Evidence map›Paper›PMID 23118208›Full record

ArticleGlycobiology2013

A phenotype survey of 36 mutant mouse strains with gene-targeted defects in glycosyltransferases or glycan-binding proteins.

Sally L Orr, Dzung Le, Jeffrey M Long, Peter Sobieszczuk, Bo Ma, Hua Tian, Xiaoqun Fang, James C Paulson, Jamey D Marth, Nissi Varki

Abstract read
In one paragraph

Article in Glycobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
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

35 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Glycosylation in Cancer.Handbook of experimental pharmacology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Metabolic control of T cell immune response through glycans in inflammatory bowel disease.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  17. Article
  18. Review
  19. Review
  20. Review
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

10 authors.

Sally L OrrDepartment of Pathology, University of California, San Diego, La Jolla, CA 92093-0687, USA.
Dzung Le
Jeffrey M Long
Peter Sobieszczuk
Bo Ma
Hua Tian
Xiaoqun Fang
James C Paulson
Jamey D Marth
Nissi Varki

Funding

Structural Basis of Immune Recognition of Glycosylated AntigensU54GM062116 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SASISEKHARAN, RAM · 2001 to 2010
$80.3M
GLYCOSYLTRANSFERASE FUNCTION IN DEVELOPMENT AND DISEASER01DK048247 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JAMEY MARTH · 1994 to 2026
$9.4M
Intramural NIH HHSNIDDK NIH HHS R01 DK048247NIGMS NIH HHS U54 GM062116NIGMS NIH HHS U54 GM62116
6 · The paper itself

Abstract

The consortium for functional glycomics (CFG) was a large research initiative providing networking and resources for investigators studying the role of glycans and glycan-binding proteins in health and disease. Starting in 2001, six scientific cores were established to generate data, materials and new technologies. By the end of funding in 2011, the mouse phenotype core (MPC) submitted data to a website from the phenotype screen of 36 mutant mouse strains deficient in a gene for either a glycan-binding protein (GBP) or glycosyltransferase (GT). Each mutant strain was allotted three months for analysis and screened by standard phenotype assays used in the fields of immunology, histology, hematology, coagulation, serum chemistry, metabolism and behavior. Twenty of the deficient mouse strains had been studied in other laboratories, and additional tests were performed on these strains to confirm previous observations and discover new data. The CFG constructed 16 new homozygous mutant mouse strains and completed the initial phenotype screen of the majority of these new mutant strains. In total, >300 phenotype changes were observed, but considering the over 100 assays performed on each strain, most of the phenotypes were unchanged. Phenotype differences include abnormal testis morphology in GlcNAcT9- and Siglec-H-deficient mice and lethality in Pomgnt1-deficient mice. The numerous altered phenotypes discovered, along with the consideration of the significant findings of normality, will provide a platform for future characterization to understand the important roles of glycans and GBPs in the mechanisms of health and disease.

Indexed as

PhenotypeAnimalsGene TargetingGlycosyltransferasesHomozygoteLectinsMiceMice, Inbred C57BLMice, Mutant StrainsMutationGlycosyltransferasesLectins

Identifiers

PMID23118208
PMCPMC3605971

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.