Editors' Summary: This Replication Study did not reproduce those experiments in the original paper that it attempted to reproduce.

The HOXB13 binding partner MEIS1 suppresses prostate cancer proliferation, invasion, and metastasis by promoting expression of the anti-oncogenic extracellular proteoglycan Decorin.

The Anaphase Promoting Complex/Cyclosome is regulated by sumoylation to ensure timely mitotic exit in human cells.

Prostate cancer resistance to androgen receptor antagonist therapy occurs by way of tumors impeding local glucocorticoid metabolism and inactivation and thereby permitting sustained glucocorticoids to stimulate up-regulated glucocorticoid receptor.

The ISR kinase GCN2 is critical for maintaining tumor amino acid levels to facilitate growth, suggesting a novel therapeutic strategy for the treatment of prostate cancer by inducing starvation for essential amino acids.

A comprehensive molecular interrogation of CREB5 interactions identified changes in protein and chromatin interactions of FOXA1 that promoted therapy resistance in prostate cancer cells.

A mechanistic link between TLE3 loss and glucocorticoid receptor-mediated androgen receptor inhibitor resistance supports the rationale to target GR during anti-hormonal treatment in castrate-resistant prostate cancer.

The yeast APC/C cryo-EM structure reveals substantial similarities with the human APC/C structure but also important differences in mechanisms of phosphorylation-dependent regulation and activation by coactivators.

FLEXIQuant-LF provides the framework to enable large-scale identification of differentially modified peptides and quantification of their modification extent in label-free mass spectrometry data without prior knowledge of the modification type.