Genetic and proteomic screening with Wolbachia's CidB enzyme reveal the mechanisms and targets of cytoplasmic incompatibility (CI).

This review serves as a gateway to experimental, conceptual, and quantitative themes of cytoplasmic incompatibility (CI) and outlines significant gaps in the understanding of CI's mechanism that are ripe for investigation.

Yersinia pseudotuberculosis and enteropathogenic Escherichia coli promote pathogenicity by deamidating the ubiquitin-like protein NEDD8 to block ubiquitin-dependent trafficking of Perforin-2, which is an effector of innate immunity.

Differentiation of mitotic errors occurring during late embryonic development from the well-characterized first division defects provides new insight into the mechanisms of Wolbachia-induced cytoplasmic incompatibility.

Localized lignin impregnations, forming a pan-endodermal net-like diffusion barrier strongly relies on stabilizing signals from neighbors.

A newly discovered cytoplasmic intermediate filament in water bears may help these animals to resist extreme environmental conditions.

Low expression of Cbfb may be the cause of osteoarthritis, and local admission of Cbfb may rescue and protect against osteoarthritis through decreasing Wnt/β-catenin signaling, and increasing Hippo/Yap signaling and Tgfβ/Smad2/3 signaling in osteoarthritis articular cartilage.

Aberrant cytoskeletal intermediate filament networks in the C. elegans intestine are associated with hyperphosphorylated intermediate filament proteins and impact not only intestinal cell structure but have also detrimental consequences for organismal well-being.

The extrinsic cue NGF and the intrinsic signal Islet1 converge at the level of the Runx1/CBFβ transcription factor complex formation to promote differentiation of a major nociceptor subtype.

An analysis of more than 3000 randomized controlled trials published in JAMA, the Lancet and NEJM has identified 396 medical reversals.