Evidence map›Paper›PMID 35878408›Full record

ArticleThe Journal of cell biology2022

The inositol 5-phosphatase INPP5B regulates B cell receptor clustering and signaling.

Alaa Droubi, Connor Wallis, Karen E Anderson, Saifur Rahman, Aloka de Sa, Taufiq Rahman, Len R Stephens, Philip T Hawkins, Martin Lowe

Open access · hybridAbstract read
In one paragraph

Article in The Journal of cell biology, 2022. 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
1.1field-weighted citation impact, top 24% 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. TheCells · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Regulation of INPP5E in Ciliogenesis, Development, and Disease.International journal of biological sciences · 2025
    Review
  7. Fine-Tuned Expression of Evolutionarily Conserved Signaling Molecules in theInternational journal of molecular sciences · 2024
    Article
  8. Review
  9. Article
  10. The Arf family GTPases: Regulation of vesicle biogenesis and beyond.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Review
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Alaa DroubiFaculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Connor WallisFaculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Karen E AndersonInositide Laboratory, Babraham Institute, Cambridge, UK.ORCID 0000-0002-7394-6660
Saifur RahmanDepartment of Pharmacology, University of Cambridge, Cambridge, UK.ORCID 0000-0002-6811-5133
Aloka de SaFaculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Taufiq RahmanDepartment of Pharmacology, University of Cambridge, Cambridge, UK.ORCID 0000-0003-3830-5160
Len R StephensInositide Laboratory, Babraham Institute, Cambridge, UK.
Philip T HawkinsInositide Laboratory, Babraham Institute, Cambridge, UK.
Martin LoweFaculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.ORCID 0000-0002-9331-8143
University of Manchester · GBBabraham Institute · GBUniversity of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council BB/PO13384/1Biotechnology and Biological Sciences Research Council BB/S014799/1Biotechnology and Biological Sciences Research Council BBS/E/B/000C0415Medical Research Council MR/L011840/1Wellcome Trust 222757/Z/21/Z
6 · The paper itself

Abstract

Upon antigen binding, the B cell receptor (BCR) undergoes clustering to form a signalosome that propagates downstream signaling required for normal B cell development and physiology. BCR clustering is dependent on remodeling of the cortical actin network, but the mechanisms that regulate actin remodeling in this context remain poorly defined. In this study, we identify the inositol 5-phosphatase INPP5B as a key regulator of actin remodeling, BCR clustering, and downstream signaling in antigen-stimulated B cells. INPP5B acts via dephosphorylation of the inositol lipid PI(4,5)P2 that in turn is necessary for actin disassembly, BCR mobilization, and cell spreading on immobilized surface antigen. These effects can be explained by increased actin severing by cofilin and loss of actin linking to the plasma membrane by ezrin, both of which are sensitive to INPP5B-dependent PI(4,5)P2 hydrolysis. INPP5B is therefore a new player in BCR signaling and may represent an attractive target for treatment of B cell malignancies caused by aberrant BCR signaling.

Indexed as

ActinsInositol Polyphosphate 5-PhosphatasesReceptors, Antigen, B-CellB-LymphocytesHumansPhosphatidylinositol 4,5-DiphosphatePhosphoinositide 5-PhosphatasesPhosphoric Monoester HydrolasesActinsInositol Polyphosphate 5-PhosphatasesPhosphatidylinositol 4,5-DiphosphatePhosphoinositide 5-PhosphatasesPhosphoric Monoester HydrolasesReceptors, Antigen, B-Cell

Identifiers

PMID35878408
PMCPMC9351708
OpenAlexW4287837689

What Socratic holds

Textmetadata
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 Socratic graph.