https://www.selleckchem.com/products/a-674563.html Together, these data indicate that the TUBA1A-rich microtubule tracks that are assembled during development are essential for mature neuron function and maintenance of synapses over time.Significance Statement Defects in axonal trafficking have been reported in models of movement disorders, but it has been unclear if trafficking defects are coincident or causative. Our results suggest that deficits in TUBA1A αTubulin can cause trafficking defects that impair synaptic maintenance leading to a movement disorder without axon degeneration or impacting myelination or neuron survival. Copyright © 2020 Buscaglia et al.T cell receptor (TCR)-based therapeutic cells and agents have emerged as a new class of effective cancer therapies. These therapies work on cells that express intracellular cancer-associated proteins by targeting peptides displayed on major histocompatibility complex receptors. However, cross-reactivities of these agents to off-target cells and tissues have resulted in serious, sometimes fatal, adverse events. We have developed a high throughput genetic platform (termed "PresentER") that encodes MHC-I peptide minigenes for functional immunological assays and determines the reactivities of TCR-like therapeutic agents against large libraries of MHC-I ligands. In this report, we demonstrated that PresentER could be used to identify the on-and-off targets of T cells and TCR mimic antibodies using in vitro co-culture assays or binding assays. We found dozens of MHC-I ligands that were cross-reactive with two TCR mimic antibodies and two native TCRs and that were not easily predictable by other methods. Copyright ©2020, American Association for Cancer Research.Patients with hematological cancers have improved outcomes after treatment with bispecific antibodies that bind to CD3 on T cells and that redirect T cells towards cancer cells. However, clinical benefit against solid tumors remains to be shown. We made a bis