Evidence map›Paper›PMID 30889230›Full record

ArticlePloS one2019

Predicting mutations deleterious to function in beta-lactamase TEM1 using MM-GBSA.

Christopher Negron, David A Pearlman, Guillermo Del Angel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Disrupting Cu trafficking as a potential therapy for cancer.Frontiers in molecular biosciences · 2022
    Article
  5. Anti-cancer activity ofBioinformation · 2022
    Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Christopher NegronSchrödinger, New York, New York, United States of America.ORCID 0000-0002-5802-8482
David A PearlmanSchrödinger, New York, New York, United States of America.
Guillermo Del AngelAlexion Pharmaceuticals Inc., Boston, Massachusetts, United States of America.
Schrodinger (United States) · USAlexion Pharmaceuticals (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Missense mutations can have disastrous effects on the function of a protein. And as a result, they have been implicated in numerous diseases. However, the majority of missense variants only have a nominal impact on protein function. Thus, the ability to distinguish these two classes of missense mutations would greatly aid drug discovery efforts in target identification and validation as well as medical diagnosis. Monitoring the co-occurrence of a given missense mutation and a disease phenotype provides a pathway for classifying functionally disrupting missense mutations. But, the occurrence of a specific missense variant is often extremely rare making statistical links challenging to infer. In this study, we benchmark a physics-based approach for predicting changes in stability, MM-GBSA, and apply it to classifying mutations as functionally disrupting. A large and diverse dataset of 990 residue mutations in beta-lactamase TEM1 is used to assess performance as it is rich in both functionally disrupting mutations and functionally neutral/beneficial mutations. On this dataset, we compare the performance of MM-GBSA to alternative strategies for predicting functionally disrupting mutations. We observe that the MM-GBSA method obtains an area under the curve (AUC) of 0.75 on the entire dataset, outperforming all other predictors tested. More importantly, MM-GBSA's performance is robust to various divisions of the dataset, speaking to the generality of the approach. Though there is one notable exception: Mutations on the surface of the protein are the mutations that are the most difficult to classify as functionally disrupting for all methods tested. This is likely due to the many mechanisms available to surface mutations to disrupt function, and thus provides a direction of focus for future studies.

Indexed as

Mutation, MissenseBacterial Proteinsbeta-LactamasesDatabases, GeneticEnzyme StabilityGenes, BacterialHumansBacterial Proteinsbeta-Lactamasesbeta-lactamase TEM-1

Identifiers

PMID30889230
PMCPMC6424398
OpenAlexW2924162540

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.