32 research outputs found
Semiflexible Filamentous Composites
Inspired by the ubiquity of composite filamentous networks in nature we
investigate models of biopolymer networks that consist of interconnected floppy
and stiff filaments. Numerical simulations carried out in three dimensions
allow us to explore the microscopic partitioning of stresses and strains
between the stiff and floppy fractions c_s and c_f, and reveal a non-trivial
relationship between the mechanical behavior and the relative fraction of stiff
polymer: when there are few stiff polymers, non-percolated stiff ``inclusions``
are protected from large deformations by an encompassing floppy matrix, while
at higher fractions of stiff material the stiff network is independently
percolated and dominates the mechanical response.Comment: Phys. Rev. Lett, to appear (4 pages, 2 figures
Characterization of STAT6 Target Genes in Human B Cells and Lung Epithelial Cells
Using ChIP Seq, we identified 556 and 467 putative STAT6 target sites in the Burkitt's lymphoma cell line Ramos and in the normal lung epithelial cell line BEAS2B, respectively. We also examined the positions and expression of transcriptional start sites (TSSs) in these cells using our TSS Seq method. We observed that 44 and 132 genes in Ramos and BEAS2B, respectively, had STAT6 binding sites in proximal regions of their previously reported TSSs that were up-regulated at the transcriptional level. In addition, 406 and 109 of the STAT6 target sites in Ramos and BEAS2B, respectively, were located in proximal regions of previously uncharacterized TSSs. The target genes identified in Ramos and BEAS2B cells in this study and in Th2 cells in previous studies rarely overlapped and differed in their identity. Interestingly, ChIP Seq analyses of histone modifications and RNA polymerase II revealed that chromatin formed an active structure in regions surrounding the STAT6 binding sites; this event also frequently occurred in different cell types, although neither STAT6 binding nor TSS induction was observed. The rough landscape of STAT6-responsive sites was found to be shaped by chromatin structure, but distinct cellular responses were mainly mediated by distinct sets of transcription factors