Evidence map›Paper›PMID 26706316›Full record

ArticleThe Journal of biological chemistry2016

Phospholipase C-related Catalytically Inactive Protein Is a New Modulator of Thermogenesis Promoted by β-Adrenergic Receptors in Brown Adipocytes.

Kana Oue, Jun Zhang, Kae Harada-Hada, Satoshi Asano, Yosuke Yamawaki, Masaki Hayashiuchi, Hisako Furusho, Takashi Takata, Masahiro Irifune, Masato Hirata and 1 more

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 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Oral administration ofJournal of oral microbiology · 2024
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  5. Uncoupling Protein 1 Does Not Produce Heat without Activation.International journal of molecular sciences · 2022
    Review
  6. Progesterone receptor isoform B regulates theProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
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

11 authors at 3 institutions in 1 country.

Kana OueFrom the Departments of Cellular and Molecular Pharmacology, Dental Anesthesiology, and.
Jun ZhangFrom the Departments of Cellular and Molecular Pharmacology.
Kae Harada-HadaFrom the Departments of Cellular and Molecular Pharmacology.
Satoshi AsanoFrom the Departments of Cellular and Molecular Pharmacology.
Yosuke YamawakiFrom the Departments of Cellular and Molecular Pharmacology.
Masaki HayashiuchiFrom the Departments of Cellular and Molecular Pharmacology.
Hisako FurushoOral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8553 and.
Takashi TakataOral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8553 and.
Masahiro IrifuneDental Anesthesiology, and.
Masato Hiratathe Laboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan.
Takashi KanematsuFrom the Departments of Cellular and Molecular Pharmacology, tkanema2@hiroshima-u.ac.jp.
Hiroshima University · JPHiroshima University Hospital · JPKyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phospholipase C-related catalytically inactive protein (PRIP) was first identified as an inositol 1,4,5-trisphosphate-binding protein, and was later found to be involved in a variety of cellular events, particularly those related to protein phosphatases. We previously reported that Prip knock-out (KO) mice exhibit a lean phenotype with a small amount of white adipose tissue. In the present study, we examined whether PRIP is involved in energy metabolism, which could explain the lean phenotype, using high-fat diet (HFD)-fed mice. Prip-KO mice showed resistance to HFD-induced obesity, resulting in protection from glucose metabolism dysfunction and insulin resistance. Energy expenditure and body temperature at night were significantly higher in Prip-KO mice than in wild-type mice. Gene and protein expression of uncoupling protein 1 (UCP1), a thermogenic protein, was up-regulated in Prip-KO brown adipocytes in thermoneutral or cold environments. These phenotypes were caused by the promotion of lipolysis in Prip-KO brown adipocytes, which is triggered by up-regulation of phosphorylation of the lipolysis-related proteins hormone-sensitive lipase and perilipin, followed by activation of UCP1 and/or up-regulation of thermogenesis-related genes (e.g. peroxisome proliferator-activated receptor-γ coactivator-1α). The results indicate that PRIP negatively regulates UCP1-mediated thermogenesis in brown adipocytes.

Indexed as

LipolysisThermogenesisAdipocytes, BrownAnimalsDietary FatsIon ChannelsMiceMice, KnockoutMitochondrial ProteinsNuclear Receptor CoactivatorsObesityUncoupling Protein 1Dietary FatsIon ChannelsMitochondrial ProteinsNcoa6 protein, mouseNuclear Receptor CoactivatorsUcp1 protein, mouseUncoupling Protein 1adipocyteadipose tissue metabolismlipolysisobesitythermogenesisuncoupling protein

Identifiers

PMID26706316
PMCPMC4759193
OpenAlexW2288051797

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.