• Publications
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Inducible Nitric-oxide Synthase Generates Superoxide from the Reductase Domain*
TLDR
Electron paramagnetic resonance measurements demonstrate that inducible NOS does generate O⨪2, and this mainly occurs at the flavin-binding sites of the reductase domain. Expand
Enhanced Electron Flux and Reduced Calmodulin Dissociation May Explain “Calcium-independent” eNOS Activation by Phosphorylation*
TLDR
Results suggest that a negative charge imposed at serine 1179, either by phosphorylation or by replacement with aspartate, increases eNOS catalytic activity by increasing electron flux at the reductase domain and by reducing calmodulin dissociation from activated eN OS when calcium levels are low. Expand
Characterization of the helicase activity of the Escherichia coli RecBCD enzyme using a novel helicase assay.
TLDR
It is shown that recBCD enzyme molecules are able to catalytically unwind additional ds DNA substrates subsequent to initiation, unwinding, and dissociation from a previous dsDNA molecule. Expand
Nox4 NADPH Oxidase Mediates Peroxynitrite-dependent Uncoupling of Endothelial Nitric-oxide Synthase and Fibronectin Expression in Response to Angiotensin II
TLDR
It is demonstrated that, in MCs, Ang II induces endothelial nitric-oxide synthase (eNOS) uncoupling with enhanced generation of reactive oxygen species (ROS) and decreased production of NO, providing the first evidence that uncoupled eNOS is responsible for Ang II-induced MC fibronectin accumulation. Expand
An Autoinhibitory Control Element Defines Calcium-regulated Isoforms of Nitric Oxide Synthase*
TLDR
It is shown that cNOS isoforms contain a unique polypeptide insert in their FMN binding domains which is not shared with iNOS or other related flavoproteins, and this strongly suggest that the insert is an autoinhibitory control element, docking with a site on cN OSs which impedes calmodulin binding and enzymatic activation. Expand
Intrinsic and extrinsic modulation of nitric oxide synthase activity.
The Role of Tetrahydrobiopterin in the Regulation of Neuronal Nitric-oxide Synthase-generated Superoxide*
  • G. Rosen, P. Tsai, +5 authors S. Pou
  • Chemistry, Medicine
  • The Journal of Biological Chemistry
  • 25 October 2002
TLDR
It has been hypothesized that in the absence of or under nonsaturating levels of l-arginine where O2 reduction is the primary outcome of NOS activation, H4B promotes the generation of H2O2 at the expense of O 2 ⨪ . Expand
Sestrin 2 and AMPK Connect Hyperglycemia to Nox4-Dependent Endothelial Nitric Oxide Synthase Uncoupling and Matrix Protein Expression
TLDR
It is demonstrated that, in glomerular mesangial cells (MCs), endothelial nitric oxide synthase (eNOS) is uncoupled upon exposure to high glucose (HG), with enhanced generation of reactive oxygen species (ROS) and decreased production of Nitric oxide and peroxynitrite mediates the effects of HG on eNOS dysfunction. Expand
The C Terminus of Mouse Macrophage Inducible Nitric-oxide Synthase Attenuates Electron Flow through the Flavin Domain*
TLDR
It is proposed that the C-terminal tail of nitric-oxide synthase (NOS) flavin domains curls back to interact with the flavin domain in such a way as to modulate the interaction between the two flavin moieties. Expand
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