Evidence map›Paper›PMID 27494936›Full record

ArticleJournal of lipid research2016

An LPL-specific monoclonal antibody, 88B8, that abolishes the binding of LPL to GPIHBP1.

Christopher M Allan, Mikael Larsson, Xuchen Hu, Cuiwen He, Rachel S Jung, Alaleh Mapar, Constance Voss, Kazuya Miyashita, Tetsuo Machida, Masami Murakami and 6 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. GPIHBP1 on oligodendrocytes binds lipoprotein lipase within the human brain.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. A protein of capillary endothelial cells, GPIHBP1, is crucial for plasma triglyceride metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. 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

16 authors at 4 institutions in 3 countries.

Christopher M AllanDepartments of Medicine University of California Los Angeles, Los Angeles, CA.
Mikael LarssonDepartments of Medicine University of California Los Angeles, Los Angeles, CA.
Xuchen HuDepartments of Medicine University of California Los Angeles, Los Angeles, CA.
Cuiwen HeDepartments of Medicine University of California Los Angeles, Los Angeles, CA.
Rachel S JungDepartments of Medicine University of California Los Angeles, Los Angeles, CA.
Alaleh MaparDepartments of Medicine University of California Los Angeles, Los Angeles, CA.
Constance VossDepartments of Medicine University of California Los Angeles, Los Angeles, CA.
Kazuya MiyashitaGunma University, Graduate School of Medicine, Maebashi, Japan.
Tetsuo MachidaGunma University, Graduate School of Medicine, Maebashi, Japan.
Masami MurakamiGunma University, Graduate School of Medicine, Maebashi, Japan.
Katsuyuki NakajimaGunma University, Graduate School of Medicine, Maebashi, Japan.
André BensadounDivision of Nutritional Science, Cornell University, Ithaca, NY.
Michael PlougFinsen Laboratory, Rigshospitalet, Copenhagen N, Denmark; Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen N, Denmark.
Loren G FongDepartments of Medicine University of California Los Angeles, Los Angeles, CA. Electronic address: lfong@mednet.ucla.edu.
Stephen G YoungDepartments of Medicine University of California Los Angeles, Los Angeles, CA; Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA. Electronic address: sgyoung@mednet.ucla.edu.
Anne P BeigneuxDepartments of Medicine University of California Los Angeles, Los Angeles, CA. Electronic address: abeigneux@mednet.ucla.edu.
University of California, Los Angeles · USGunma University · JPCornell University · USUniversity of Copenhagen · DK

Funding

UCLA-Caltech Medical Scientist Training ProgramT32GM008042 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A, DAWSON, DAVID WAYNE · 1985 to 2023
$29.9M
The Lipin Protein Family and Triglyceride Metabolism P01HL090553 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2008 to 2018
$23.3M
Refining Physiologic Mechanisms for Intravascular Triglyceride MetabolismR01HL087228 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEIGNEUX, ANNE, FONG, LOREN GI · 2007 to 2024
$7.8M
Vascular Biology Training GrantT32HL069766 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2002 to 2022
$7.4M
Defining mechanisms for lipid transport across capillary endothelial cellsR01HL125335 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2015 to 2017
$1.2M
NHLBI NIH HHS P01 HL090553NHLBI NIH HHS R01 HL087228NHLBI NIH HHS R01 HL125335NHLBI NIH HHS T32 HL069766NIGMS NIH HHS T32 GM008042
6 · The paper itself

Abstract

LPL contains two principal domains: an amino-terminal catalytic domain (residues 1-297) and a carboxyl-terminal domain (residues 298-448) that is important for binding lipids and binding glycosylphosphatidylinositol-anchored high density lipoprotein binding protein 1 (GPIHBP1) (an endothelial cell protein that shuttles LPL to the capillary lumen). The LPL sequences required for GPIHBP1 binding have not been examined in detail, but one study suggested that sequences near LPL's carboxyl terminus (residues ∼403-438) were crucial. Here, we tested the ability of LPL-specific monoclonal antibodies (mAbs) to block the binding of LPL to GPIHBP1. One antibody, 88B8, abolished LPL binding to GPIHBP1. Consistent with those results, antibody 88B8 could not bind to GPIHBP1-bound LPL on cultured cells. Antibody 88B8 bound poorly to LPL proteins with amino acid substitutions that interfered with GPIHBP1 binding (e.g., C418Y, E421K). However, the sequences near LPL's carboxyl terminus (residues ∼403-438) were not sufficient for 88B8 binding; upstream sequences (residues 298-400) were also required. Additional studies showed that these same sequences are required for LPL binding to GPIHBP1. In conclusion, we identified an LPL mAb that binds to LPL's GPIHBP1-binding domain. The binding of both antibody 88B8 and GPIHBP1 to LPL depends on large segments of LPL's carboxyl-terminal domain.

Indexed as

Amino Acid SubstitutionAnimalsAntibodies, Monoclonal, Murine-DerivedCell LineDrosophila melanogasterHumansLipoprotein LipaseMutation, MissenseProtein BindingProtein DomainsReceptors, LipoproteinAntibodies, Monoclonal, Murine-DerivedGPIHBP1 protein, humanLipoprotein LipaseLPL protein, humanReceptors, Lipoproteinchylomicronsendothelial cellsglycosylphosphatidylinositol-anchored high density lipoprotein binding protein 1lipids/chemistrylipolysis and fatty acid metabolismlipoprotein lipasetriglycerides

Identifiers

PMID27494936
PMCPMC5036369
OpenAlexW2526340886

What OpenQuestion holds

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Registered trials

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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.