Paracrine rescue of MYR1-deficient mutants reveals limitations of pooled CRISPR screens.

is an intracellular parasite that subverts host cell functions via secreted virulence factors. Up to 70% of parasite-controlled changes in the host transcriptome rely on the MYR1 protein, which is required for the translocation of secreted proteins into the host cell. Mice infected with MYR1 knock-out (KO) strains survive infection, supporting a paramount function of MYR1-dependent secreted proteins in virulence and proliferation.

Analysis of Complement Factor H gene polymorphisms and their association with clinical manifestations ofleptospirosis.

Leptospirosis is caused by pathogenic leptospires, posing a significant public health problem. Host susceptibility to Leptospira infection is a multifactorial trait, and the host's genetic background can influence both the establishment of infection and the severity of the disease. Complement Factor H (FH) plays a crucial role in the interaction between pathogenic bacteria and the host.

Development of personalized profiles of students with autism spectrum disorder for interactive interventions with robots to enhance language and social skills.

The inclusion of students with autism spectrum disorder (ASD) in mainstream education (primary and secondary, in the range of 4-5 to 8-10 years old) is a complex task that has long challenged both educators and health professionals. However, the correct use of digital technologies such as personalization settings and interaction with robots has clearly shown how these new technologies can benefit ASD students. However, it is essential to characterize the profile, problems, and needs of each student, since it is not possible to generalize an accessible approach for all users.

TRIM65 regulates innate immune signaling by enhancing K6-linked ubiquitination of IRF3 and its chromatin recruitment.

Viral infection triggers a rapid and effective cellular response primarily mediated by interferon β (IFNβ), which induces an antiviral state through complex signaling cascades. To maintain a robust antiviral response while preventing excessive activation, the induction of IFNβ and downstream signaling are tightly regulated. Members of the tripartite-motif (TRIM) family of E3 ubiquitin (Ub) ligases play crucial roles in modulating these processes.