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Updated: May 29, 2026

A Bilingual Computational Workflow for Identifying Potential PLK1 Inhibitors in American Sign Language and English
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Identification of novel small molecules that elevate Klotho expression.

Gwendalyn D King1, CiDi Chen, Mickey M Huang

  • 1Boston University School of Medicine, Department of Biochemistry, 72 East Concord Street K304, Boston, MA 02118, USA.

The Biochemical Journal
|September 24, 2011
PubMed
Summary

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Researchers identified compounds that boost Klotho (KL) levels, a protein linked to aging and longevity. These compounds may offer new therapeutic strategies for healthier aging and age-related diseases.

Area of Science:

  • Biochemistry
  • Gerontology
  • Pharmacology

Background:

  • Klotho (KL) deficiency in mice mimics human aging disorders and reduces lifespan.
  • KL protein levels decline with age, suggesting its maintenance could promote healthy aging and modify disease.
  • KL plays a crucial role in regulating aging processes and longevity.

Purpose of the Study:

  • To identify compounds that activate Klotho (KL) transcription using a high-throughput screening approach.
  • To validate and characterize compounds that increase KL expression and protein levels.
  • To investigate the functional impact of KL-boosting compounds on fibroblast growth factor 23 (FGF23) signaling.

Main Methods:

  • A high-throughput screen utilizing a luciferase reporter system driven by the KL promoter.

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A Bilingual Computational Workflow for Identifying Potential PLK1 Inhibitors in American Sign Language and English
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Published on: April 3, 2026

  • In vitro validation of hit compounds in opossum kidney and rat choroid plexus cells.
  • Assay of FGF23 signaling, including ERK phosphorylation, in response to compounds, with KL siRNA knockdown.

    • Main Results:

    • Compounds were identified that elevated luciferase expression by at least 30%, indicating KL transcriptional activation.
    • Validated compounds dose-dependently increased KL protein levels in kidney and choroid plexus cells without cytotoxicity.
    • Compounds G-I augmented ERK phosphorylation in FGFR-transfected cells, an effect blocked by KL siRNA, confirming functional KL pathway modulation.

    Conclusions:

    • The identified compounds serve as valuable tools for elucidating KL regulatory mechanisms.
    • These compounds demonstrate potential for developing pharmacological interventions to modulate KL activity.
    • Further optimization of these compounds could lead to novel therapeutic strategies for age-related diseases and longevity enhancement.