Evidence map›Paper›PMID 41446266›Full record

ArticlebioRxiv : the preprint server for biology2025

Characterizing the Effects of Protein Glycosylation Perturbation on Phosphorylation Signaling.

Effram Wei, Hongyi Liu, Michael Betenbaugh, Hui Zhang

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Effram WeiDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Whiting School of Engineering, Baltimore, MD 21218, USA.ORCID 0009-0006-6204-8861
Hongyi LiuDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Michael BetenbaughDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Whiting School of Engineering, Baltimore, MD 21218, USA.
Hui ZhangDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Whiting School of Engineering, Baltimore, MD 21218, USA.ORCID 0000-0001-8726-7098

Funding

Proteogenomic Characterization of Tumor Tissues and Preclinical Models with High PrecisionU24CA271079 · NCI · JOHNS HOPKINS UNIVERSITY · PI DANIEL Wanyui CHAN, Hui Zhang · 2022 to 2026
$6.6M
Biomarker Reference LaboratoryU2CCA271895 · NCI · JOHNS HOPKINS UNIVERSITY · PI DANIEL Wanyui CHAN · 2023 to 2026
$4.6M
Development of a panel of multiplex biomarkers for the early detection of pancreatic ductal adenocarcinoma and high-risk lesionsU01CA274514 · NCI · JOHNS HOPKINS UNIVERSITY · PI Randall Brand, DANIEL Wanyui CHAN · 2023 to 2026
$3.2M
NCI NIH HHS U01 CA274514NCI NIH HHS U24 CA271079NCI NIH HHS U2C CA271895
6 · The paper itself

Abstract

Protein glycosylation and phosphorylation constitute two pervasive regulatory layers in mammalian cells, yet the effects that protein glycosylation play in phosphorylation signaling remain poorly understood. Here we show that controlled perturbation of N-linked glycan biosynthesis through glycoengineering fundamentally rewires phosphorylation signaling networks in human cells. Using comprehensive proteomics approaches, we simultaneously profiled the global proteome, glycoproteome, and phosphoproteome in engineered HEK293 cells designed to eliminate core fucosylation while enhancing sialylation and reducing GlcNAc branching complexity. Glycoengineering emerged as the dominant source of molecular variation across all datasets, with over 9,800 intact glycopeptides identified of which 3,400 are significantly altered, establishing a remodeled baseline cellular state. Upon serum stimulation, engineered cells not only exhibited markedly decreased phosphorylation responses compared to wild-type cells, but comprehensively re-wired to prefer signaling away from canonical EGFR/mTOR growth pathways. These findings establish a systematic framework for targeting glycosylation-phosphorylation regulation and nominate glycan-dependent signaling nodes as potential therapeutic vulnerabilities in glycosylation-remodeled disease states.

Indexed as

glycoengineeringglycosylationphosphorylationproteomicsserum starvationserum stimulation

Identifiers

PMID41446266
PMCPMC12724710

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.