Thesis (Ph. D.)--University of Missouri--Columbia, 1997. / "December 1997." Typescript. Vita. Includes bibliographical references (leaves 100-109). Also available on the Internet.

Thesis (Ph. D.)--University of Hong Kong, 2008. / Includes bibliographical references (leaf 96-139) Also available in print.

Thesis (Ph. D.)--University of Missouri--Columbia, 1997. / Typescript. Vita. Includes bibliographical references (leaves: 100-109). Also available on the Internet.

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 232-263). Also available in print.

Thesis (Ph. D.)--Joint Program in Biological Oceanography (Massachusetts Institute of Technology, Dept. of Biology, and the Woods Hole Oceanographic Institution), 2000. / Vita. Includes bibliographical references.

Thesis (Ph.D.)--University of California, San Francisco, 2004. / Bibliography: leaves 85-92. Also available online.

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 232-263). Also available online.

Thesis (M. Phil.)--University of Hong Kong, 2010. / Includes bibliographical references (leaves 61-64). Also available in print.

Thesis (Ph. D.)--Massachusetts Institute of Technology and Woods Hole Oceanographic Institution Joint Program in Oceanography/Applied Ocean Science and Engineering, 2000. / "Funding was provided by grants from WHOI's Rinehart Coastal Research Center and Ocean Ventures Fund, a National Science Foundation graduate fellowship, grant CC-S-611002-001-C from the Office of Naval Research, and broad financial support from WHOI's Education Department. Includes bibliographical references.

Human Natural Killer (NK) cells are regulated by a variety of germ-line encoded activating and inhibitory receptors. Broadly, activating receptors detect ligands that are expressed or up-regulated on cancerous or infected cells, while inhibitory receptors bind self-molecules to induce tolerance against healthy cells. Highly homologous pairs of activating and inhibitory receptors are also expressed on NK cells, including Killer Ig-like Receptors KIR2DL1 and KIR2DS1, which bind the same ligands, class I MHC proteins from the C2 group. Here, two super-resolution microscopy techniques, stimulated emission depletion (STED) and ground state depletion microscopy followed by individual molecule return (GSDIM) were used to examine the nanometre-scale organization of KIR2DL1 and KIR2DS1, as well as molecules engaged in their signalling. Both receptors were observed to constitutively assemble in nanometre-scale clusters at the surface of NK cells but displayed differential patterns of clustering - the activating receptor KIR2DS1 formed nanoclusters 2.3-fold larger than its inhibitory counterpart KIR2DL1. Site-directed mutagenesis established that the size of nanoclusters was controlled by transmembrane amino-acid 233, a lysine in KIR2DS1. Mutated variant of KIR2DS1 in which lysine 233 was substituted with alanine formed significantly smaller clusters than the wild-type KIR2DS1. Reciprocally, substitution of isoleucine found at position 233 in KIR2DL1 sequence with lysine resulted in the receptor assembling into larger clusters. Super-resolution microscopy also revealed two ways in which KIR nanoclusters impact signalling. First, KIR2DS1 and DAP12 nanoclusters were juxtaposed in the resting-cell state but coalesced upon receptor ligation. Second, quantitative super-resolution microscopy revealed that membrane-proximal clusters of the kinase ZAP-70 or phosphatase SHP-1, as well as their phosphorylated active forms, were more often found in contact with larger KIR nanoclusters. Together, this work has established that size of KIR nanoclusters depends on the transmembrane sequence and impacts downstream signalling.