Evidence map›Paper›PMID 19218240›Full record

ArticleThe Journal of biological chemistry2009

BLNK binds active H-Ras to promote B cell receptor-mediated capping and ERK activation.

Yasuhiro Imamura, Akihisa Oda, Takashi Katahira, Kenji Bundo, Kelly A Pike, Michael J H Ratcliffe, Daisuke Kitamura

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. BLNK negatively regulates innate antifungal immunity through inhibiting c-Cbl-mediated macrophage migration.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Review
  3. Aberrant B-Cell Activation in Systemic Lupus Erythematosus.Kidney diseases (Basel, Switzerland) · 2022
    Review
  4. Article
  5. [Structure and function of B-cell linker and its role in the development of B cell-related diseases].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
    Article
  6. Mechanisms of central tolerance for B cells.Nature reviews. Immunology · 2017
    Review
  7. High Frequency and Poor Outcome of Philadelphia Chromosome-Like Acute Lymphoblastic Leukemia in Adults.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
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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

7 authors at 3 institutions in 2 countries.

Yasuhiro ImamuraDivision of Molecular Biology, Research Institute for Biological Sciences, Tokyo University of Science, 2669 Yamazaki, Noda, Chiba 278-0022, Japan.
Akihisa Oda
Takashi Katahira
Kenji Bundo
Kelly A Pike
Michael J H Ratcliffe
Daisuke Kitamura
Tokyo University of Science · JPSunnybrook Health Science Centre · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cross-linked B cell receptor (BCR) aggregates on the cell surface, then assembles into the "cap" where Ras is co-localized, and transduces various intracellular signals including Ras-ERK activation. BCR signals induce proliferation, differentiation, or apoptosis of B cells depending on their maturational stage. The adaptor protein BLNK binds various signaling proteins and Igalpha, a signaling subunit of the BCR complex, and plays an important role in the BCR signal transduction. BLNK was shown to be required for activation of ERK, but not of Ras, after BCR cross-linking, raising a question how BLNK facilitates ERK activation. Here we demonstrate that BLNK binds the active form of H-Ras, and their binding is facilitated by BCR cross-linking. We have identified a 10-amino acid Ras-binding domain within BLNK that is necessary for restoration of BCR-mediated ERK activation in BLNK-deficient B cells and for anti-apoptotic signaling. The Ras-binding domain fused with a CD8alpha-Igalpha chimeric receptor could induce prolonged ERK phosphorylation, transcriptional activation of Elk1, as well as the capping of the receptor in BLNK-deficient B cells. These results indicate that BLNK recruits active H-Ras to the BCR complex, which is essential for sustained surface expression of BCR in the form of the cap and for the signal leading to functional ERK activation.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisCD8 AntigensCell DifferentiationCell ProliferationChickensChlorocebus aethiopsCOS CellsExtracellular Signal-Regulated MAP KinasesHumansMicePhosphorylationras ProteinsReceptors, Antigen, B-CellAdaptor Proteins, Signal TransducingB cell linker proteinCD8 AntigensExtracellular Signal-Regulated MAP Kinasesras ProteinsReceptors, Antigen, B-Cell

Identifiers

PMID19218240
PMCPMC2665102
OpenAlexW1976914214

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.