Evidence map›Paper›PMID 21757756›Full record

ArticleThe Journal of biological chemistry2011

Involvement of PRIP, phospholipase C-related, but catalytically inactive protein, in bone formation.

Koshiro Tsutsumi, Miho Matsuda, Miho Kotani, Akiko Mizokami, Ayako Murakami, Ichiro Takahashi, Yoshihiro Terada, Takashi Kanematsu, Kiyoko Fukami, Tadaomi Takenawa and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 35% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
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  5. 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

12 authors at 4 institutions in 1 country.

Koshiro TsutsumiLaboratory of Molecular and Cellular Biochemistry, Kyushu University, Fukuoka 812-8582, Japan; Division of Fixed Prosthodontics, Kyushu University, Fukuoka 812-8582, Japan.
Miho MatsudaLaboratory of Molecular and Cellular Biochemistry, Kyushu University, Fukuoka 812-8582, Japan.
Miho KotaniLaboratory of Molecular and Cellular Biochemistry, Kyushu University, Fukuoka 812-8582, Japan; Division of Orthodontics, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan.
Akiko MizokamiLaboratory of Molecular and Cellular Biochemistry, Kyushu University, Fukuoka 812-8582, Japan.
Ayako MurakamiDivision of Orthodontics, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan.
Ichiro TakahashiDivision of Orthodontics, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan.
Yoshihiro TeradaDivision of Fixed Prosthodontics, Kyushu University, Fukuoka 812-8582, Japan.
Takashi KanematsuLaboratory of Molecular and Cellular Biochemistry, Kyushu University, Fukuoka 812-8582, Japan.
Kiyoko FukamiLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Science, Tokyo 192-0392, Japan.
Tadaomi TakenawaDivision of Lipid Biochemistry, Graduate School of Medicine, Kobe University, Kobe 650-0017, Japan.
Eijiro JimiDepartment of Molecular Signaling and Biochemistry, Kyushu Dental College, Kitakyushu 803-8580, Japan.
Masato HirataLaboratory of Molecular and Cellular Biochemistry, Kyushu University, Fukuoka 812-8582, Japan. Electronic address: hirata1@dent.kyushu-u.ac.jp.
Kyushu University · JPKyushu Dental University · JPKobe University · JPTokyo University of Pharmacy and Life Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PRIP (phospholipase C-related, but catalytically inactive protein) is a novel protein isolated in this laboratory. PRIP-deficient mice showed increased serum gonadotropins, but decreased gonadal steroid hormones. This imbalance was similar to that for the cause of bone disease, such as osteoporosis. In the present study, therefore, we analyzed mutant mice with special reference to the bone property. We first performed three-dimensional analysis of the femur of female mice. The bone mineral density and trabecular bone volume were higher in mutant mice. We further performed histomorphometrical assay of bone formation parameters: bone formation rate, mineral apposition rate, osteoid thickness, and osteoblast number were up-regulated in the mutant, indicating that increased bone mass is caused by the enhancement of bone formation ability. We then cultured primary cells isolated from calvaria prepared from both genotypes. In mutant mice, osteoblast differentiation, as assessed by alkaline phosphatase activity and the expression of osteoblast differentiation marker genes, was enhanced. Moreover, we analyzed the phosphorylation of Smad1/5/8 in response to bone morphogenetic protein, with longer phosphorylation in the mutant. These results indicate that PRIP is implicated in the negative regulation of bone formation.

Indexed as

AnimalsBone and BonesCatalysisCell DifferentiationFemaleFemurMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalNuclear Receptor CoactivatorsOsteoblastsOsteoclastsOsteogenesisOvariectomyPhosphorylationNcoa6 protein, mouseNuclear Receptor CoactivatorsSmad ProteinsType C Phospholipases

Identifiers

PMID21757756
PMCPMC3162462
OpenAlexW1994295418

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.