Evidence map›Paper›PMID 25653040›Full record

ArticleScientific reports2015

Deficiency of Capicua disrupts bile acid homeostasis.

Eunjeong Kim, Sungjun Park, Nahyun Choi, Jieon Lee, Jeehyun Yoe, Soeun Kim, Hoe-Yune Jung, Kyong-Tai Kim, Hyojin Kang, John D Fryer and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

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  12. Deletion Timing ofImmune network · 2020
    Article
  13. Article
  14. Article
  15. Regulation and function of capicua in mammals.Experimental & molecular medicine · 2020
    Review
  16. Article
  17. Review
  18. Article
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  20. Review
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

13 authors at 4 institutions in 2 countries.

Eunjeong KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Sungjun ParkDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Nahyun ChoiDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Jieon LeeDepartment of Chemical Engineering, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Jeehyun YoeDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Soeun KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Hoe-Yune JungDivision of Integrative Bioscience and Biotechnology, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Kyong-Tai Kim1] Department of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea [2] Division of Integrative Bioscience and Biotechnology, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Hyojin KangNational Institute of Supercomputing and Networking, Korea Institute of Science and Technology Information, Daejeon 305-806, Republic of Korea.
John D FryerDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Huda Y ZoghbiHoward Hughes Medical Institute, Departments of Molecular and Human Genetics, and Neuroscience, Baylor College of Medicine, and Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX 77030, USA.
Daehee Hwang1] Division of Integrative Bioscience and Biotechnology, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea [2] Center for Plant Aging Research, Institute for Basic Science, Daegu Gyeongbuk Institute of Science and Technology, Daegu, 711-873, Republic of Korea.
Yoontae Lee1] Department of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea [2] Division of Integrative Bioscience and Biotechnology, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
Pohang University of Science and Technology · KRDaegu Gyeongbuk Institute of Science and Technology · KRKorea Institute of Science & Technology Information · KRMayo Clinic in Florida · US

Funding

MOLECULAR STUDIES OF SPINOCEREBELLAR ATAXIA TYPE 1R01NS027699 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI HUDA Y ZOGHBI · 1989 to 2026
$8.8M
Steps towards a paternal gene activation therapy for Angelman syndromeU54HD083092 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI NELSON, DAVID LOREN, NEUL, JEFFREY L · 2014 to 2019
$7.8M
MOLECULAR STUDIES OF SPINOCEREBELLAR ATAXIS TYPE IR37NS027699 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ZOGHBI, HUDA Y · 2015 to 2021
$2.8M
Howard Hughes Medical InstituteNICHD NIH HHS U54 HD083092NINDS NIH HHS NS27699NINDS NIH HHS R01 NS027699NINDS NIH HHS R37 NS027699
6 · The paper itself

Abstract

Capicua (CIC) has been implicated in pathogenesis of spinocerebellar ataxia type 1 and cancer in mammals; however, the in vivo physiological functions of CIC remain largely unknown. Here we show that Cic hypomorphic (Cic-L(-/-)) mice have impaired bile acid (BA) homeostasis associated with induction of proinflammatory cytokines. We discovered that several drug metabolism and BA transporter genes were down-regulated in Cic-L(-/-) liver, and that BA was increased in the liver and serum whereas bile was decreased within the gallbladder of Cic-L(-/-) mice. We also found that levels of proinflammatory cytokine genes were up-regulated in Cic-L(-/-) liver. Consistent with this finding, levels of hepatic transcriptional regulators, such as hepatic nuclear factor 1 alpha (HNF1α), CCAAT/enhancer-binding protein beta (C/EBPβ), forkhead box protein A2 (FOXA2), and retinoid X receptor alpha (RXRα), were markedly decreased in Cic-L(-/-) mice. Moreover, induction of tumor necrosis factor alpha (Tnfα) expression and decrease in the levels of FOXA2, C/EBPβ, and RXRα were found in Cic-L(-/-) liver before BA was accumulated, suggesting that inflammation might be the cause for the cholestasis in Cic-L(-/-) mice. Our findings indicate that CIC is a critical regulator of BA homeostasis, and that its dysfunction might be associated with chronic liver disease and metabolic disorders.

Indexed as

HomeostasisAnimalsBile Acids and SaltsBlood Chemical AnalysisCytokinesFemaleGene Expression ProfilingGene Expression RegulationGenotypeInflammation MediatorsLiverMiceMice, KnockoutPhenotypeRepressor ProteinsTranscription FactorsBile Acids and SaltsCic protein, mouseCytokinesInflammation MediatorsRepressor ProteinsTranscription Factors

Identifiers

PMID25653040
PMCPMC4317698
OpenAlexW2017676825

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.