Philip T. Edeen

This study identifies PIKI-1 as a Class II PI3K essential for PI(3,4)P2 production and early endosomal function in C. elegans, showing its role in suppressing NEKL-related molting defects.

This study identifies TAT-1 as a phosphatidylserine flippase required for normal endosomal function and molting in C. elegans, linking it to NEKL-2/3 and endocytic processes.

The paper identifies catp-1 as a suppressor of molting defects in nekl-2; nekl-3 mutants in C. elegans, suggesting it modulates membrane trafficking by altering electrochemical gradients.

This study identifies novel functions of the conserved phosphatase PTPN-22 in C. elegans, showing its role in molting, cell adhesion, and cytoskeletal regulation through genetic and proteomic analyses.

This paper identifies ADM-2 as a negative regulator of molting in C. elegans, showing it inhibits molting by regulating LRP-1 and endocytic trafficking.

The paper shows that transitioning through the L2d stage can rescue molting defects in C. elegans with reduced NEKL function by restoring transcriptional defects associated with molting.