Evidence map›Paper›PMID 26113483›Full record

ArticleScientific reports2015

Structural and Physical Basis for Anti-IgE Therapy.

Jon D Wright, Hsing-Mao Chu, Chun-Hsiang Huang, Che Ma, Tse Wen Chang, Carmay Lim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
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  7. Article
  8. Article
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  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Biological therapies for atopic dermatitis: An update.Experimental and therapeutic medicine · 2019
    Review
  17. New treatment directions in food allergy.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2018
    Review
  18. Article
  19. Oral immunotherapy for food allergy.Seminars in immunology · 2017
    Review
  20. Critical and direct involvement of the CD23 stalk region in IgE binding.The Journal of allergy and clinical immunology · 2017
    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

6 authors at 3 institutions in 1 country.

Jon D Wright1] Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan [2] The Genomics Research Center, Academia Sinica 115, Taiwan.
Hsing-Mao ChuThe Genomics Research Center, Academia Sinica 115, Taiwan.
Chun-Hsiang HuangThe Genomics Research Center, Academia Sinica 115, Taiwan.
Che MaThe Genomics Research Center, Academia Sinica 115, Taiwan.
Tse Wen ChangThe Genomics Research Center, Academia Sinica 115, Taiwan.
Carmay Lim1] Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan [2] Department of Chemistry, National Tsing Hua University, Hsinchu 300, Taiwan.
Genomics Research Center, Academia Sinica · TWInstitute of Biomedical Sciences, Academia Sinica · TWNational Tsing Hua University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Omalizumab, an anti-IgE antibody, used to treat severe allergic asthma and chronic idiopathic urticaria, binds to IgE in blood or membrane-bound on B lymphocytes but not to IgE bound to its high (FcεRI) or low (CD23) affinity receptor. Mutagenesis studies indicate overlapping FcεRI and omalizumab-binding sites in the Cε3 domain, but crystallographic studies show FcεRI and CD23-binding sites that are far apart, so how can omalizumab block IgE from binding both receptors? We report a 2.42-Å omalizumab-Fab structure, a docked IgE-Fc/omalizumab-Fab structure consistent with available experimental data, and the free energy contributions of IgE residues to binding omalizumab, CD23, and FcεRI. These results provide a structural and physical basis as to why omalizumab cannot bind receptor-bound IgE and why omalizumab-bound IgE cannot bind to CD23/FcεRI. They reveal the key IgE residues and their roles in binding omalizumab, CD23, and FcεRI.

Indexed as

Amino Acid SequenceAnti-Asthmatic AgentsAntibodies, Anti-IdiotypicAsthmaBinding SitesCrystallography, X-RayHumansImmunoglobulin EModels, MolecularMutationOmalizumabProtein BindingProtein Structure, TertiaryReceptors, IgEAnti-Asthmatic AgentsAntibodies, Anti-Idiotypicanti-IgE antibodiesImmunoglobulin EOmalizumabReceptors, IgE

Identifiers

PMID26113483
PMCPMC4481376
OpenAlexW2268022034

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.