What does this research mean for the field?

A guanine-to-adenine transition at codon 244 is responsible for the glycine-to-aspartic acid mutation in the human beta-actin gene found in neoplastic fibroblasts, resulting in the loss of a HaeIII restriction site. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

October 1, 1984Molecular and Cellular Biology

Molecular Cloning and Characterization of Mutant and Wild-Type Human β-Actin Genes

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Population

Human fetal gene library and human fibroblasts (normal and neoplastic)

Design

Preclinical

Authors

JLJohn LeavittUniversity of California, Santa Cruz PGPeter W. GunningUniversity of Southern California PPPatricia PorrecaPalo Alto Institute

Discussion

Member takes

Implication

No clinical implications yet; leaves open the functional impact of beta-actin mutations in neoplasia.

Structured PICO

Population

Human fetal gene library and human fibroblasts (normal and neoplastic)

Intervention

Homologous recombination using pi AN7 beta 1 miniplasmid

Outcome

Isolation and characterization of functional beta-actin genes

The study successfully isolated and characterized human beta-actin genes, identifying the specific nucleotide transition responsible for a known mutation in neoplastic fibroblasts.

Cite This Study

Leavitt et al. (1984) studied this question.

synapsesocial.com/papers/6a1bf986ea84844e355f4194 https://doi.org/10.1128/mcb.4.10.1961-1969.1984

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Molecular Cloning and Characterization of Mutant and Wild-Type Human β-Actin Genes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Molecular Cloning and Characterization of Mutant and Wild-Type Human β-Actin Genes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider