Showing papers by "Sandra L. Schmid published in 2012"
TL;DR: It is reported that Disabled homolog 2 (Dab2), a cargo-specific adaptor protein for Clathrin, is essential to mediate the proangiogenic function of BMP2 signaling and decreases phosphorylation of SMAD-1, 5, and 8, indicating that Dab2 plays an essential role in determining the outcome of B MP signaling within endothelial cells.
57 citations
TL;DR: It is speculated that the evolution of metazoan dynamin coincided with the specialized need for regulated CME during neurotransmission in eukaryotic cells.
Abstract: Whereas clathrin-mediated endocytosis (CME) exists in all eukaryotic cells, we first detect classical dynamin in Ichthyosporid, a single-cell, metazoan precursor. Based on a key functional residue in its pleckstrin homology domain, we speculate that the evolution of metazoan dynamin coincided with the specialized need for regulated CME during neurotransmission.
16 citations
TL;DR: Structural studies of dynamin are used to study nucleotide-dependent conformational changes required for dynamin-catalyzed fission and identify dynamin partners that function synergistically with dynamin to catalyze membrane fission from SUPER templates.
1 citations
TL;DR: 3D maps of ΔPRD-dynamin with three crystal structures docked into the map, the GMP-PCP GG domain (GTPase domain-GED fragment), the stalk domain from another dynamin family member, MxA, and the PH domain from dynamin are calculated and the location and interactions between the domains are predicted.
1 citations
TL;DR: The authors used a variety of cell biological and biochemical methods to identify profound structural defects in brush border microvilli, but their resilient subject animal compensated structurally by redistributing intermediate filaments and the normally basolateral myosin-1c to the apical microVilli, and functionally by upregulating normal mucosal repair mechanisms.
Abstract: Figure 2B of this paper shows two Eppendorf tubes containing mouse feces that illustrate the unexpectedly normal functionality of the intestinal tract of knockout mice lacking brush border myosin (myosin-1a; Tyska et al., 2005). The authors used a variety of cell biological and biochemical methods to identify profound structural defects in brush border microvilli. However, their resilient subject animal compensated structurally by redistributing intermediate filaments and the normally basolateral myosin-1c to the apical microvilli, and functionally by upregulating normal mucosal repair mechanisms. This paper illustrates the perseverance and ingenuity of both the scientist and the subject.