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FLASH GENE

Symbol

SLC2A8

contributors: mct - updated : 18-03-2020

HGNC name	solute carrier family 2, (facilitated glucose transporter) member 8
HGNC id	13812

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	a short extracellular loop between transmembrane domain (TM) 1and TM2 and a long loop between TM9 and TM10
	a [D/E]XXXL[L/I]-type dileucine sorting signal that has been postulated to retain the protein in an endosomal/lysosomal compartment via interactions with clathrin adaptor protein (AP) complexes , and SLC2A8 and SLC2A12 both contain a similar [DE]XXXL[LI] dileucine sorting signal in their N- terminus

HOMOLOGY

interspecies

homolog to rattus Glut1-5

Homologene

FAMILY

solute carrier family 2

CATEGORY

transport carrier

SUBCELLULAR LOCALIZATION	plasma membrane
	intracellular
	intracellular,cytoplasm,organelle,endosome
	intracellular,cytoplasm,organelle,lysosome
text	located at the plasma membrane as well as within spermatozoa in the acrosomal region
	associated with a specific intracellular compartment in which it may play an as-yet-uncharacterized role
	localized in a late endosomal/lysosomal compartment of spermatocytes and spermatids

basic FUNCTION	insulin regulated facilitative glucose transporter
	transport facilitator playing a major role in the fuel supply of mature spermatozoa, and is a potential target for inhibition of sperm cell function
	class 3 sugar transport facilitator, not playing a significant role for maintenance of whole body glucose homeostasis
	plays an important role in the energy metabolism of sperm cells
	potential role in the so far unexplored substrate transport across intracellular membranes
	activities of the enigmatic transporters SLC2A8 and SLC2A11 are required for proliferation and viability in myeloma, albeit because of functionalities probably distinct from whole-cell glucose supply
	is a facilitative glucose and fructose transporter
	is essential for hepatocyte fructose transport and fructose-induced macrosteatosis
	SLC2A4 and SLC2A8 trafficking is impaired in the diabetic atria and rescued by insulin treatment
	is likely a mammalian trehalose transporter required for hepatocyte trehalose-induced autophagy and signal transduction
	SLC2A1 and SLC2A8 both transporters are involved in glucose uptake into cis-Golgi, supporting lactose synthesis

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

facilitated diffusion transport

PATHWAY

metabolism

carbohydrate

signaling

a component

INTERACTION

DNA

RNA

small molecule

protein	regulates enterocyte fructose transport by regulating SLC2A12, and disrupted SLC2A8 function has deleterious long-term metabolic sequelae
	hepatic TM4SF5 modulated SLC2A8 localization and activity through transient binding, leading to steatosis-related fructose uptake and lipogenesis

cell & other

REGULATION

induced by

hormones

Other

recruitment of SLC2A8 to the endocytic machinery occurs via direct interaction of the dileucine motif with beta2-adaptin, and endocytosis might be the main site at which it is likely to be regulated

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional     --over   in human IUGR-affected pregnancies on the maternal aspect of the placenta (extravillous trophoblastic (EVT) cytoplasm) compared to control

Susceptibility

Variant & Polymorphism

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed cancer     therapeutic strategy entailing selective SLC2A4, SLC2A11, SLC2A8 inhibition to specifically target aberrant glucose metabolism in cancer diabete type 2   is a promising target in the prevention of diet-induced obesity, and type 2 diabetes mellitus in males diabete metabolic syndrom   is a promising target in the prevention of diet-induced obesity, metabolic syndrome in males

ANIMAL & CELL MODELS

	behavioral alterations of Slc2a8 -/- mice are due to dysfunctions in neuronal processes presumably as a consequence of defects in the glucose metabolism
	Glut8KO mice exhibited significantly greater jejunal fructose uptake at baseline and after high-fructose diet (HFrD) feeding vs. wild-type mice