Evidence map›Paper›PMID 30009791›Full record

ArticleExperimental cell research2018

TCEA1 regulates the proliferative potential of mouse myeloid cells.

Taomei Yang, Haoran Cui, Mingxin Wen, Johannes Zuber, Scott C Kogan, Guangwei Wei

Open access · greenAbstract read
In one paragraph

Article in Experimental cell research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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  6. GLI3: a mediator of genetic diseases, development and cancer.Cell communication and signaling : CCS · 2020
    Review
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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 3 institutions in 3 countries.

Taomei YangDepartment of Cell Biology and Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University School of Medicine, Jinan, Shandong, China. Electronic address: zmyangtao@163.com.
Haoran CuiDepartment of Cell Biology and Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University School of Medicine, Jinan, Shandong, China. Electronic address: cuihr1027@163.com.
Mingxin WenDepartment of Anatomy and Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University School of Medicine, Jinan, Shandong, China. Electronic address: wen20042302079@163.com.
Johannes ZuberResearch Institute of Molecular Pathology (IMP), Vienna BioCenter (VBC), 1030 Vienna, Austria; Medical University of Vienna, Vienna BioCenter (VBC), 1030 Vienna, Austria. Electronic address: johannes.zuber@imp.ac.at.
Scott C KoganDepartment of Laboratory Medicine, University of California San Francisco, CA, USA. Electronic address: scott.kogan@ucsf.edu.
Guangwei WeiDepartment of Cell Biology and Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University School of Medicine, Jinan, Shandong, China. Electronic address: gwwei@email.sdu.edu.cn.
Shandong University · CNUniversity of California, San Francisco · USVienna Biocenter · AT

Funding

Molecular Mechanisms of Leukemogenesis by PMLRAR alphaR01CA095274 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KOGAN, SCOTT C. · 2002 to 2013
$2.7M
NCI NIH HHS R01 CA095274
6 · The paper itself

Abstract

Leukemia is a malignance with complex pathogenesis and poor prognosis. Discovery of noval regulators amenable to leukemia could be of value to gain insight into the pathogenesis, diagnosis and prognosis of leukemia. Here, we conducted a large-scale shRNA library screening for functional regulators in the development of myeloid cells in primary cells. We identified eighteen candidate regulators in the primary screening. Those genes cover a wide range of cellular functions, including gene expression regulation, intracellular signaling transduction, nucleotide excision repair, cell cycle control and transcription regulation. In both primary screening and validation, shRNAs targeting Tcea1, encoding the transcription elongation factor A (SII) 1, exhibited the greatest influence on the proliferative potential of cells. Knocking down the expression of Tcea1 in the 32Dcl3 myeloid cell line led to enhanced proliferation of myeloid cells and blockage of myeloid differentiation induced by G-CSF. In addition, silence of Tcea1 inhibited apoptosis of myeloid cells. Thus, Tcea1 was identified as a gene which can influence the proliferative potential, survival and differentiation of myeloid cells. These findings have implications for how transcriptional elongation influences myeloid cell development and leukemic transformation.

Indexed as

AnimalsCell DifferentiationCell LineDNA-Binding ProteinsGene Expression RegulationGranulocyte Colony-Stimulating FactorHematopoiesisMiceMyeloid CellsSignal TransductionTranscriptional Elongation FactorsTranscription FactorsDNA-Binding ProteinsGranulocyte Colony-Stimulating FactorTranscriptional Elongation FactorsTranscription Factorstranscription factor S-IIDifferentiationMyelopoiesisProliferative potentialTCEA1

Identifiers

PMID30009791
PMCPMC6816334
OpenAlexW2883579439

What OpenQuestion holds

Textmetadata
LicenceTDM
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.