Evidence map›Paper›PMID 41509511›Full record

ArticleSynthetic and systems biotechnology2026

Leveraging ANXA1 to enhance recombinant protein yields in CHO cells: A UPR-Mediated bioprocessing approach.

Qi Zhao, Hui-Jie Zhang, Ming-Ming Han, Jumai Abiti, Yan-Ju Dong, Jia-Ning Wang, Jiang-Tao Lu, Wen Wang, Xi Zhang, Shao-Lei Geng and 5 more

Abstract read
In one paragraph

Article in Synthetic and systems biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
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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

15 authors.

Qi ZhaoSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Hui-Jie ZhangSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Ming-Ming HanSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Jumai AbitiSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Yan-Ju DongSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Jia-Ning WangSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Jiang-Tao LuSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Wen WangSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Xi ZhangSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.
Shao-Lei GengInternational Joint Laboratory of Recombinant Drug Protein Expression System, Xinxiang, Henan, 453003, China.
Le-Le QiuSchool of Basic Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, China.
Xiao-Yin WangInternational Joint Laboratory of Recombinant Drug Protein Expression System, Xinxiang, Henan, 453003, China.
Zi-Chun HuaFaculty of Pharmaceutical Sciences, Xinxiang Medical University, Xinxiang, 453003, China.
Tian-Yun WangInternational Joint Laboratory of Recombinant Drug Protein Expression System, Xinxiang, Henan, 453003, China.
Yan-Long JiaSchool of Pharmacy, Xinxiang Medical University, Xinxiang, Henan, 453003, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chinese hamster ovary (CHO) cells undergo endoplasmic reticulum stress (ERS) during intensive recombinant protein production, triggering the unfolded protein response (UPR) to balance cell survival and protein output. Nevertheless, key regulatory components of this process remain incompletely characterized. In this study, we demonstrate that Annexin A1 (ANXA1) functions as a UPR suppressor in CHO cells. Employing the PiggyBac transposon system, we generated a stable ANXA1-knockdown cell line exhibiting a 4.5-fold increase in recombinant antibody expression and a 4.2-fold increase in specific productivity. Pharmacological inhibition using AC2-26 similarly enhanced recombinant protein expression in low-productivity cell populations. Mechanistically, ANXA1 depletion remodeled the UPR by activating the PERK-eIF2α-ATF4 and IRE1-XBP1 branches. This activation upregulaed ATF4, Bip, and XBP1s; suppressed CHOP; reduced apoptosis; and enhanced autophagic flux. Metabolic profiling revealed increased glucose and lactate utilization, while glutamine consumption and ammonia flux remained unchanged. Collectively, these findings establish that ANXA1 depletion enhances recombinant protein biosynthesis through coordinated pro-survival mechanisms. Targeting ANXA1 thus represents an innovative cell engineering strategy for optimizing CHO cell platforms in industrial biopharmaceutical manufacturing.

Indexed as

Annexin A1 (ANXA1)Chinese hamster ovary (CHO) cellsGenetic engineeringRecombinant preotein expressionUnfolded protein response (UPR)

Identifiers

PMID41509511
PMCPMC12775871

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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.