What is the clinical evidence from this study?

Study design: Other. Population: Malignant transformation. Intervention: PKR variants (PKR-M1 and PKR-M7) vs. Wild-type PKR (PKR-WT). Primary outcome: mRNA translation inhibition, eIF-2 alpha phosphorylation levels, and growth rates.

July 1, 1995Journal of Biological ChemistryOpen Access

Molecular Mechanisms Responsible for Malignant Transformation by Regulatory and Catalytic Domain Variants of the Interferon-induced Enzyme RNA-dependent Protein Kinase

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Key result

PKR variants PKR-M1 and PKR-M7 functioned as transdominant inhibitors of wild-type PKR, with PKR-M7 inhibiting at stoichiometric levels and causing greater reductions in eIF-2 alpha phosphorylation.

Population

Reticulocyte translation extracts, in vitro kinase assays with purified reagents, and transformed cell lines…

Comparison

PKR variants containing either a mutation in… vs Wild-type PKR (PKR-WT)

Design

Preclinical

Authors

GBGlen N. BarberImmunité et Cancer RJRosemary JagusUniversity of Maryland, Baltimore ÉMÉliane MeursCentre National de la Recherche Scientifique

Discussion

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Implication

PKR-M1/M7 may inhibit eIF-2α in models; leaves open their role in malignant transformation.

Structured PICO

Population

Reticulocyte translation extracts, in vitro kinase assays with purified reagents, and transformed cell lines overexpressing PKR variants

Intervention

PKR variants containing either a mutation in catalytic domain II (PKR-M1) or a deletion of RNA binding domain I (PKR-M7)

Comparator

Wild-type PKR (PKR-WT)

Outcome

Biological and biochemical properties including mRNA translation inhibition, eIF-2 alpha phosphorylation levels, and growth ratessurrogate

PKR variants M1 and M7 exhibit distinct biochemical properties and mechanisms of transdominant inhibition, providing insights into their roles in malignant transformation.

Cite This Study

Barber et al. (1995) studied Malignant transformation. PKR variants (PKR-M1 and PKR-M7) vs. Wild-type PKR (PKR-WT) was evaluated on mRNA translation inhibition, eIF-2 alpha phosphorylation levels, and growth rates. PKR variants PKR-M1 and PKR-M7 functioned as transdominant inhibitors of wild-type PKR, with PKR-M7 inhibiting at stoichiometric levels and causing greater reductions in eIF-2 alpha phosphorylation.

synapsesocial.com/papers/6a944cff7779db04076e49d8 https://doi.org/10.1074/jbc.270.29.17423

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Molecular Mechanisms Responsible for Malignant Transformation by Regulatory and Catalytic Domain Variants of the Interferon-induced Enzyme RNA-dependent Protein Kinase

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Molecular Mechanisms Responsible for Malignant Transformation by Regulatory and Catalytic Domain Variants of the Interferon-induced Enzyme RNA-dependent Protein Kinase

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider