Kinetochore microtubule dynamics and attachment stability are regulated by Hec1.

By J. DeLuca, Walter E. Gall, C. Ciferri, D. Cimini, A. Musacchio, E. Salmon. Cell, 2006

805 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Bub3 reads phosphorylated MELT repeats to promote spindle assembly checkpoint signaling (2013, background): “In a few well-characterized cases, phosphorylation negatively regulates protein interactions at the kinetochore (e.g., Cheeseman et al., 2006; DeLuca et al., 2006; Meadows et al., 2011; Rosenberg et al., 2011).”
The conserved KMN network constitutes the core microtubule-binding site of the kinetochore. (2006, background): “…work from DeLuca and coworkers has demonstrated that expression of a Ndc80/Hec1 mutant in human cells which is unable to be phosphorylated by Aurora B, causes an increase in incorrect kinetochore-microtubule attachments and chromosome segregation defects (DeLuca et al., 2006 [this issue of Cell]).”
Shared and separate functions of polo-like kinases and aurora kinases in cancer (2010, background): “In this conformation, it can phosphorylate several kinetochore-associated proteins, such as highly expressed in cancer (HEC1; also known as NDC80), DSN1 (also known as KNL3) and KNL1 (also known as CASC5 or blinkin) thereby modifying the microtubule binding affinity of the KMN network”