High-Fidelity Reprogrammed Human IPSCs Have a High Efficacy of DNA Repair and Resemble hESCs in Their MYC Transcriptional Signature.

Human induced pluripotent stem cells (hiPSCs) are reprogrammed from adult or progenitor somatic cells and must make substantial adaptations to ensure genomic stability in order to become "embryonic stem cell- (ESC-) like." The DNA damage response (DDR) is critical for maintenance of such genomic integrity. Herein, we determined whether cell of origin and reprogramming method influence the DDR of hiPSCs.

Histone deacetylase inhibitors decrease NHEJ both by acetylation of repair factors and trapping of PARP1 at DNA double-strand breaks in chromatin.

Histone deacetylase inhibitors (HDACi) induce acetylation of histone and non-histone proteins, and modulate the acetylation of proteins involved in DNA double-strand break (DSB) repair. Non-homologous end-joining (NHEJ) is one of the main pathways for repairing DSBs. Decreased NHEJ activity has been reported with HDACi treatment.

Cation exchange on the surface of gold nanorods with a polymerizable surfactant: polymerization, stability, and toxicity evaluation.

Gold nanorods were synthesized using a seed-mediated wet chemical approach with a quaternary ammonium surfactant, cetyltrimethylammonium bromide (CTAB), that forms a bilayer on the surface of the nanorods. The CTAB molecules in the bilayer were exchanged with a similar polymerizable analog, 11-(acryloyloxy) undecyltrimethyl ammonium bromide (p-CTAB). Mass spectrometric analysis of the degree of exchange of CTAB for p-CTAB, after gold digestion, gave 77 +/- 3 and 23 +/- 1% for p-CTAB and CTAB, respectively.

Cellular uptake and cytotoxicity of gold nanorods: molecular origin of cytotoxicity and surface effects.

Gold nanorods of different aspect ratios are prepared using the growth-directing surfactant, cetyltrimethylammonium bromide (CTAB), which forms a bilayer on the gold nanorod surface. Toxicological assays of CTAB-capped nanorod solutions with human colon carcinoma cells (HT-29) reveal that the apparent cytotoxicity is caused by free CTAB in solution. Overcoating the nanorods with polymers substantially reduces cytotoxicity.