Evidence map›Paper›PMID 36596852›Full record

ArticleExperimental & molecular medicine2023

TPX2 prompts mitotic survival via the induction of BCL2L1 through YAP1 protein stabilization in human embryonic stem cells.

Yun-Jeong Kim, Young-Hyun Go, Ho-Chang Jeong, Eun-Ji Kwon, Seong-Min Kim, Hyun Sub Cheong, Wantae Kim, Hyoung Doo Shin, Haeseung Lee, Hyuk-Jin Cha

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.3field-weighted citation impact, top 8% of its field
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

11 citing papers in PubMed, 16 citations in OpenAlex.

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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

10 authors at 5 institutions in 2 countries.

Yun-Jeong KimCollege of Pharmacy, Seoul National University, Seoul, 08826, Republic of Korea.
Young-Hyun GoDepartment of Life Sciences, Sogang University, Seoul, 04107, Republic of Korea.
Ho-Chang JeongDepartment of Life Sciences, Sogang University, Seoul, 04107, Republic of Korea.
Eun-Ji KwonCollege of Pharmacy, Seoul National University, Seoul, 08826, Republic of Korea.
Seong-Min KimCollege of Pharmacy, Seoul National University, Seoul, 08826, Republic of Korea.
Hyun Sub CheongDrug Information Research Institute, College of Pharmacy, Sookmyung Women's University, Seoul, 04310, Republic of Korea.
Wantae KimDepartment of Biochemistry, College of Natural Sciences, Chungnam National University, Daejeon, 34134, Republic of Korea.
Hyoung Doo ShinDepartment of Life Sciences, Sogang University, Seoul, 04107, Republic of Korea.
Haeseung LeeCollege of Pharmacy, Pusan National University, Busan, 46241, Korea.
Hyuk-Jin ChaCollege of Pharmacy, Seoul National University, Seoul, 08826, Republic of Korea. hjcha93@snu.ac.kr.ORCID http://orcid.org/0000-0001-9277-2662
Seoul National University · KRSogang University · KRChungnam National University · KRPusan National University · KRSookmyung Women's University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic alterations have been reported for decades in most human embryonic stem cells (hESCs). Survival advantage, a typical trait acquired during long-term in vitro culture, results from the induction of BCL2L1 upon frequent copy number variation (CNV) at locus 20q11.21 and is one of the strongest candidates associated with genetic alterations that occur via escape from mitotic stress. However, the underlying mechanisms for BCL2L1 induction remain unknown. Furthermore, abnormal mitosis and the survival advantage that frequently occur in late passage are associated with the expression of BCL2L1, which is in locus 20q11.21. In this study, we demonstrated that the expression of TPX2, a gene located in 20q11.21, led to BCL2L1 induction and consequent survival traits under mitotic stress in isogenic pairs of hESCs and human induced pluripotent stem cells (iPSCs) with normal and 20q11.21 CNVs. High Aurora A kinase activity by TPX2 stabilized the YAP1 protein to induce YAP1-dependent BCL2L1 expression. A chemical inhibitor of Aurora A kinase and knockdown of YAP/TAZ significantly abrogated the high tolerance to mitotic stress through BCL2L1 suppression. These results suggest that the collective expression of TPX2 and BCL2L1 from CNV at loci 20q11.21 and a consequent increase in YAP1 signaling promote genome instability during long-term in vitro hESC culture.

Indexed as

Human Embryonic Stem CellsInduced Pluripotent Stem CellsAurora Kinase Abcl-X ProteinCell Cycle ProteinsDNA Copy Number VariationsHumansMicrotubule-Associated ProteinsAurora Kinase ABCL2L1 protein, humanbcl-X ProteinCell Cycle ProteinsMicrotubule-Associated ProteinsTPX2 protein, human

Identifiers

PMID36596852
PMCPMC9898288
OpenAlexW4313455512

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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.