Browsing by Author "Gülsuner, Hilal Ünal"

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Open Access
Multi-domain short peptide molecules for in situ synthesis and biofunctionalization of gold nanoparticles for integrin-targeted cell uptake
(American Chemical Society, 2015) Gülsuner, Hilal Ünal; Ceylan, Hakan; Güler, Mustafa O.; Tekinay, Ayse B.
We describe design and synthesis model of multidomain (modular) peptides (MDPs), which direct a reaction cascade coupling the synthesis and surface functionalization of gold nanoparticles (AuNPs) in a single step. The synthesis is achieved via simple mixing of the aqueous solutions of auric acid and MDPs at room temperature without the addition of any surfactants or toxic intermediate reagents. This method allows facile control over the nanoparticle size between ∼2–15 nm, which opens a practical window for biomedical applications. In contrast to the conventional citrate-mediated methods, peptide-mediated synthesis and stabilization provide increased colloidal stability to AuNPs. As a proof of this concept, we demonstrate active targeting of human breast adenocarcinoma cell line (MCF7) using the one-step-prepared engineered AuNPs. Overall, we propose a single-step, chemically greener, biologically safer method for the synthesis and surface functionalization of gold nanoparticles in a size-controlled manner. The chemical versatility of the MDP design broadens the applicability of this strategy, thereby emerging as a successful alternative for the currently available nanoparticle preparation technologies.
Open Access
Reply to tzoulis et al.: genetic and clinical heterogeneity of essential tremor
(National Academy of Sciences, 2015) Gülsuner, Hilal Ünal; Gülsuner, S.; Mercan, F.; Onat, Onur Emre; Walsh, T.; Shahin, H.; Lee, M.; Dogu, O.; Kansu, T.; Topaloglu, H.; Elibol, B.; Akbostanci, C.; King, M. -C.; Özçelik, Tayfun; Tekinay, Ayse B.
In addressing our recent report of HTRA2 p.G399S as the gene and mutation responsible for essential tremor and subsequent Parkinson disease in a large kindred (1), Tzoulis et al. (2) screened this mutation in patients with Parkinson disease, essential tremor, tremulous cervical dystonia, and nontremulous cervical dystonia patients, and did not find a significant difference in carrier frequency compared with the general population. Their observation replicates our experience, in that in the kindred of our study, HTRA2 p.G399S was responsible for essential tremor and, among homozygotes, for Parkinson disease, but as we reported, this allele was not responsible for essential tremor in other families from the same population. Both these observations support the conclusion that essential tremor is a heterogeneous disease, both clinically and genetically (3). In addition to HTRA2, two other genes for essential tremor have been identified: DNAJC13 and FUS, and still other responsible genes have been mapped to chromosomes 2p22-24, 3q13, and 6p23 (1, 4). In any one patient, mutation at only one of these genes is sufficient for development of essential tremor, but the responsible gene differs among patients. These two features—the severity of individual causal mutations and different responsible genes in different families—are characteristic of genetic heterogeneity of complex diseases generally (5). Phenotypic features of a genetically heterogeneous disease may offer clues as to the responsible gene. In the family harboring mutation in HTRA2, Parkinson disease appeared after more than a decade of essential tremor. Also, cervical dystonia was not among the presenting signs in any of the family members. These clinical features differ from the series of patients screened by Tzoulis et al. Some of the patients screened by Tzoulis et al. may harbor HTRA2 mutations other than p.G399S that would be revealed by more complete sequencing; this would be interesting to learn. It is also possible that mutations in the other known genes for essential tremor may be present in these patients. If not, then these patients, like those from the other kindreds in our series, offer the opportunity to identify additional causal genes for essential tremor.