Evidence map›Paper›PMID 30026232›Full record

ArticleThe Journal of biological chemistry2018

Krüppel-like factor 10 (KLF10) is transactivated by the transcription factor C/EBPβ and involved in early 3T3-L1 preadipocyte differentiation.

Yuan Liu, Wan-Qiu Peng, Ying-Ying Guo, Yang Liu, Qi-Qun Tang, Liang Guo

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 38 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

6 authors at 2 institutions in 1 country.

Yuan LiuFrom the Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education, Institute of Stem Cell Research and Regenerative Medicine of Institutes of Biomedical Sciences, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology and Metabolism of Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Wan-Qiu PengFrom the Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education, Institute of Stem Cell Research and Regenerative Medicine of Institutes of Biomedical Sciences, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology and Metabolism of Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Ying-Ying GuoFrom the Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education, Institute of Stem Cell Research and Regenerative Medicine of Institutes of Biomedical Sciences, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology and Metabolism of Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Yang LiuFrom the Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education, Institute of Stem Cell Research and Regenerative Medicine of Institutes of Biomedical Sciences, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology and Metabolism of Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Qi-Qun TangFrom the Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education, Institute of Stem Cell Research and Regenerative Medicine of Institutes of Biomedical Sciences, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology and Metabolism of Zhongshan Hospital, Fudan University, Shanghai 200032, China qqtang@shmu.edu.cn.
Liang GuoFrom the Key Laboratory of Metabolism and Molecular Medicine of the Ministry of Education, Institute of Stem Cell Research and Regenerative Medicine of Institutes of Biomedical Sciences, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology and Metabolism of Zhongshan Hospital, Fudan University, Shanghai 200032, China liangguo@fudan.edu.cn.
Fudan University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue stores energy and plays an important role in energy homeostasis. CCAAT/enhancer-binding protein β (C/EBPβ) is an important early transcription factor for 3T3-L1 preadipocyte differentiation, facilitating mitotic clonal expansion (MCE) and transactivating C/EBPα and peroxisome proliferator-activated receptor-γ (PPARγ) to promote adipogenesis. C/EBPβ is induced early, but the expression of antimitotic C/EBPα and PPARγ is not induced until ∼48 h. The delayed expression of C/EBPα and PPARγ is thought to ensure MCE progression, but the molecular mechanism for this delay remains elusive. Here, we show that the zinc-finger transcription factor Krüppel-like factor 10 (KLF10) is induced after adipogenic induction and that its expression positively correlates with that of C/EBPβ but inversely correlates with expression of C/EBPα and PPARγ. C/EBPβ bound to the KLF10 promoter and transactivated its expression during MCE. KLF10 overexpression in 3T3-L1 preadipocyte repressed adipogenesis and decreased C/EBPα and PPARγ expression, whereas siRNA-mediated down-regulation of KLF10 enhanced adipogenesis and increased C/EBPα and PPARγ expression. Luciferase assays revealed an inhibitory effect of KLF10 on C/EBPα promoter activity. Using promoter deletion and mutation analysis, we identified a KLF10-binding site within the proximal promoter region of C/EBPα. Furthermore, KLF10 interacted with and recruited histone deacetylase 1 (HDAC1) to the C/EBPα promoter, decreasing acetylated histone H4 on the C/EBPα promoter and inactivating C/EBPα transcription. Because C/EBPα can transactivate PPARγ, our results suggest a mechanism by which expression of C/EBPα and PPARγ is delayed via KLF10 expression and shed light on the negative feedback loop for C/EBPβ-regulated adipogenesis in 3T3-L1 preadipocyte.

Indexed as

AdipogenesisTranscriptional Activation3T3-L1 CellsAnimalsCCAAT-Enhancer-Binding Protein-alphaCell DifferentiationEarly Growth Response Transcription FactorsFeedback, PhysiologicalKruppel-Like Transcription FactorsMicePPAR gammaTime FactorsCCAAT-Enhancer-Binding Protein-alphaEarly Growth Response Transcription FactorsKLF10 protein, mouseKruppel-Like Transcription FactorsPPAR gamma3T3-L1 preadipocytesadipocyte differentiationadipogenesisadipose tissueCCAAT-enhancer-binding protein (C/EBP)C/EBPβcell proliferationhistone deacetylase 1 (HDAC1)Kruppel-like factor (KLF)Krüppel-like factor (KLF)mitotic clonal expansiontranscription regulation

Identifiers

PMID30026232
PMCPMC6130933
OpenAlexW2883446651

What OpenQuestion holds

Textmetadata
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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.