Evidence map›Paper›PMID 40559997›Full record

ReviewProteomes2025

Advances in the Study of Protein Deamidation: Unveiling Its Influence on Aging, Disease Progression, Forensics and Therapeutic Efficacy.

Sunil S Adav

Abstract readReview
In one paragraph

Review in Proteomes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. 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

1 author.

Sunil S AdavSchool of Materials Science and Engineering, Nanyang Technological University, 50 Nanyang Avenue, Singapore 639798, Singapore.ORCID 0000-0002-8559-4885

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein deamidation, a nonenzymatic post-translational modification that converts asparagine and glutamine residues into their acidic forms, such as aspartic acid, iso-aspartic acid, or glutamic acid, has emerged as a pivotal process affecting protein stability and function. Once considered a minor biochemical occurrence, deamidation is now recognized for its significant role in aging, age-associated diseases, disease progression, cancer, and therapeutic efficacy. This review explores the recent advances in understanding protein deamidation, its impact on cellular homeostasis, protein misfolding, and age-related and chronic diseases including neurodegeneration and cancer. The study also highlights the challenges posed by deamidation in biopharmaceuticals, where it compromises therapeutic stability and efficacy. Advancements in state-of-the-art analytical techniques and computational approaches for identifying deamidation sites and predicting deamidation-prone regions are discussed, along with deeper insights into how deamidation affects protein structure and function. Based on the current insights, this review underscores the dual role of deamidation as both a natural regulatory process and a contributor to pathological states, providing a roadmap for future research in aging biology, disease mechanisms, and therapeutics.

Indexed as

agingbiopharmaceuticalscancerdeamidationdementiaforensics

Identifiers

PMID40559997
PMCPMC12196754

What OpenQuestion holds

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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.