The subject of this review is the colloidal quantum dot (QD) and specifically the interaction of the QD with proximate molecules. It covers various functions of these molecules, including (i) ligands for the QDs, coupled electronically or vibrationally to localized surface states or to the delocalized states of the QD core, (ii) energy or electron donors or acceptors for the QDs, and (iii) structural components of QD assemblies that dictate QD-QD or QD-molecule interactions. Research on interactions of ligands with colloidal QDs has revealed that ligands determine not only the excited state dynamics of the QD but also, in some cases, its ground state electronic structure. Specifically, the article discusses (i) measurement of the electronic structure of colloidal QDs and the influence of their surface chemistry, in particular, dipolar ligands and exciton-delocalizing ligands, on their electronic energies; (ii) the role of molecules in interfacial electron and energy transfer processes involving QDs, including electron-to-vibrational energy transfer and the use of the ligand shell of a QD as a semipermeable membrane that gates its redox activity; and (iii) a particular application of colloidal QDs, photoredox catalysis, which exploits the combination of the electronic structure of the QD core and the chemistry at its surface to use the energy of the QD excited state to drive chemical reactions.

Colloidal semiconductor nanocrystals, or "quantum dots" (QDs), have several optical and chemical properties that give them the potential to enable nonincremental increases in the efficiencies of many types of photocatalytic reactions relevant for energy conversion and organic synthesis. Colloidal photocatalysts have many desirable characteristics of both heterogeneous and homogeneous catalysts but come with their own particular set of challenges. This viewpoint outlines some of the obstacles one first encounters when driving reactions with these colloids and offers some strategies for overcoming these obstacles, including ways to extend their excited state lifetimes, prevent corrosion by photogenerated holes, and choose a surface chemistry and buffering system for maximum colloidal stability over a range of environmental conditions.

Cyclin-dependent kinase 1 (Cdk1)/cyclin B1 complex is the driving force for mitotic entry, and its activation is tightly regulated by the G2/M checkpoint. We originally reported that a novel protein C53 (also known as Cdk5rap3 and LZAP) potentiates DNA damage-induced cell death by modulating the G2/M checkpoint. More recently, Wang et al. (2007) found that C53/LZAP may function as a tumor suppressor by way of inhibiting NF-κB signaling. We report here the identification of C53 protein as a novel regulator of Cdk1 activation. We found that knockdown of C53 protein causes delayed Cdk1 activation and mitotic entry. During DNA damage response, activation of checkpoint kinase 1 and 2 (Chk1 and Chk2) is partially inhibited by C53 overexpression. Intriguingly, we found that C53 interacts with Chk1 and antagonizes its function. Moreover, a portion of C53 protein is localized at the centrosome, and centrosome-targeting C53 potently promotes local Cdk1 activation. Taken together, our results strongly suggest that C53 is a novel negative regulator of checkpoint response. By counteracting Chk1, C53 promotes Cdk1 activation and mitotic entry in both unperturbed cell-cycle progression and DNA damage response.

Silver molecules are chromophores with diverse spectra and rich photophysics, and DNA strands act as ligands that develop specific molecular silver species. For example, C4AC4T*C3GT4 selectively yields a Ag10 6+ fluorophore with λex/λem = 490/550 nm. This single-stranded DNA coordinates and protects the cluster, and its integrity was challenged by breaking the phosphodiester backbone at the innocuous T*. The resulting C4AC4T and C3GT4 fragments also develop the same Ag10 6+ fluorophore but only when all three components (two fragments + Ag) are present. This C4AC4T/C3GT4/Ag10 6+ complex is favored by higher DNA concentrations and preferentially forms when hybridization forces C4AC4T and C3GT4 onto a shared DNA duplex. The C4AC4T/C3GT4 assembly reverses when the cluster photodegrades, which suggests that the cluster is labile. C4AC4T forms an alternate cluster at low temperatures, but C3GT4 recovers the λ = 490 nm fluorophore at higher temperatures. Thus, the reciprocal interactions between the host DNA strands and the cluster adduct combine to create a highly specific, split-DNA fluorescent Ag cluster capable of sensing target DNA sequences with high specificity and on–off contrast.

Increasing the fraction of 1H,1H,2H,2H-perfluorodecanethiol (PFDT) in the mixed-PFDT/oleate ligand shell of a PbS quantum dot (QD) dramatically reduces the permeability of the ligand shell to alkyl-substituted benzoquinones (s-BQs), as measured by a decrease in the efficiency of collisional photoinduced electron transfer. Replacing only 21% of the oleates on the QD surface with PFDT reduces the yield of photo-oxidation by tetramethyl BQ by 68%. Experiments with s-BQ quenchers of two different sizes reveal that the degree of protection provided by the PFDT-doped monolayer, relative to a decanethiolate (DT)-doped monolayer at similar coverage, is due to both size exclusion (PFDT is larger and more rigid than DT), and the oleophobicity of PFDT. This work demonstrates the usefulness of fluorinated ligands in designing molecule-selective and potentially corrosion-inhibiting surface coatings for QDs for applications as robust emitters or high fidelity sensing platforms.