ArticleThe EMBO journal2015
The BAFFling function of Syk in B-cell homeostasis.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- CD19 Deficiency Leads to Dysregulation of Phosphoinositide 3-Kinase-Protein Kinase B (Journal of clinical practice and research · 2025Article
- Sin1/mTORC2 regulate B cell growth and metabolism by activating mTORC1 and Myc.Cellular & molecular immunology · 2019Article
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The TNF receptor family member BAFFR is essential for providing mature B cells with pro-survival signals and has recently been claimed to transduce these, though not exclusively, via a Syk-dependent signaling hub that feeds into ERK/AKT activation. In this issue of The EMBO Journal, Hobeika et al (2015) describe a synergistic prosurvival scenario involving BAFFR and CD19, which remains functional under Syk null conditions and is able to maintain mature B-cell survival. The authors hence propose a BAFFR-/CD19-driven mechanism to act in parallel with homeostatic NF-κB/AKT activation in non-stimulated B cells.
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