Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing 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.
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
12 authors.
Xi Kong *Laboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China.
Nan Jiang *Laboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China.
Shaowei Chen *Department of Reproductive Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, China.
Xingyou Zhang *Luzhou New Drug Evaluation and Research Center, Luzhou, China.
An HuangLaboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China.
Li HuLaboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China.
Simeng YiLaboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China.
Shigang YinLaboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China.ORCID http://orcid.org/0000-0003-0955-917X
Jianhua PengLaboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China.ORCID http://orcid.org/0000-0003-3348-9538
Yong JiangLaboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China. jiangyong@swmu.edu.cn.ORCID http://orcid.org/0000-0002-0490-3405
Huangfan XieLaboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China. xie1991@swmu.edu.cn.ORCID http://orcid.org/0000-0002-6342-4316
Bingqing XieLaboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University; Institute of Brain Science, Southwest Medical University, Luzhou, China. bingqingxie@swmu.edu.cn.ORCID http://orcid.org/0000-0001-9433-1641
Funding
National Natural Science Foundation of China (National Science Foundation of China) 32300675National Natural Science Foundation of China (National Science Foundation of China) 32400598National Natural Science Foundation of China (National Science Foundation of China) 52435006
6 · The paper itself
Abstract
In human embryos, major zygotic genome activation (ZGA) initiates at the 8-cell (8C) blastomere stage, marking the start of the ontogenesis program. Recent advancements have shown that primed human pluripotent stem cells (hPSCs) can be reprogrammed to 8C-like cells (8CLCs) with totipotent characteristics in vitro. However, the key regulators driving this transition remain largely unexplored. In this study, we identify OTX2 as a key factor that establishes a repressive barrier to the induction of 8CLCs from primed hPSCs. Our findings reveal that OTX2 deletion greatly enhances the generation of TPRX1-EGFP
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.
OTX2 inhibits human pluripotent stem cell reprogramming toward 8-cell-like and morula-like states. · full record | OpenQuestion