Evidence map›Paper›PMID 30042821›Full record

ArticleOncotarget2018

The regulatory interplay between Oct-1 isoforms contributes to hematopoiesis and the isoforms imbalance correlates with a malignant transformation of B cells.

Elizaveta V Pankratova, Alexander G Stepchenko, Irina D Krylova, Tatiana N Portseva, Sofia G Georgieva

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. MYCN Gene Is Activated by High-Level Expression of Stress-Inducible Isoform of Oct-1 Transcription Factor in Human Neuroblastoma Cells.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2026
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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.

Elizaveta V Pankratova *Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Alexander G Stepchenko *Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Irina D KrylovaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Tatiana N PortsevaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Sofia G GeorgievaEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Engelhardt Institute of Molecular Biology · RUPirogov Russian National Research Medical University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oct-1(POU2F1) is a DNA-binding transcription regulator and its level being highly increased in many human cancers. Oct-1 is present in the human cells as a family of functionally different isoforms which are transcribed from alternative promoters. Here, we have demonstrated that expression patterns of Oct-1 isoforms change during differentiation of hematopoetic progenitor cells (CD34+) (HPCs) to the B (CD19+) and T (CD3+) cells. While Oct-1L is expressed at a high level in the CD34+ HPCs, its expression level drops dramatically during the T-cell differentiation, although remains nearly the same in B-cells. We have described the novel human Oct-1R isoform which is conserved in mammals and is B cell-specific. Oct-1R was found in B cells, but not in HPCs. Oct-1R is transcribed from the same promoter as Oct-1L, another lymphocyte-specific isoform. Overexpression of Oct-1R and Oct-1L in the Namalwa cells leads to the repression of many genes involved in B-lymphocyte differentiation and signal transduction. Thus these isoforms may regulate the particular stages of development of normal B cells and maintain their proper differentiation status. However the extremely high level of Oct-1L isoform observed in the B-lymphoblast tumor cell lines indicated that the excess of Oct-L seem likely to considerably decrease the differentiation ability of these cells. Oct-1 may serve as a therapeutic target for many tumors, but it should be noted that in a tumor the content of a certain isoform Oct-1, rather than the total Oct-1 protein, can be increased.

Indexed as

hematopoietic cells differentiationisoformsmolecular therapeutic targetPOU2F1

Identifiers

PMID30042821
PMCPMC6057458
OpenAlexW2851272792

What OpenQuestion holds

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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.