23 research outputs found
On Upward Drawings of Trees on a Given Grid
Computing a minimum-area planar straight-line drawing of a graph is known to
be NP-hard for planar graphs, even when restricted to outerplanar graphs.
However, the complexity question is open for trees. Only a few hardness results
are known for straight-line drawings of trees under various restrictions such
as edge length or slope constraints. On the other hand, there exist
polynomial-time algorithms for computing minimum-width (resp., minimum-height)
upward drawings of trees, where the height (resp., width) is unbounded.
In this paper we take a major step in understanding the complexity of the
area minimization problem for strictly-upward drawings of trees, which is one
of the most common styles for drawing rooted trees. We prove that given a
rooted tree and a grid, it is NP-hard to decide whether
admits a strictly-upward (unordered) drawing in the given grid.Comment: Appears in the Proceedings of the 25th International Symposium on
Graph Drawing and Network Visualization (GD 2017
Melittin-Induced Inhibition and Aggregation of Ca-ATPase in Skeletal Muscle Sarcoplasmic Reticulum: A Comparative Study
Pubertal development and its influences on bone mineral density in Australian children and adolescents with cystic fibrosis
Background: Pubertal delay is thought to contribute to suboptimal peak bone mass acquisition in young people with cystic fibrosis (CF), leading to an increased fracture incidence. This study aims to compare pubertal development in young people with CF with that of a local healthy population and assess the influence it has on areal bone mineral density (aBMD)
A major advance of tropical Andean glaciers during the Antarctic cold reversal
International audienc
Mutation and Phosphorylation Change the Oligomeric Structure of Phospholamban in Lipid Bilayers
Drosophila UTX Coordinates with p53 to Regulate ku80 Expression in Response to DNA Damage
UTX is known as a general factor that activates gene transcription during development. Here, we demonstrate an additional essential role of UTX in the DNA damage response, in which it upregulates the expression of ku80 in Drosophila, both in cultured cells and in third instar larvae. We further showed that UTX mediates the expression of ku80 by the demethylation of H3K27me3 at the ku80 promoter upon exposure to ionizing radiation (IR) in a p53-dependent manner. UTX interacts physically with p53, and both UTX and p53 are recruited to the ku80 promoter following IR exposure in an interdependent manner. In contrast, the loss of utx has little impact on the expression of ku70, mre11, hid and reaper, suggesting the specific regulation of ku80 expression by UTX. Thus, our findings further elucidate the molecular function of UTX
Identification of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel target of bisphenol A.
Bisphenol A (BPA) forms the backbone of plastics and epoxy resins used to produce packaging for various foods and beverages. BPA is also an estrogenic disruptor, interacting with human estrogen receptors (ER) and other related nuclear receptors. Nevertheless, the effects of BPA on human health remain unclear. The present study identified DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel BPA-binding protein. DNA-PKcs, in association with the Ku heterodimer (Ku70/80), is a critical enzyme involved in the repair of DNA double-strand breaks. Low levels of DNA-PK activity are previously reported to be associated with an increased risk of certain types of cancer. Although the Kd for the interaction between BPA and a drug-binding mutant of DNA-PKcs was comparatively low (137 nM), high doses of BPA were required before cellular effects were observed (100-300 μM). The results of an in vitro kinase assay showed that BPA inhibited DNA-PK kinase activity in a concentration-dependent manner. In M059K cells, BPA inhibited the phosphorylation of DNA-PKcs at Ser2056 and H2AX at Ser139 in response to ionizing radiation (IR)-irradiation. BPA also disrupted DNA-PKcs binding to Ku70/80 and increased the radiosensitivity of M059K cells, but not M059J cells (which are DNA-PKcs-deficient). Taken together, these results provide new evidence of the effects of BPA on DNA repair in mammalian cells, which are mediated via inhibition of DNA-PK activity. This study may warrant the consideration of the possible carcinogenic effects of high doses of BPA, which are mediated through its action on DNA-PK
