Dual photoluminescence peaks observed during the synthesis of colloidal PbS nanosheets reveal their growth mechanism - two-dimensional attachments of the quantum dots. Well-grown nanosheets show the photoluminescence linewidth of 95 meV at room temperature. Aged nanosheets in toluene have enhanced photoluminescence with intensity improved by an order of magnitude.

Catalyst‐free, one‐pot synthesis of colloidal PbSe nanorods is demonstrated. The co‐solvent chloroalkanes play a critical role in driving a one‐dimensional growth of PbSe nanorods. The formation of the nanorod is likely governed by the anisotropic growth of the crystal due to the different reactivity of the facets. The photoluminescence quantum yield of the nanorods is above 25%, indicating well‐passivated surfaces. (© 2016 WILEY‐VCH Verlag GmbH &Co. KGaA, Weinheim)

Protein kinase Cs (PKCs) are activated by lipids in the plasma membrane and bind to a scaffold assembled on the epidermal growth factor (EGF) receptor (EGFR). Understanding how this complex is routed is important, because this determines whether EGFR is degraded, terminating signaling. Here, cells were preincubated in EGF-tagged gold nanoparticles, then allowed to internalize them in the presence or absence of a phorbol ester PKC activator. PKC colocalized with EGF-tagged nanoparticles within 5 min and migrated with EGFR-bearing vesicles into the cell. Two conformations of PKC-epsilon were distinguished by different primary antibodies. One, thought to be enzymatically active, was on endosomes and displayed a binding site for antibody RR (R&D). The other, recognized by Genetex green (GG), was soluble, on actin-rich structures, and loosely bound to vesicles. During a 15-min chase, EGF-tagged nanoparticles entered large, perinuclear structures. In phorbol ester-treated cells, vesicles bearing EGF-tagged nanoparticles tended to enter this endocytic recycling compartment (ERC) without the GG form. The correlation coefficient between the GG (inactive) and RR conformations on vesicles was also lower. Thus, active PKC has a Charon-like function, ferrying vesicles to the ERC, and inactivation counteracts this function. The advantage conferred on cells by aggregating vesicles in the ERC is unclear.

No abstract

No abstract