• Publications
  • Influence
Hypoxia regulates expression of the endothelin-1 gene through a proximal hypoxia-inducible factor-1 binding site on the antisense strand.
TLDR
An active hypoxia-inducible factor 1 (HIF-1) binding site is identified starting at position -118 upstream of the transcription start site on the non-coding DNA strand, and mutation of this site eliminated induction by Hypoxia without affecting basal (aerobic) expression, and the mutated sequence did not display hyp oxia-specific binding of Hif-1. Expand
Molecular Regulation of the Endothelin-1 Gene by Hypoxia
TLDR
It is reported that the HIF-1 binding site alone is not sufficient for the response to hypoxia but requires an additional 50 base pairs of flanking sequence that includes binding sites for the factors activator protein-1 (AP-1), GATA-2, and CAAT-binding factor (NF-1). Expand
Amyloid-beta peptide activates cultured astrocytes: morphological alterations, cytokine induction and nitric oxide release.
TLDR
Treatment of rat cortical astrocyte cultures with aggregated Abeta 1-42 peptide induces activation, as assessed by reactive morphological changes and upregulation of selective glial mRNA and proteins, such as the inflammatory cytokine interleukin-1beta. Expand
S100β Induces Neuronal Cell Death Through Nitric Oxide Release from Astrocytes
TLDR
The data support the idea that overexpression of S100β may be an exacerbating factor in the neurodegeneration of Alzheimer's disease. Expand
S100β Stimulates Inducible Nitric Oxide Synthase Activity and mRNA Levels in Rat Cortical Astrocytes (*)
TLDR
The data indicate that S100β can induce a potent activation of inducible NOS in astrocytes, an observation that might have relevance to the role of S100 β in neuropathology. Expand
The organization of the human GSTP1-1 gene promoter and its response to retinoic acid and cellular redox status.
TLDR
It is shown that the expression of GSTP1 is regulated by the redox status of the cell, and the effect of NAC was shown to be mediated largely by the AP1 site, since mutation of this site abolished the induction by NAC. Expand
Effects of a calcimimetic compound and naturally activating mutations on the human Ca2+ receptor and on Ca2+ receptor/metabotropic glutamate chimeric receptors.
TLDR
Interactions between four different ADH mutations located in the amino-terminal extracellular domain of R-568 and Leu125Pro suggest that the mGluR1 7TM domain may be more permissive for activation than the 7 TM domain of the CaR. Expand
CCAAT/Enhancer-binding Protein-β Regulates Interferon-induced Transcription through a Novel Element*
TLDR
A novel role for C/EBP-β in the IFN-signaling pathways is identified as a gene coding for the pleiotropic transcription factor, CCAAT/enhancer-binding protein-β (C/E BP-β), which binds to GATE and induces gene expression. Expand
Alterations in the interaction between iron regulatory proteins and their iron responsive element in normal and Alzheimer's diseased brains.
TLDR
The appearance of the single IRE/IRP complex in Alzheimer's brain extracts is associated with relatively high endogenous ribonuclease activity, and it is proposed that elevated RNase activity is one mechanism by which the iron regulatory system becomes dysfunctional. Expand
ERK1 and ERK2 activate CCAAAT/enhancer-binding protein-beta-dependent gene transcription in response to interferon-gamma.
TLDR
A new IFN-gamma-stimulated pathway that operates C/EBP-beta-regulated gene expression independent of JAK1 is described and it is shown that ERKs are activated by IFN -gamma to stimulate C/ EBP- beta-dependent expression. Expand
...
1
2
3
4
5
...