ReviewJournal of molecular evolution2015
Significance of the evolutionary α1,3-galactosyltransferase (GGTA1) gene inactivation in preventing extinction of apes and old world monkeys.
Review in Journal of molecular evolution, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Distribution of Bacterial α1,3-Galactosyltransferase Genes in the Human Gut Microbiome.Frontiers in immunology · 2019Pooled it
- Human monoclonal antibodies targeting α-Gal restrict IgE engagement of α-Gal syndrome allergens.The Journal of clinical investigation · 2026Article
- Alpha-gal xenoantigens in bioprosthetic valve recipients: clinical implications for bioprosthesis longevity.Journal of cardiothoracic surgery · 2026Review
- Alpha-Gal syndrome unveiled: decoding the glycan-driven red meat allergy.Glycoconjugate journal · 2026Review
- Liver Xenotransplantation: From Early Primate Trials to the First-in-Human Porcine Bridging Therapies.Journal of clinical medicine · 2026Review
- Chemically Defined Non-human Glycans Comprising Galactose-α1-3-Galactose (α-Gal) Epitopes Glycoengineered into the Fragment Antigen-Binding (Fab) Domain of Cetuximab Differentially Affect Human Anti-α-Gal Immunoglobulin E (IgE) Binding.ACS pharmacology & translational science · 2026Article
- A Human Monoclonal Antibody Targeting α-Gal Ameliorates Experimental Cutaneous Leishmaniasis.The Journal of infectious diseases · 2026Article
- The Role ofPathogens (Basel, Switzerland) · 2025Article
- Exploring the relationship betweenComputational and structural biotechnology journal · 2024Review
- IgE and anaphylaxis specific to the carbohydrate alpha-gal depend on IL-4.The Journal of allergy and clinical immunology · 2024Article
- The Acari Hypothesis, IV: revisiting the role of hygiene in allergy.Frontiers in allergy · 2024Article
- Influence of microbiota-driven natural antibodies on dengue transmission.Frontiers in immunology · 2024Article
- Validation of an anti-α-Gal IgE fluoroenzyme-immunoassay for the screening of patients at risk of severe anaphylaxis to cetuximab.BMC cancer · 2023Article
- High-risk groups for alpha-gal sensitization.Allergologie select · 2023Article
- Emerging Nano-/Biotechnology Drives Oncolytic Virus-Activated and Combined Cancer Immunotherapy.Research (Washington, D.C.) · 2023Article
- Genetic and structural basis of the human anti-α-galactosyl antibody response.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Immunological Risk Assessment of Xenogeneic Dural Patch by Comparing with Raw Material via GTKO Mice.BioMed research international · 2022Article
- Poly-L-Lysine-Based αGal-Glycoconjugates for Treating Anti-αGal IgE-Mediated Diseases.Frontiers in immunology · 2022Article
- Current and Future Strategies for the Diagnosis and Treatment of the Alpha-Gal Syndrome (AGS).Journal of asthma and allergy · 2022Review
- Kcnk3, Ggta1, and Gpr84 are involved in hyperbaric oxygenation preconditioning protection on cerebral ischemia-reperfusion injury.Experimental brain research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The α1,3-galactosyltransferase (α1,3GT or GGTA1) gene displays unique evolutionary characteristics. This gene appeared early in mammalian evolution and is absent in other vertebrates. The α1,3GT gene is active in marsupials, nonprimate placental mammals, lemurs (prosimians) and New World monkeys, encoding the α1,3GT enzyme that synthesizes a carbohydrate antigen called "α-gal epitope." The α-gal epitope is present in large numbers on cell membrane glycolipids and glycoproteins. The α1,3GT gene was inactivated in ancestral Old World monkeys and apes by frameshift single-base deletions forming premature stop codons. Because of this gene inactivation, humans, apes, and Old World monkeys lack α-gal epitopes and naturally produce an antibody called the "anti-Gal antibody" which binds specifically to α-gal epitopes and which is the most abundant antibody in humans. The evolutionary event that resulted in the inactivation of the α1,3GT gene in ancestral Old World primates could have been mediated by a pathogen endemic to Eurasia-Africa landmass that exerted pressure for selection of primate populations lacking the α-gal epitope. Once the α-gal epitope was eliminated, primates could produce the anti-Gal antibody, possibly as means of defense against pathogens expressing this epitope. This assumption is supported by the fossil record demonstrating an almost complete extinction of apes in the late Miocene and failure of Old World monkeys to radiate into multiple species before that period. A present outcome of this evolutionary event is the anti-Gal-mediated rejection of mammalian xenografts expressing α-gal epitopes in humans, apes, and Old World monkeys.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.