SOCS3 deficiency drives the primed to naive pluripotency transition by sustaining STAT3 activation.

Renhong Lu, Suoni Huang, Mingyang Du, Xiumiao Yang, Junyang Liu, Zheyi Lin, Jian Yang

Abstract read

In one paragraph

Article in Frontiers in genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

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5 · Who and what money

Authors and funding

7 authors.

Renhong Lu *State Key Laboratory of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.

Suoni Huang *State Key Laboratory of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.

Mingyang DuJinzhou Medical University, Jinzhou, China.

Xiumiao YangJinzhou Medical University, Jinzhou, China.

Junyang LiuState Key Laboratory of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.

Zheyi LinState Key Laboratory of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.

Jian YangState Key Laboratory of Cardiology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: The transition between naive and primed pluripotency is governed by dynamic signaling networks and transcriptional circuits. While the janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway is the master driver of naive pluripotency, the intrinsic negative feedback mechanisms that restrict its activation in primed epiblast stem cells (EpiSCs) remain incompletely defined. This study aimed to characterize the functional role of Suppressor of Cytokine Signaling 3 (SOCS3) in the primed-to-naive pluripotency transition. Methods: CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats)/Cas9 (CRISPR-associated protein 9) -mediated Results: Conclusion: SOCS3 acts as a pivotal inducible barrier to the primed-to-naive pluripotency transition. Eliminating SOCS3-mediated negative regulation to sustain STAT3 activation is an effective strategy to overcome stem cell reprogramming barriers, providing a key target for the precise manipulation of pluripotent stem cell (PSC) fate.

Indexed as

EpiSCsESCspluripotent stem cellsreprogrammed naive ESCsSOCS3

Identifiers

PMID42544337

DOI10.3389/fgene.2026.1857225

PMCPMC13429239

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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.