Tripeptide Self-Assembled Monolayers as Biocompatible Surfaces for Cytochrome Electrochemistry.

Biocompatible tripeptide self-assembled monolayers (SAMs) are designed with a carboxylate group on the terminal amino acid (glutamate, aspartate, or amino adipate) to electrostatically attract the lysine groups around the heme crevice in horse heart cytochrome (cyt ), creating an electroactive protein/tripeptide/Au interfacial structure. Exposing the peptide/Au electrode to cyt resulted in an 11 ± 3 pmol/cm electroactive protein surface coverage. Topographical images of the interfacial structure are obtained down to single-protein resolution by atomic force microscopy.

The nociceptin pharmacophore site for opioid receptor binding derived from the NMR structure and bioactivity relationships.

Nociceptin, a 17 amino acid opioid-like peptide that has an inhibitory effect on synaptic transmission in the nervous system, is involved in learning, memory, attention, and emotion and is also implicated in the perception of pain and visual, auditory, and olfactory functions. In this study, we investigated the NMR solution structure of nociceptin in membrane-like environments (trifluoroethanol and SDS micelles) and found it to have a relatively stable helix conformation from residues 4-17 with functionally important N-terminal residues being folded aperidoically on top of the helix. In functional assays for receptor binding and calcium flux, alanine-scanning variants of nociceptin indicated that functionally important residues generally followed helix periodicity, consistent with the NMR structural model.

Side-chain anchoring strategy for solid-phase synthesis of peptide acids with C-terminal cysteine.

Many naturally occurring peptide acids, e.g., somatostatins, conotoxins, and defensins, contain a cysteine residue at the C-terminus.

Anti-tumor activity of the novel angiogenesis inhibitor anginex.

Anginex is a novel cytokine-like peptide with potent anti-angiogenic activity, which operates specifically against angiogenically-activated endothelial cells via prevention of cell adhesion/migration on the extracellular matrix and subsequent induction of apoptosis. Here, we demonstrate that anginex inhibits tumor growth in vivo in mouse xenograft models. In the MA148 ovarian carcinoma model, tumor growth was inhibited dose-dependently by up to 80% when systemically administered via osmotic mini-pumps starting at the time of tumor cell inoculation.