Evidence map›Paper›PMID 23955076›Full record

ArticleOncogene2014

Inducible expression of hyperactive Syk in B cells activates Blimp-1-dependent terminal differentiation.

E Hug, E Hobeika, M Reth, H Jumaa

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  18. Mechanistic rationale for targeting the unfolded protein response in pre-B acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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

4 authors at 1 institution in 1 country.

E Hug1] BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-Universität, Freiburg, Germany [2] Department of Molecular Immunology, Faculty of Biology, Albert-Ludwigs-Universität, Freiburg, Germany [3] Max-Planck-Institute of Immunobiology and Epigenetics, Freiburg, Germany.
E Hobeika1] Department of Molecular Immunology, Faculty of Biology, Albert-Ludwigs-Universität, Freiburg, Germany [2] Max-Planck-Institute of Immunobiology and Epigenetics, Freiburg, Germany.
M Reth1] BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-Universität, Freiburg, Germany [2] Department of Molecular Immunology, Faculty of Biology, Albert-Ludwigs-Universität, Freiburg, Germany [3] Max-Planck-Institute of Immunobiology and Epigenetics, Freiburg, Germany.
H Jumaa1] BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs-Universität, Freiburg, Germany [2] Department of Molecular Immunology, Faculty of Biology, Albert-Ludwigs-Universität, Freiburg, Germany [3] Max-Planck-Institute of Immunobiology and Epigenetics, Freiburg, Germany.
University of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The non-receptor protein tyrosine kinase Syk (spleen tyrosine kinase) is an important mediator of signal transduction in B cells. By acting downstream of the B-cell antigen receptor, Syk promotes signaling pathways involved in proliferation, differentiation and survival of B cells. To study the oncogenic potential of Syk, we generated a mouse model for the inducible expression of the leukemia-derived TEL-Syk fusion protein exhibiting constitutive kinase activity. To achieve B-cell-specific expression of TEL-Syk in adult mice, we used a tamoxifen-inducible Cre mouse line. This study shows that inducible expression of TEL-Syk in B cells leads to transient proliferation and subsequent plasma cell differentiation. However, it does not lead to B-cell transformation. Instead, Syk activation induces the tumor suppressor B-lymphocyte-induced maturation protein-1 (Blimp-1), which interferes with the expression of the antiapoptotic protein Bcl-2. Combined induction of TEL-Syk with transgenic expression of Bcl-2 results in a severe phenotype and plasma cell expansion. Our results suggest that deregulated Syk activity by itself is not sufficient for the transformation of B cells, as downstream effectors, such as Blimp-1, limit the survival and expansion of the activated B cell.

Indexed as

Cell DifferentiationAnimalsApoptosisBiomarkersB-LymphocytesCell SurvivalGene ExpressionIntegrasesIntracellular Signaling Peptides and ProteinsMiceMice, TransgenicMutationPhenotypePlasma CellsPositive Regulatory Domain I-Binding Factor 1Protein-Tyrosine KinasesBiomarkersCre recombinaseIntegrasesIntracellular Signaling Peptides and ProteinsPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseProtein-Tyrosine KinasesRecombinant Fusion ProteinsSyk KinaseSyk protein, mouseTamoxifenTranscription Factors

Identifiers

PMID23955076
OpenAlexW2006750556

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.