Gregory R. Palardy

TL;DR: Cell transplantation studies suggest that mib function is essential in the signaling cell for efficient activation of Notch in neighboring cells, and observations support a model for Notch activation where the Delta-Notch interaction is followed by endocytosis of Delta and transendocyTosis of the Notch extracellular domain by the signalingcell.

TL;DR: It is shown that immunization with myelin basic protein and proteolipid protein determinants results in clinical disease with significant demyelination and intermolecular "determinant spreading" is associated with clinical autoimmune disease in primates.

TL;DR: Treatment with MP4, a chimeric, recombinant polypeptide containing human myelin basic protein and human proteolipid protein epitopes, prevented clinical symptoms and did not exacerbate disease in primates and proved specific Ag-directed therapy can be effective and nontoxic in primates.

TL;DR: Transgenic mice selected to have relatively higher B cell numbers produced anti‐TAChR titers equal to B6 mice and a predominance of Th1‐induced antibody isotypes were observed in certain experiments, indicating the incidence and severity of clinical disease was variable following immunizations.

TL;DR: It is shown that elimination of the Mind bomb1 Interaction Domain (MID) or mutation of specific conserved motifs in this domain prevents effective Mib1-mediated ubiquitylation and internalization of DeltaD, which can activate Notch in trans and suppress early neurogenesis when mRNA encoding it is ectopically expressed in zebrafish embryos.