Evidence map›Paper›PMID 40412387›Full record

ArticleAmerican journal of human genetics2025

Prioritizing disease-associated missense variants with chemoproteomic-detected amino acids.

Maria F Palafox, Lisa Boatner, Blake R Wilde, Heather Christofk, Keriann M Backus, Valerie A Arboleda

Abstract read
In one paragraph

Article in American journal of human genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Maria F PalafoxDepartment of Human Genetics, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Department of Pathology and Lab Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Department of Biological Chemistry, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA.
Lisa BoatnerDepartment of Biological Chemistry, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Department of Chemistry and Biochemistry, College of Arts and Sciences, UCLA, Los Angeles, CA 90095, USA.
Blake R WildeDepartment of Biological Chemistry, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA 90095, USA.
Heather ChristofkDepartment of Biological Chemistry, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Molecular Biology Institute, UCLA, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, UCLA, Los Angeles, CA 90095, USA.
Keriann M BackusDepartment of Biological Chemistry, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Department of Chemistry and Biochemistry, College of Arts and Sciences, UCLA, Los Angeles, CA 90095, USA; Molecular Biology Institute, UCLA, Los Angeles, CA 90095, USA; DOE Institute for Genomics and Proteomics, UCLA, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, UCLA, Los Angeles, CA 90095, USA. Electronic address: kbackus@mednet.ucla.edu.
Valerie A ArboledaDepartment of Human Genetics, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Department of Pathology and Lab Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA; Molecular Biology Institute, UCLA, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, UCLA, Los Angeles, CA 90095, USA; Department of Computational Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA. Electronic address: varboleda@mednet.ucla.edu.

Funding

UCLA SPORE in Brain CancerP50CA211015 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GANG LI · 2017 to 2026
$25.2M
CHEMISTRY BIOLOGY INTERFACE TRAINING PROGRAMT32GM008496 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MAYNARD, HEATHER D · 1993 to 2019
$6.3M
Nutrient Regulation of Cancer Cell GrowthR01CA215185 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Heather Christofk · 2018 to 2026
$4.3M
A systems-level approach to decipher the protein interactome.DP2GM146246 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BACKUS, KERIANN MARIE · 2021 to 2024
$2.3M
Metabolic Control of Hair Follicle Stem Cell Homeostasis and TumorigenesisR01AR070245 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHRISTOFK, HEATHER, LOWRY, WILLIAM E · 2018 to 2022
$2.1M
Unraveling correlations between Mendelian and common disease using functional genomicsDP5OD024579 · OD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARBOLEDA, VALERIE A · 2017 to 2021
$1.9M
NCI NIH HHS P50 CA211015NCI NIH HHS R01 CA215185NIAMS NIH HHS R01 AR070245NIGMS NIH HHS DP2 GM146246NIGMS NIH HHS T32 GM008496NIH HHS DP5 OD024579
6 · The paper itself

Abstract

Missense variants are the most common type of protein-altering genetic variation. Due to their wide-ranging potential functional consequences, missense variants are challenging to interpret and, as a result, are often classified as unknown pathogenicity or as variants of uncertain significance (VUSs). Genomic-based predictive tools have made significant inroads into the challenge of accurately pinpointing functional missense variants by providing genome-wide assessments of deleteriousness or potential pathogenicity. Complementary to these tools, here we provide an initial study into the utility of harnessing protein-based measures of amino acid reactivity to delineate functionally significant missense variants. These reactivity measurements, which are generated using mass spectrometry-based chemoproteomic methods, have already proved capable of pinpointing functional sites on proteins, which provide the added value of delineating potential sites suitable for drug-development efforts. Here, using published chemoproteomic datasets for three specific privileged amino acids, cysteine, lysine, and tyrosine, we assessed the utility of proteomic reactivity measurements to identify clinically important variants and regions within monogenic-disease-associated genes. We found that genes where amino acids are detected via chemoproteomics are enriched for monogenic-disease phenotypes, indicative of functional importance. Chemoproteomic-detected amino acids (CpDAAs) are enriched at and around sites with known pathogenic missense variants when assessed with either one- or three-dimensional protein structures. To further illustrate the utility of our findings, we found that regions at or around CpDAAs in fumarate hydratase (FH) were enriched for VUSs and pathogenic variants, which we validate through demonstration of an altered FH oligomerization state. Collectively, our study highlights the potential of chemoproteomic and genetic data integration for enhancing the identification of functional genetic variants and protein sites with potential value for drug-development efforts.

Indexed as

Amino AcidsGenetic Predisposition to DiseaseMutation, MissenseProteomicsHumansAmino Acidscancer predispositionchemoproteomicsclinical geneticscysteinegenomicslysineMendelian diseasemissense variationproteomicstyrosine

Identifiers

PMID40412387
PMCPMC12256893

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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.