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Articles by W Deng
Total Records ( 3 ) for W Deng
  Y Cheng , W Wu , S Ashok Kumar , D Yu , W Deng , T Tripic , D. C King , K. B Chen , Y Zhang , D Drautz , B Giardine , S. C Schuster , W Miller , F Chiaromonte , G. A Blobel , M. J Weiss and R. C. Hardison

The transcription factor GATA1 regulates an extensive program of gene activation and repression during erythroid development. However, the associated mechanisms, including the contributions of distal versus proximal cis-regulatory modules, co-occupancy with other transcription factors, and the effects of histone modifications, are poorly understood. We studied these problems genome-wide in a Gata1 knockout erythroblast cell line that undergoes GATA1-dependent terminal maturation, identifying 2616 GATA1-responsive genes and 15,360 GATA1-occupied DNA segments after restoration of GATA1. Virtually all occupied DNA segments have high levels of H3K4 monomethylation and low levels of H3K27me3 around the canonical GATA binding motif, regardless of whether the nearby gene is induced or repressed. Induced genes tend to be bound by GATA1 close to the transcription start site (most frequently in the first intron), have multiple GATA1-occupied segments that are also bound by TAL1, and show evolutionary constraint on the GATA1-binding site motif. In contrast, repressed genes are further away from GATA1-occupied segments, and a subset shows reduced TAL1 occupancy and increased H3K27me3 at the transcription start site. Our data expand the repertoire of GATA1 action in erythropoiesis by defining a new cohort of target genes and determining the spatial distribution of cis-regulatory modules throughout the genome. In addition, we begin to establish functional criteria and mechanisms that distinguish GATA1 activation from repression at specific target genes. More broadly, these studies illustrate how a "master regulator" transcription factor coordinates tissue differentiation through a panoply of DNA and protein interactions.

  L. F Allard , A Borisevich , W Deng , R Si , M Flytzani Stephanopoulos and S. H. Overbury

High-resolution aberration-corrected electron microscopy was performed on a series of catalysts derived from a parent material, 2 at.% Au/Fe2O3 (WGC ref. no. 60C), prepared by co-precipitation and calcined in air at 400°C, and a catalyst prepared by leaching surface gold from the parent catalyst and exposed to various treatments, including use in the water–gas shift reaction at 250°C. Aberration-corrected JEOL 2200FS (JEOL USA, Peabody, MA) and Vacuum Generators HB-603U STEM instruments were used to image fresh, reduced, leached, used and re-oxidized catalyst samples. A new in situ heating technology (Protochips Inc., Raleigh, NC, USA), which permits full sub-Ångström imaging resolution in the JEOL 2200FS was used to study the effects of temperature on the behavior of gold species. A remarkable stability of gold to redox treatments up to 400°C, with atomic gold decorating step surfaces of iron oxide was identified. On heating the samples in vacuum to 700°C, it was found that monodispersed gold began to sinter to form nanoparticles above 500°C. Gold species internal to the iron oxide support material was shown to diffuse to the surface at elevated temperature, coalescing into discrete nanocrystals. The results demonstrate the value of in situ heating for understanding morphological changes in the catalyst with elevated temperature treatments.

  P Jiang , S. N Rushing , C. w Kong , J Fu , D. K. T Lieu , C. W Chan , W Deng and R. A. Li

Human embryonic stem cells (hESCs) can self-renew while maintaining their pluripotency. Direct reprogramming of adult somatic cells to induced pluripotent stem cells (iPSCs) has been reported. Although hESCs and human iPSCs have been shown to share a number of similarities, such basic properties as the electrophysiology of iPSCs have not been explored. Previously, we reported that several specialized ion channels are functionally expressed in hESCs. Using transcriptomic analyses as a guide, we observed tetraethylammonium (TEA)-sensitive (IC50 = 3.3 ± 2.7 mM) delayed rectifier K+ currents (IKDR) in 105 of 110 single iPSCs (15.4 ± 0.9 pF). IKDR in iPSCs displayed a current density of 7.6 ± 3.8 pA/pF at +40 mV. The voltage for 50% activation (V1/2) was –7.9 ± 2.0 mV, slope factor k = 9.1 ± 1.5. However, Ca2+-activated K+ current (IKCa), hyperpolarization-activated pacemaker current (If), and voltage-gated sodium channel (NaV) and voltage-gated calcium channel (CaV) currents could not be measured. TEA inhibited iPSC proliferation (EC50 = 7.8 ± 1.2 mM) and viability (EC50 = 5.5 ± 1.0 mM). By contrast, 4-aminopyridine (4-AP) inhibited viability (EC50 = 4.5 ± 0.5 mM) but had less effect on proliferation (EC50 = 0.9 ± 0.5 mM). Cell cycle analysis further revealed that K+ channel blockers inhibited proliferation primarily by arresting the mitotic phase. TEA and 4-AP had no effect on iPSC differentiation as gauged by ability to form embryoid bodies and expression of germ layer markers after induction of differentiation. Neither iberiotoxin nor apamin had any function effects, consistent with the lack of IKCa in iPSCs. Our results reveal further differences and similarities between human iPSCs and hESCs. A better understanding of the basic biology of iPSCs may facilitate their ultimate clinical application.

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