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Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Tumor suppressor protein (p)53, is a regulator of NF-kappaB repression by the glucocorticoid receptor

Samantha H Murphy1, Kotaro Suzuki, Michael Downes

  • 1Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA

Proceedings of the National Academy of Sciences of the United States of America
|September 28, 2011
PubMed

Insights

The tumor suppressor p53 is crucial for glucocorticoids to inhibit inflammation by blocking NF-κB. Loss of p53 hinders this process and impairs glucocorticoid effectiveness in models of inflammation and shock.

Area of Science:

  • Molecular Biology
  • Immunology
  • Cancer Biology

Background:

  • Glucocorticoids suppress inflammation by inhibiting NF-κB signaling.
  • The precise molecular mechanisms of glucocorticoid-mediated NF-κB repression are not fully understood.
  • Identifying novel regulators is key to understanding glucocorticoid action.

Purpose of the Study:

  • To identify novel genes involved in glucocorticoid repression of NF-κB.
  • To elucidate the role of the tumor suppressor p53 in this pathway.

Main Methods:

  • High-throughput siRNA oligo screening was employed.
  • NF-κB and glucocorticoid receptor (GR) target gene transcription were analyzed.
  • A mouse model of LPS shock was used to assess glucocorticoid rescue of death.

Main Results:

  • Loss of p53 impaired glucocorticoid repression of NF-κB target genes.
  • p53 deficiency also impaired GR target gene transcription.
  • p53 loss severely compromised glucocorticoid-mediated survival in LPS shock.

Conclusions:

  • p53 plays a significant role in mediating the anti-inflammatory effects of glucocorticoids.
  • Aberrant p53 activity may impact the efficacy of glucocorticoids in treating inflammatory conditions, including those in tumors.

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