August 15, 2025Nature CommunicationsOpen Access

Multivalent interactions with CCR4–NOT and PABPC1 determine mRNA repression efficiency by tristetraprolin

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Authors

FPFilip PekovicNational Institutes of Health WLWi S. LaiNational Institute of Environmental Health Sciences JCJoshua CorboFrederick National Laboratory for Cancer Research

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Implication

Experimental analysis reveals tristetraprolin accelerates mRNA decay in vitro, suggesting multivalent binding with CCR4–NOT enhances poly(A) tail shortening.

Key Points

Tristetraprolin boosts mRNA deadenylation, emphasizing the role of multivalent interactions in the CCR4–NOT complex.
Purified protein assays demonstrated enhanced deadenylation activity with CCR4–NOT in the presence of tristetraprolin.
Observational analysis revealed phosphorylation is critical for tristetraprolin's interaction with PABPC1, influencing mRNA stability.
These findings imply targeted modulation of mRNA decay could be leveraged for therapeutic interventions.

Cite This Study

Pekovic et al. (2025) studied this question.

synapsesocial.com/papers/68a365560a429f797332b0cb https://doi.org/10.1038/s41467-025-62741-7

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Implication

Experimental analysis reveals tristetraprolin accelerates mRNA decay in vitro, suggesting multivalent binding with CCR4–NOT enhances poly(A) tail shortening.

Multivalent interactions with CCR4–NOT and PABPC1 determine mRNA repression efficiency by tristetraprolin

Discussion

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Implication

Key Points

Cite This Study

Multivalent interactions with CCR4–NOT and PABPC1 determine mRNA repression efficiency by tristetraprolin

Discussion

Member takes

Implication

Key Points

Cite This Study

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