Evidence map›Paper›PMID 24903886›Full record

ArticleCurrent protocols in chemical biology2014

Rapid assays for lectin toxicity and binding changes that reflect altered glycosylation in mammalian cells.

Pamela Stanley, Subha Sundaram

Abstract read
In one paragraph

Article in Current protocols in chemical biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Flow Cytometric Examination of Galectin Binding to Red Blood Cells.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  3. Impact ofFrontiers in cellular and infection microbiology · 2025
    Article
  4. Article
  5. Article
  6. 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

2 authors at 1 institution in 1 country.

Pamela StanleyDepartment of Cell Biology, Albert Einstein College of Medicine, New York, New York.
Subha SundaramDepartment of Cell Biology, Albert Einstein College of Medicine, New York, New York.
Albert Einstein College of Medicine · US

Funding

Lectin Resistant Tumor Cells and Functional GlycomicsR01GM105399 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STANLEY, PAMELA M · 2013 to 2022
$3.6M
NIGMS NIH HHS R01 GM105399NIGMS NIH HHS R01GM105399
6 · The paper itself

Abstract

Glycosylation engineering is used to generate glycoproteins, glycolipids, or proteoglycans with a more defined complement of glycans on their glycoconjugates. For example, a mammalian cell glycosylation mutant lacking a specific glycosyltransferase generates glycoproteins, and/or glycolipids, and/or proteoglycans with truncated glycans missing the sugar transferred by that glycosyltransferase, as well as those sugars that would be added subsequently. In some cases, an alternative glycosyltransferase may then use the truncated glycans as acceptors, thereby generating a new or different glycan subset in the mutant cell. Another type of glycosylation mutant arises from gain-of-function mutations that, for example, activate a silent glycosyltransferase gene. In this case, glycoconjugates will have glycans with additional sugar(s) that are more elaborate than the glycans of wild type cells. Mutations in other genes that affect glycosylation, such as nucleotide sugar synthases or transporters, will alter the glycan complement in more general ways that usually affect several types of glycoconjugates. There are now many strategies for generating a precise mutation in a glycosylation gene in a mammalian cell. Large-volume cultures of mammalian cells may also generate spontaneous mutants in glycosylation pathways. This article will focus on how to rapidly characterize mammalian cells with an altered glycosylation activity. The key reagents for the protocols described are plant lectins that bind mammalian glycans with varying avidities, depending on the specific structure of those glycans. Cells with altered glycosylation generally become resistant or hypersensitive to lectin toxicity, and have reduced or increased lectin or antibody binding. Here we describe rapid assays to compare the cytotoxicity of lectins in a lectin resistance test, and the binding of lectins or antibodies by flow cytometry in a glycan-binding assay. Based on these tests, glycosylation changes expressed by a cell can be revealed, and glycosylation mutants classified into phenotypic groups that may reflect a loss-of-function or gain-of-function mutation in a specific gene involved in glycan synthesis.

Indexed as

AnimalsBiological AssayCell LineCell SurvivalCHO CellsColoring AgentsCricetulusFlow CytometryGlycoconjugatesGlycosylationLectinsPolysaccharidesTetrazolium SaltsThiazolesColoring AgentsGlycoconjugatesLectinsPolysaccharidesTetrazolium SaltsThiazolesthiazolyl blueantibodiesCHO cellsengineer glycansglycan bindingglycosylation mutantslectinsmammalian cells

Identifiers

PMID24903886
PMCPMC4114153
OpenAlexW1868416060

What OpenQuestion holds

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LicenceTDM
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.