By binding to Fc gamma receptor IIb, amyloid beta induces a series of phosphorylation events that mediate the damaging effects of hyperphosphorylated tau proteins in Alzheimer's disease.

Tat uses unexpected regulatory mechanisms to reprogram target immune cells to promote viral replication and rewire pathways beneficial for HIV.

AFF4 increases the combined selectivity of HIV Tat and TAR for super elongation complexes 330-fold over P-TEFb alone.

A new Cereblon-recruiting bifunctional tau ligand, QC-01-175, promotes aberrant tau degradation and rescue of stress vulnerability in human neuronal cell models of tauopathy.

Mechanistic insight into the chaperone-like activity of NMNAT to phosphorylated Tau reveals a connection between NAD⁺metabolism and Tau homeostasis.

Amphiphysin I is identified as a new substrate of AEP, and the resultant fragment induces synaptic dysfunction and promotes tau hyperphosphorylation via activating CDK5 kinase.

External hydrodynamic forcing on each flagellum of Chlamydomonas reinhardtii reveals a leader-follower relation between the two flagella in the synchronous beating.

Tau deposition in the aging brain follows patterns of functional connectivity that correspond to specific neural memory networks, and this relationship is strengthened in the presence of amyloid-β.

Liquid-liquid phase separation of tau is demonstrated to be an equilibrium state, stable only within a narrow range near physiological conditions, and thus has the capacity to regulate biological processes.

Cryo-EM structures of heparin-induced tau filaments differ from those observed in neurodegenerative disease, illustrating their structural versatility, and prompting questions about the relevance of in vitro amyloid models.