Evidence map›Paper›PMID 42839642›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

SEC Mediates m

Zhijing Zhang, Jingyi Xu, Yonghong Wu, Yitong Qu, Xinglin Hu, Yuchen Sun, Yanshuang Wu, Zhonghua Liu, Jiaqiang Wang, Lei Lei

Abstract read
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In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. 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

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

10 authors.

Zhijing ZhangKey Laboratory of Animal Cellular and Genetic Engineering of Heilongjiang Province, Northeast Agricultural University, Harbin, Heilongjiang, China.ORCID https://orcid.org/0000-0002-7777-8414
Jingyi XuDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, China.
Yonghong WuDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, China.
Yitong QuDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, China.ORCID https://orcid.org/0009-0005-1491-5417
Xinglin HuDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, China.ORCID https://orcid.org/0000-0003-0311-5332
Yuchen SunDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, China.ORCID https://orcid.org/0000-0003-2688-3932
Yanshuang WuDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, China.
Zhonghua LiuKey Laboratory of Animal Cellular and Genetic Engineering of Heilongjiang Province, Northeast Agricultural University, Harbin, Heilongjiang, China.ORCID https://orcid.org/0000-0002-9199-6493
Jiaqiang WangKey Laboratory of Animal Cellular and Genetic Engineering of Heilongjiang Province, Northeast Agricultural University, Harbin, Heilongjiang, China.ORCID https://orcid.org/0000-0002-1758-3316
Lei LeiDepartment of Histology and Embryology, School of Basic Medical Sciences, Harbin Medical University, Harbin, Heilongjiang, China.ORCID https://orcid.org/0000-0002-5239-7009

Funding

National Natural Science Foundation of China 32671086
6 · The paper itself

Abstract

backgroundInduced pluripotent stem cell (iPSC) reprogramming and embryonic stem cell (ESC) differentiation represent opposite models of cell identity transition, yet their regulatory mechanisms remain incompletely understood. Here, we identify the Super Elongation Complex (SEC), the most pivotal regulators of transcription pause release, as a central driver of cell identity transition in both models.

resultsSEC depletion markedly impairs iPSC reprogramming efficiency, particularly during the early stage, by suppressing core reprogramming genes, including Klf4 and Myc, thereby disrupting key reprogramming events, such as cell-cycle progression and activation of the pluripotency network. Mechanistically, SEC activates the expression of Klf4 and Myc by promoting the release of pre-established paused RNA polymerase II (RNA Pol II). Moreover, SEC also cooperates with METTL3 to facilitate N6-methyladenosine (m

conclusionsThese findings establish SEC as a shared regulator of cell identity transition in both iPSC reprogramming and ESC differentiation. Elucidating the mechanisms by which SEC drives cell identity transitions provides a foundation for further investigation into diverse cell identity transitions under physiological and pathological conditions.

Indexed as

cell identity transitioniPSCsm6A modificationSECtranscription pause release

Identifiers

PMID42839642
PMCPMC13643097

What OpenQuestion holds

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Registered trials

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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.