Evidence map›Paper›PMID 27542413›Full record

ArticleThe Journal of biological chemistry2016

Hepatic Loss of Borealin Impairs Postnatal Liver Development, Regeneration, and Hepatocarcinogenesis.

Lu Li, Dan Li, Feng Tian, Jin Cen, Xiaotao Chen, Yuan Ji, Lijian Hui

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Effect of PGV-1 on ApoptosisTurkish journal of pharmaceutical sciences · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Observational
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

7 authors at 6 institutions in 1 country.

Lu LiFrom the State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai and the University of Chinese Academy of Sciences, and.
Dan LiFrom the State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai and lidan@sibcb.ac.cn.
Feng Tianthe Department of Pathology, Zhongshan Hospital, Fudan University, Fenglin Road 180, Shanghai, China.
Jin CenFrom the State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai and.
Xiaotao ChenFrom the State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai and.
Yuan Jithe Department of Pathology, Zhongshan Hospital, Fudan University, Fenglin Road 180, Shanghai, China.
Lijian HuiFrom the State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai and ljhui@sibcb.ac.cn.
Chinese Academy of Sciences · CNCenter for Excellence in Molecular Cell Science · CNFudan University · CNShanghai Institutes for Biological Sciences · CNUniversity of Chinese Academy of Sciences · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Borealin, a member of the chromosomal passenger complex, plays a key regulatory role at centromeres and the central spindle during mitosis. Loss of Borealin leads to defective cell proliferation and early embryonic lethality. The in vivo functions of Borealin in mammalian postnatal development, tissue homeostasis, and tumorigenesis remain elusive. We specifically analyzed the role of Borealin in regulating postnatal liver development, damage-induced liver regeneration, and liver carcinogenesis using mice carrying conditional Borealin alleles. Perinatal loss of Borealin caused increased genome ploidy and enlarged cell size in hepatocytes, likely due to the impaired function of the chromosomal passenger complex in mitosis. Borealin deletion also showed attenuated expansion of Sox9

Indexed as

Liver RegenerationAnimalsCell Cycle ProteinsCell SizeChromosomal Proteins, Non-HistoneHepatocyte Nuclear Factor 4HepatocytesLiverLiver NeoplasmsMiceMice, Mutant StrainsPloidiesProto-Oncogene Proteins c-metSOX9 Transcription FactorStem CellsCDCA8 protein, mouseCell Cycle ProteinsChromosomal Proteins, Non-HistoneHepatocyte Nuclear Factor 4Hnf4a protein, mouseProto-Oncogene Proteins c-metSox9 protein, mouseSOX9 Transcription FactorBorealincell cyclehepatocellular carcinomaliver cancerliver developmentliver injuryliver progenitor-like cellstem cells

Identifiers

PMID27542413
PMCPMC5076522
OpenAlexW2517006279

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.