Preventing activity of the kinase tumor progression locus 2 modulates microglial activation, reduces T-cell brain infiltration, and is neuroprotective in disease models.

Aurora A kinase, an anti-cancer drug target, can be activated by two independent mechanisms.

Cryo-EM structures of human TPC2 channel in the ligand-bound and apo states reveal the structural mechanism of PI(3,5)P₂ lipid regulated gating of TPC2.

The lysosomal ion channel TPC2 emerges as an example of an ion channel in which ion selectivity is not fixed but rather agonist-selective.

The protein hyaluronan-mediated motility receptor interacts with microtubules to enhance their stability and recruits TPX2 to promote microtubule emanation in neurons.

A combination of cryo-electron microscopy of TPX2 bound to microtubules and in vitro reconstitution experiments reveals a novel microtubule interaction mode that explains how TPX2 promotes microtubule nucleation and stabilization.

The TPL corepressor binds to the core mediator complex through MED21 to inhibit transcription while simultaneously priming repressed genes for rapid reactivation.

A sequential reaction pathway involving TPX2, augmin and γ-TuRC governs the assembly and architecture of branched microtubule networks.

The protein TPX2 and the protein complex augmin together recruit the microtubule nucleator γ-TuRC to a pre-existing microtubule where they initiate branching microtubule nucleation.