Takeshi Matsuzawa

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: This study engineered macrophages encoding a tandem fluorescently tagged LC3b autophagosome reporter along with stably integrated short hairpin RNAs to demonstrate IFN-γ–induced autophagy required JAK 1/2, PI3K, and p38 MAPK but not STAT1, revealing a novel p38MAPK-dependent, STAT1-independent autophagic pathway that bypasses Irgm1.

TL;DR: It is shown that Irgm1 targets the mycobacterial phagosome through lipid-mediated interactions with phosphatidylinositol-3,4-bisphosphate (PtdIns) and PtdIns(3, 4,5)P3 and facilitates the engagement of IrGM1 with its fusogenic effectors at the site of infection, thereby ensuring pathogen-directed responses during innate immunity.

TL;DR: The recent clarification of known family members, their cellular biochemistry and host defense functions as a means to understanding the complex innate immune response engendered in higher vertebrates such as humans and mice are discussed.