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Rab35 Regulates an Endocytic Recycling Pathway Essential for the Terminal Steps of Cytokinesis
Cytokinesis is the final step of cell division and leads to the physical separation of the daughter cells. After the ingression of a cleavage membrane furrow that pinches the mother cell, futureExpand
Moesin and its activating kinase Slik are required for cortical stability and microtubule organization in mitotic cells
Cell division requires cell shape changes involving the localized reorganization of cortical actin, which must be tightly linked with chromosome segregation operated by the mitotic spindle. How thisExpand
Heat shock protein 70 binding inhibits the nuclear import of apoptosis-inducing factor
Heat shock protein 70 (HSP70) can inhibit apoptosis by neutralizing and interacting with apoptosis-inducing factor (AIF), a mitochondrial flavoprotein that translocates upon apoptosis induction toExpand
A Global Census of Fission Yeast Deubiquitinating Enzyme Localization and Interaction Networks Reveals Distinct Compartmentalization Profiles and Overlapping Functions in Endocytosis and Polarity
Proteomic, localization, and enzymatic activity screens in fission yeast reveal how deubiquitinating enzyme localization and function are tuned.
AIF and cyclophilin A cooperate in apoptosis-associated chromatinolysis
Cyclophilin A (CypA) was determined to interact with apoptosis-inducing factor (AIF) by mass spectroscopy, coimmunoprecipitation, pull-down assays, and molecular modeling. During the initial,Expand
An ARF6/Rab35 GTPase Cascade for Endocytic Recycling and Successful Cytokinesis
Cytokinesis bridge instability leads to binucleated cells that can promote tumorigenesis in vivo. Membrane trafficking is crucial for animal cell cytokinesis, and several endocytic pathways regulatedExpand
Protein degradation in DNA damage response.
DNA damage is a major threat to genome integrity. To reduce its deleterious effects, cells have developed coordinated responses, collectively referred to as the "DNA damage response" pathway (DDR).Expand
Mutations affecting the conserved acidic WNK1 motif cause inherited hyperkalemic hyperchloremic acidosis.
Gain-of-function mutations in the WNK1 and WNK4 genes are responsible for Familial Hyperkalemic Hypertension (FHHt), a rare inherited disorder characterized by arterial hypertension and hyperkalemiaExpand
Severe Arterial Hypertension from Cullin 3 Mutations Is Caused by Both Renal and Vascular Effects.
BACKGROUND Mutations in four genes, WNK lysine deficient protein kinase 1 and 4 (WNK1 and WNK4), kelch like family member 3 (KLHL3), or Cullin 3 (CUL3), can result in familial hyperkalemicExpand