ArticleEvolutionary bioinformatics online2007
An insulin-like modular basis for the evolution of glucose transporters (GLUT) with implications for diabetes.
Article in Evolutionary bioinformatics online, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Selection for Molecularly Complementary Modules (MCMs) Drives the Origins and Evolution of Pleiofunctional, Epistatic Interactomes (PEIs).Life (Basel, Switzerland) · 2026Review
- Co-Evolution of Opioid and Adrenergic Ligands and Receptors: Shared, Complementary Modules Explain Evolution of Functional Interactions and Suggest Novel Engineering Possibilities.Life (Basel, Switzerland) · 2021Article
- Mutual Enhancement of Opioid and Adrenergic Receptors by Combinations of Opioids and Adrenergic Ligands Is Reflected in Molecular Complementarity of Ligands: Drug Development Possibilities.International journal of molecular sciences · 2019Article
- Rapid Non-Enzymatic Glycation of the Insulin Receptor under Hyperglycemic Conditions Inhibits Insulin Binding In Vitro: Implications for Insulin Resistance.International journal of molecular sciences · 2017Article
- tRNA evolution from the proto-tRNA minihelix world.Transcription · 2016Article
- Glucose binds to the insulin receptor affecting the mutual affinity of insulin and its receptor.Cellular and molecular life sciences : CMLS · 2009Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose transporters (GLUT) are twelve-transmembrane spanning proteins that contain two pores capable of transporting glucose and dehydroascorbate in and out of cells. The mechanism by which transport is effected is unknown. An evolutionarily-based hypothesis for the mechanism of glucose transport is presented here based on reports that insulin has multiple binding sites for glucose. It is proposed that insulin-like peptides were incorporated as modular elements into transmembrane proteins during evolution, resulting in glucose transporting capacity. Homology searching reveals that all GLUT contain multiple copies of insulin-like regions. These regions map onto a model of GLUT in positions that define the glucose transport cores. This observation provides a mechanism for glucose transport involving the diffusion of glucose from one insulin-like glucose-binding region to another. It also suggests a mechanism by which glucose disregulation may occur in both type 1 and type 2 diabetes: insulin rapidly self-glycates under hyperglycemic conditions. Insulin-like regions of GLUT may also self-glycate rapidly, thereby interfering with transport of glucose into cells and disabling GLUT sensing of blood glucose levels. All aspects of the hypothesis are experimentally testable.
Identifiers
19430606PMC2674801W1496201023What 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.