Differential translation of mRNA isoforms underlies oncogenic activation of cell cycle kinase Aurora A

The paper identifies that differential translation of AURKA mRNA isoforms, regulated by miRNA and alternative polyadenylation, contributes to oncogenic activation of Aurora A in breast cancer.

Revisiting degron motifs in human AURKA required for its targeting by APC/C-FZR1

This study redefines AURKA degron motifs, showing the N-terminal A-box functions as a D-box and the C-terminal D-box is not a degron but a structural motif essential for AURKA's active conformation.

The E3 ubiquitin ligase HECTD1 contributes to cell cycle progression through an effect on mitosis

This study shows that HECTD1 ubiquitin ligase activity promotes cell cycle progression through its role in mitosis by affecting chromosome alignment and spindle assembly checkpoint activity.

A Focused Small-Molecule Screen Identifies PHA-680626 as an Amphosteric Inhibitor Disrupting the Interaction between Aurora-A and N-Myc

This study identifies PHA-680626 as an amphosteric inhibitor that disrupts the AURKA/N-Myc interaction, reducing N-Myc levels and cell viability in neuroblastoma cells.

Selective targeting of non-centrosomal AURKA functions through use of a targeted protein degradation tool

This study characterizes a PROTAC-based degrader of AURKA, showing differential targeting of subcellular AURKA pools and distinct phenotypic effects compared to traditional inhibitors.

Evidence that polyploidy in esophageal adenocarcinoma originates from mitotic slippage caused by defective chromosome attachments

This study identifies mitotic slippage due to defective chromosome attachments as the origin of polyploidy in esophageal adenocarcinoma.

AURKA destruction is decoupled from its activity at mitotic exit but suppresses interphase activity

The paper investigates AURKA activity regulation, finding that its inactivation at mitotic exit depends on TPX2 degradation, not AURKA destruction, and that FZR1 suppresses interphase AURKA activity.

Regulation of mitochondrial dynamics by Aurora A kinase

This study shows that Aurora A kinase associates with mitochondria and influences their dynamics, affecting mitochondrial morphology in different cell lines.