The molecular mechanisms of peroxisome biogenesis have begun to emerge; in contrast, relatively little is known about how the organelle functions as cells age. In this report, we characterize age-related changes in peroxisomes of human cells. We show that aging compromises peroxisomal targeting signal 1 (PTS1) protein import, affecting in particular the critical antioxidant enzyme catalase. The number and appearance of peroxisomes are altered in these cells, and the organelles accumulate the PTS1-import receptor, Pex5p, on their membranes. Concomitantly, cells produce increasing amounts of the toxic metabolite hydrogen peroxide, and we present evidence that this increased load of reactive oxygen species may further reduce peroxisomal protein import and exacerbate the effects of aging

Purpose-To investigate the molecular mechanism underlying intrinsic resistance to Experimental Design-Western blots and real-time RT-PCR were used to determine levels of Mcl-1 after Conclusions-Our results demonstrate that sequestration of Bim by Mcl-1 is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML. HHS Public AccessAuthor manuscript Clin Cancer Res. Author manuscript; available in PMC 2017 September 01.

NiO is a p-type wide bandgap semiconductor of use in various electronic devices ranging from solar cells to transparent transistors. This work reports the controlling of conductivity and increase of work functions by Li doping.

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