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RESEARCH ARTICLES

N-acetylation of secreted proteins in Apicomplexa is widespread and is independent of the ER acetyl-CoA transporter AT1

Mary Akinyi Nyonda,Jean-Baptiste Boyer,Lucid Belmudes,Aarti Krishnan,Paco Pino,Yohann Couté,Mathieu Brochet,Thierry Meinnel,Dominique Soldati-Favre,Carmela Giglione

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.

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Threonine phosphorylation regulates the molecular assembly and signaling of EGFR in cooperation with membrane lipids

Ryo Maeda,Hiroko Tamagaki-Asahina,Takeshi Sato,Masataka Yanagawa,Yasushi Sako

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.

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A transcriptionally repressed quiescence program is associated with paused RNA polymerase II and is poised for cell cycle re-entry

Hardik P. Gala,Debarya Saha,Nisha Venugopal,Ajoy Aloysius,Gunjan Purohit,Jyotsna Dhawan

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.

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A Zn²⁺-triggered two-step mechanism of CLIC1 membrane insertion and activation into chloride channels

Lorena Varela,Alex C. Hendry,Joseph Cassar,Ruben Martin-Escolano,Diego Cantoni,Felipe Ossa,John C. Edwards,Vahitha Abdul-Salam,Jose L. Ortega-Roldan

Summary: Identification of a two-step mechanism of CLIC1 membrane insertion based on Zn²⁺ binding and pH activation of Cl⁻ efflux.

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Metformin inactivates the cGAS-STING pathway through autophagy and suppresses senescence in nucleus pulposus cells

Chenghao Ren,Jie Jin,Chenchao Li,Jianwei Xiang,Yaosen Wu,Yifei Zhou,Liaojun Sun,Xiaolei Zhang,Naifeng Tian

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.

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Oncogenic gain of function due to p53 amyloids occurs through aberrant alteration of cell cycle and proliferation

Ambuja Navalkar,Ajoy Paul,Arunima Sakunthala,Satyaprakash Pandey,Amit Kumar Dey,Sandhini Saha,Sarthak Sahoo,Mohit Kumar Jolly,Tushar K. Maiti,Samir K. Maji

Summary: p53 amyloid formation alters key cellular pathways to induce oncogenic traits leading to cellular transformation.

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