Evidence map›Paper›PMID 34847985›Full record

ArticleBMB reports2021

Depletion of Janus kinase-2 promotes neuronal differentiation of mouse embryonic stem cells.

Mihee Oh, Sun Young Kim, Jeong-Su Byun, Seonha Lee, Won-Kon Kim, Kyoung-Jin Oh, Eun-Woo Lee, Kwang-Hee Bae, Sang Chul Lee, Baek-Soo Han

Abstract readNews
PubMed Full text at PMC
In one paragraph

Article in BMB reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Mihee OhBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.
Sun Young KimBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.
Jeong-Su ByunBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.
Seonha LeeBiodefense Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST) of Korea, Daejeon 34113, Korea.
Won-Kon KimMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST) of Korea, Daejeon 34113, Korea.
Kyoung-Jin OhMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST) of Korea, Daejeon 34113, Korea.
Eun-Woo LeeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST) of Korea, Daejeon 34113, Korea.
Kwang-Hee BaeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST) of Korea, Daejeon 34113, Korea.
Sang Chul LeeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST) of Korea, Daejeon 34113, Korea.
Baek-Soo HanBiodefense Research Center, and Metabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST) of Korea, Daejeon 34113, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Janus kinase 2 (JAK2), a non-receptor tyrosine kinase, is a critical component of cytokine and growth factor signaling pathways regulating hematopoietic cell proliferation. JAK2 mutations are associated with multiple myeloproliferative neoplasms. Although physiological and pathological functions of JAK2 in hematopoietic tissues are well-known, such functions of JAK2 in the nervous system are not well studied yet. The present study demonstrated that JAK2 could negatively regulate neuronal differentiation of mouse embryonic stem cells (ESCs). Depletion of JAK2 stimulated neuronal differentiation of mouse ESCs and activated glycogen synthase kinase 3ꞵ, Fyn, and cyclin-dependent kinase 5. Knockdown of JAK2 resulted in accumulation of GTPbound Rac1, a Rho GTPase implicated in the regulation of cytoskeletal dynamics. These findings suggest that JAK2 might negatively regulate neuronal differentiation by suppressing the GSK-3β/Fyn/CDK5 signaling pathway responsible for morphological maturation. [BMB Reports 2021; 54(12): 626-631].

Indexed as

Cell DifferentiationJanus Kinase 2Mouse Embryonic Stem CellsAnimalsCyclin-Dependent Kinase 5Glycogen Synthase Kinase 3 betaMiceNeuronsProto-Oncogene Proteins c-fynSignal TransductionCdk5 protein, mouseCyclin-Dependent Kinase 5Fyn protein, mouseGlycogen Synthase Kinase 3 betaJak2 protein, mouseJanus Kinase 2Proto-Oncogene Proteins c-fyn

Identifiers

PMID34847985
PMCPMC8728538

What OpenQuestion holds

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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.