What question did this study set out to answer?

To determine whether engineered dominant-negative Stat1 mutants can selectively down-regulate interferon-γ-induced ICAM-1 expression in airway epithelial cells.

November 1, 1997Journal of Biological ChemistryOpen Access

Targeted Inhibition of Interferon-γ-dependent Intercellular Adhesion Molecule-1 (ICAM-1) Expression Using Dominant-Negative Stat1

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Authors

MWMichael Walter DLDwight C. Look RTRose M. Tidwell

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Overview

In vitro study demonstrates targeted suppression of IFN-gamma-induced ICAM-1 by dominant-negative Stat1 mutants in human airway epithelial cells, suggesting a strategy to attenuate airway...

Key Points

To determine whether engineered dominant-negative Stat1 mutants can selectively down-regulate interferon-γ-induced ICAM-1 expression in airway epithelial cells.
Transfected a Stat1-deficient cell line with wild-type or mutant Stat1 plasmids (Tyr-701, Glu-428/429, His-713, and Ser-727) to evaluate ICAM-1 promoter activation.
Transfected primary human tracheobronchial epithelial cells (hTBECs) with Flag-tagged Stat1 constructs and examined endogenous ICAM-1 expression via dual immunofluorescence following IFN-γ stimulation.
All four Stat1 mutations reduced ICAM-1 promoter activation, with Tyr-701 and His-713 mutants displaying the strongest dominant-negative capacity to overcome co-transfected wild-type Stat1 activation.
Primary hTBECs expressing either the Tyr-701 or His-713 Stat1 mutant were completely protected from up-regulating endogenous ICAM-1 in response to IFN-γ.

Cite This Study

Walter et al. (1997) studied this question.

synapsesocial.com/papers/6a762d00cd662f67b2fbdf60 https://doi.org/10.1074/jbc.272.45.28582

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November 1, 1997Journal of Biological ChemistryOpen Access

Targeted Inhibition of Interferon-γ-dependent Intercellular Adhesion Molecule-1 (ICAM-1) Expression Using Dominant-Negative Stat1

View Full Paper

Ask AI

Bookmark

Authors

MWMichael Walter DLDwight C. Look RTRose M. Tidwell

Discussion

Member takes

Overview

In vitro study demonstrates targeted suppression of IFN-gamma-induced ICAM-1 by dominant-negative Stat1 mutants in human airway epithelial cells, suggesting a strategy to attenuate airway...

Key Points

To determine whether engineered dominant-negative Stat1 mutants can selectively down-regulate interferon-γ-induced ICAM-1 expression in airway epithelial cells.
Transfected a Stat1-deficient cell line with wild-type or mutant Stat1 plasmids (Tyr-701, Glu-428/429, His-713, and Ser-727) to evaluate ICAM-1 promoter activation.
Transfected primary human tracheobronchial epithelial cells (hTBECs) with Flag-tagged Stat1 constructs and examined endogenous ICAM-1 expression via dual immunofluorescence following IFN-γ stimulation.
All four Stat1 mutations reduced ICAM-1 promoter activation, with Tyr-701 and His-713 mutants displaying the strongest dominant-negative capacity to overcome co-transfected wild-type Stat1 activation.
Primary hTBECs expressing either the Tyr-701 or His-713 Stat1 mutant were completely protected from up-regulating endogenous ICAM-1 in response to IFN-γ.

Cite This Study

Walter et al. (1997) studied this question.

synapsesocial.com/papers/6a762d00cd662f67b2fbdf60 https://doi.org/10.1074/jbc.272.45.28582

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