| 2000 |
GLUT8 (SLC2A8) is a facilitative glucose transporter with intrinsic glucose transport activity, demonstrated by specific cytochalasin B binding (Kd=56.6 nM) and reconstitutable glucose transport in COS-7 cells transfected with GLUT8 cDNA. |
Heterologous expression in COS-7 cells, cytochalasin B binding assay, reconstituted glucose transport assay |
The Journal of biological chemistry |
High |
10821868
|
| 2000 |
GLUT8 mediates insulin-stimulated glucose uptake in mouse blastocysts; insulin induces a change in intracellular localization of GLUT8 that translates into increased glucose uptake, an effect blocked by antisense oligoprobes. |
Antisense oligoprobe inhibition, glucose uptake assay, immunolocalization in blastocysts |
Proceedings of the National Academy of Sciences of the United States of America |
High |
10860996
|
| 2000 |
GLUTX1 (GLUT8) has glucose transport activity with Km ~2 mM when expressed in Xenopus oocytes, but only after mutational suppression of an N-terminal dileucine internalization motif that normally retains the protein intracellularly; transport is inhibited by cytochalasin B and partly competed by D-fructose and D-galactose. |
Xenopus oocyte expression, transport assay, site-directed mutagenesis of dileucine motif |
The Journal of biological chemistry |
High |
10671487
|
| 2001 |
GLUT8 is retained in intracellular compartments via its N-terminal dileucine motif; mutation of this motif leads to constitutive plasma membrane expression, and blocking endocytosis with dominant-negative dynamin also causes cell surface accumulation, but unlike GLUT4, GLUT8 does not translocate to the plasma membrane in response to insulin, phorbol ester, or hyperosmolarity in rat adipose cells. |
HA-epitope tagging, transfection in primary rat adipocytes, dominant-negative dynamin co-expression, immunofluorescence |
The Biochemical journal |
High |
11513753
|
| 2002 |
GLUT8 undergoes rapid translocation to the rough endoplasmic reticulum in rat hippocampal neurons following peripheral glucose administration, as shown by immunogold electron microscopy and subcellular fractionation; this trafficking is impaired in streptozotocin diabetic rats, suggesting insulin is required for GLUT8 translocation. |
Immunogold electron microscopy, subcellular membrane fractionation, immunoblot |
The Journal of comparative neurology |
Medium |
12271485
|
| 2004 |
GLUT8 contains a [DE]XXXL[LI] late endosomal/lysosomal targeting motif; mutation of the glutamate to arginine (as in GLUT4) alters GLUT8 endocytosis and retains it at the plasma membrane; GLUT8 does not reside in a recycling vesicle pool and localizes to late endosomes/lysosomes. |
Site-directed mutagenesis, immunofluorescence, subcellular localization in 3T3L1, HEK293, CHO cells |
Traffic (Copenhagen, Denmark) |
High |
16262729
|
| 2004 |
GLUT8 translocation to the plasma membrane in neuronal N2A cells is not stimulated by insulin, IGF-1, KCl depolarization, or hypoxia; mutation of the N-terminal dileucine motif (L12,13→A12,13) constitutively localizes GLUT8 to the plasma membrane. |
GLUT8-GFP stable transfection, immunohistochemistry, subcellular fractionation, site-directed mutagenesis |
Journal of neuroscience research |
Medium |
14994344
|
| 2006 |
GLUT8 endocytosis is mediated by direct interaction of its N-terminal dileucine motif with the beta2-adaptin subunit of the AP-2 adaptor complex, targeting GLUT8 to clathrin-coated vesicles; RNAi knockdown of AP-2 mu2 subunit causes GLUT8 accumulation at the plasma membrane comparable to dominant-negative dynamin. |
Yeast two-hybrid, GST pulldown, RNAi knockdown of AP-2, immunofluorescence |
Journal of cell science |
High |
16723738
|
| 2006 |
Deletion of the Slc2a8 gene in mice results in increased hippocampal neuronal proliferation and increased P-wave duration in the heart, but does not impair normal embryonic or postnatal development or glucose homeostasis; GLUT8 is dispensable for embryonic development. |
Knockout mouse generation, cardiac electrophysiology, hippocampal BrdU incorporation assay |
Molecular and cellular biology |
High |
16705176
|
| 2009 |
Endogenous GLUT8 in spermatocytes and spermatids localizes to a late endosomal/lysosomal compartment; its N-terminal intracellular domain interacts with AP1 and AP2 (but not AP3 or AP4), and the GLUT8 N-terminal intracellular domain fused to the tailless IL-2 receptor alpha chain is sufficient to direct that chimera to intracellular membranes. |
Immunofluorescence of endogenous protein, AP complex interaction assays, chimeric protein targeting experiments |
The FEBS journal |
High |
19523115
|
| 2012 |
GLUT8 is required for hepatocyte fructose transport; GLUT8 overexpression or shRNA-mediated knockdown significantly increases or decreases radiolabeled fructose uptake in cultured hepatocytes; GLUT8-deficient mice show diminished fructose uptake, reduced de novo lipogenesis, and attenuated hepatic triglyceride/cholesterol accumulation on a high-fructose diet. |
shRNA knockdown, adenoviral overexpression, radiolabeled fructose uptake, GLUT8-deficient mouse model, hepatic lipid quantification |
The Journal of biological chemistry |
High |
24519932
|
| 2012 |
GLUT8 regulates enterocyte fructose transport; shRNA-mediated GLUT8 knockdown in Caco2 cells stimulates fructose uptake; GLUT8-deficient mice exhibit greater jejunal fructose uptake and GLUT8 deficiency leads to compensatory upregulation of GLUT12 in enterocytes. |
shRNA knockdown in Caco2 cells, GLUT8-KO mouse model, 14C-fructose uptake assay, immunoblot |
Endocrinology |
High |
22822162
|
| 2012 |
Slc2a8 deficiency in mice impairs oocyte metabolism and ATP production, and causes defective decidualization of endometrial stromal cells, leading to reduced litter size and impaired implantation; ovarian transplantation studies confirm effects on both embryo and implantation. |
Slc2a8 knockout mice, oocyte metabolic assays, ATP measurement, decidualization assay, ovarian transplantation |
Biology of reproduction |
High |
22649075
|
| 2013 |
GLUT8 transports dehydroascorbic acid (DHA) in Xenopus oocytes with Km of 3.23 mM and Vmax of 10.1 pmol/min/oocyte; DHA transport by GLUT8 is inhibited by glucose, fructose, and flavonoids (phloretin, quercetin), and maximal transport rates for DHA are lower than for 2-deoxy-D-glucose or fructose. |
Xenopus oocyte expression system, radiolabeled DHA and glucose transport assays, competitive inhibition studies |
The Journal of biological chemistry |
High |
23396969
|
| 2013 |
GLUT8 deficiency in male mice confers resistance to high-fructose diet-induced glucose intolerance and dyslipidemia, associated with enhanced hepatic PPARγ protein abundance; adenoviral GLUT8 overexpression in liver suppresses hepatic PPARγ expression, placing GLUT8 upstream of PPARγ in fructose-induced metabolic regulation. |
GLUT8-KO mice, high-fructose diet challenge, adenoviral overexpression, immunoblot for PPARγ |
Molecular endocrinology |
Medium |
24030250
|
| 2016 |
SLC2A8 (GLUT8) is a mammalian trehalose transporter; trehalose enters hepatocytes via GLUT8 (demonstrated by GC/MS, fluorescence microscopy, and radiolabeled uptake); GLUT8-deficient hepatocytes and mice resist trehalose-induced AMPK phosphorylation and autophagic induction; heterologous overexpression of the Drosophila trehalose transporter Tret1 rescues autophagic flux in GLUT8-deficient hepatocytes. |
GC/MS, fluorescence microscopy, radiolabeled trehalose uptake, GLUT8-KO mouse/hepatocytes, Tret1 rescue experiment, AMPK phosphorylation immunoblot, autophagy flux assay |
Scientific reports |
High |
27922102
|
| 2018 |
GLUT8 deficiency in mice enhances hepatic PPARα activity and FGF21 secretion during fasting; hepatic PPARα knockdown in GLUT8-deficient mice normalizes the enhanced ketogenic and FGF21 secretory responses, placing GLUT8 upstream of PPARα in the adaptive fasting response. |
GLUT8-KO mice, fasting metabolic phenotyping, adenoviral PPARα knockdown, FGF21 ELISA, mitochondrial respiratory function assays |
Endocrinology |
Medium |
29596655
|
| 2020 |
GLUT8 undergoes a lysosome-dependent cleavage reaction that releases the carboxy-terminal peptide to a separate vesicle population; GLUT8 does not transport glucose to the cell surface but is localized at the late endosomal/lysosomal interface where it may function as a sensory component of TXNIP-mediated hexosamine homeostasis. |
Splice variant cataloging, lysosomal inhibitor experiments, subcellular fractionation, immunofluorescence |
Molecular and cellular biology |
Medium |
33077497
|
| 2022 |
TM4SF5 binds GLUT8 at the cell surface and modulates its translocation to the plasma membrane; fructose treatment transiently decreases TM4SF5-GLUT8 binding, allowing GLUT8 to separate and become active for fructose uptake; Tm4sf5 suppression or knockout reduces fructose uptake, de novo lipogenesis, and steatosis. |
Co-immunoprecipitation, Tm4sf5-KO mice, in vitro fructose uptake assays, immunofluorescence of TM4SF5-GLUT8 interaction dynamics |
Molecular metabolism |
Medium |
35123128
|
| 2005 |
GLUT8 in PC12 cells and primary hippocampal neurons localizes to a perinuclear compartment partially overlapping with ER markers but not trans-Golgi, early endosomes, lysosomes, or synaptic vesicles; no stimulus tested (depolarization, PKA/PKC activation, tyrosine kinase signaling, glucose deprivation, AMPK stimulation, osmotic shock) induces GLUT8 surface translocation, and no constitutive recycling through the plasma membrane was detected. |
Recombinant adenoviral GLUT8 with extracellular myc tag, immunofluorescence, dominant-negative dynamin co-expression, anti-myc antibody internalization assay |
Endocrinology |
Medium |
16109784
|
| 2010 |
The proline at position -2 from the dileucine residues in the [DE]XXXL[LI] motif of GLUT8 influences the affinity of AP1 and AP2 for GLUT8 and is critical for intracellular sorting to lysosomes; replacing the XXX (TQP) residues in GLUT8 with those from GLUT12 (GPN) causes dramatic missorting of GLUT8 to the cell surface. |
Site-directed mutagenesis of dileucine motif flanking residues, immunofluorescence, subcellular localization in CHO/HEK293 cells |
Molecular membrane biology |
Medium |
21067453
|
| 2024 |
SLC2A8 RNAi knockdown (79% mRNA reduction) in human first-trimester trophoblast ACH-3P cells reduces glucose uptake by 11% and differentially expresses genes involved in cellular respiration, oxidative phosphorylation, and ATP synthesis, suggesting GLUT8's primary function in trophoblasts is supporting cellular respiration rather than glucose supply. |
Lentiviral RNAi knockdown, glucose uptake assay, RNA-seq transcriptomics |
Cells |
Medium |
38474355
|
| 2019 |
Endogenous GLUT8 partially co-localizes with cis-Golgi markers (58K protein, GM130) and with α-lactalbumin (a component of lactose synthase) in mammary epithelial cells, suggesting GLUT8 supplies glucose to the Golgi to support lactose synthesis. |
Immunohistochemistry, immunofluorescence co-localization with Golgi markers and lactose synthase component |
Journal of physiology and biochemistry |
Low |
31020623
|
| 2002 |
GLUT8 protein is localized to dense core vesicles of synaptic nerve endings in supraoptic nucleus and secretory granules of vasopressin-positive neurons, specifically in vasopressin (but not oxytocin) neurons, as demonstrated by immunogold electron microscopy and double immunofluorescence. |
Immunogold labeling of ultrathin cryosections, double immunofluorescence microscopy |
Endocrinology |
Medium |
11751619
|
| 2002 |
GLUT8 in spermatozoa is predominantly associated with the acrosomal region in both mouse and human sperm, with immunoreactivity at both the plasma membrane and intracellularly; expression onset in mouse testis coincides with appearance of mature spermatozoa. |
Immunohistochemistry with C-terminus-specific antiserum, developmental timing analysis |
Cell and tissue research |
Medium |
11845330
|