Evidence map›Paper›PMID 32117051›Full record

ArticleFrontiers in endocrinology2020

Both JNK1 and JNK2 Are Indispensable for Sensitized Extracellular Matrix Mineralization in IKKβ-Deficient Osteoblasts.

Qianyun Hao, Zhuangzhuang Liu, Liaoxun Lu, Lichen Zhang, Li Zuo

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 42% 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, 11 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

5 authors at 2 institutions in 1 country.

Qianyun HaoDepartment of Nephrology, Peking University People's Hospital, Beijing, China.
Zhuangzhuang LiuLaboratory of Mouse Genetics, Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang, China.
Liaoxun LuLaboratory of Mouse Genetics, Institute of Psychiatry and Neuroscience, Xinxiang Medical University, Xinxiang, China.
Lichen ZhangLaboratory of Genetic Regulators in the Immune System, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
Li ZuoDepartment of Nephrology, Peking University People's Hospital, Beijing, China.
Xinxiang Medical University · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular matrix mineralization is critical for osteogenesis, and its dysregulation could result in osteoporosis and vascular calcification. IKK/NF-κB activation inhibits differentiation of osteoblasts, and reduces extracellular matrix mineralization, however the underlying mechanisms are poorly understood. In this study, we used CRISPR/Cas9 system to permanently inactivate IKKβ in preosteoblast cells and confirmed that such cells displayed dramatic increase in extracellular matrix mineralization associated with JNK phosphorylation. Such observation was also found in our study using IKKβ-deficient primary murine osteoblasts. Interestingly, we found that in

Indexed as

AnimalsAnimals, NewbornCalcification, PhysiologicCell DifferentiationCells, CulturedExtracellular MatrixGene Knockout TechniquesI-kappa B KinaseMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9OsteoblastsOsteogenesisPhosphorylationSignal TransductionI-kappa B KinaseMitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9CRISPR/Cas9IKKβJNK1JNK2NF-κBosteoblasts

Identifiers

PMID32117051
PMCPMC7028708
OpenAlexW3006392823

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.