Summary: We explore the concept of cancer as a disease that involves abnormal regulation of cellular quiescence at every step, from malignant transformation to metastatic outgrowth.
N-acetylation of secreted proteins in Apicomplexa is widespread and is independent of the ER acetyl-CoA transporter AT1
Highlighted Article: Apicomplexan acetyl-CoA transporter 1 is indispensable for parasite development and transmission. This role is unrelated to the extensive acetylation of secreted proteins identified in apicomplexans.
Threonine phosphorylation regulates the molecular assembly and signaling of EGFR in cooperation with membrane lipids
Summary: Threonine phosphorylation at the juxtamembrane domain of EGFR is a critical step in shifting the role of EGFR from a kinase to a scaffold for signal transduction.
A transcriptionally repressed quiescence program is associated with paused RNA polymerase II and is poised for cell cycle re-entry
Summary: Promoter-proximal RNAPII stalling primes quiescent myoblasts for cell cycle re-entry. Surprisingly, Aff4, a component of the super elongation complex, is implicated in restraining the G0-G1 transition.
A Zn2+-triggered two-step mechanism of CLIC1 membrane insertion and activation into chloride channels
Summary: Identification of a two-step mechanism of CLIC1 membrane insertion based on Zn2+ binding and pH activation of Cl− efflux.
Metformin inactivates the cGAS-STING pathway through autophagy and suppresses senescence in nucleus pulposus cells
Summary: Metformin suppresses senescence via inactivating the cGAS-STING pathway through inducing autophagy, implying a new application for metformin in cGAS-STING pathway-related diseases.
Oncogenic gain of function due to p53 amyloids occurs through aberrant alteration of cell cycle and proliferation
Summary: p53 amyloid formation alters key cellular pathways to induce oncogenic traits leading to cellular transformation.