| ID | Sequence | Length | GC content |
|---|---|---|---|
| GUCCUAUUCGGGCUCCCGCCUCUGUUCAGUUCCAGAGACAAUUCAUGGG… | 2816 nt | 0.5710 | |
| GUCCUAUUCGGGCUCCCGCCUCUGUUCAGUUCCAGAGACAAUUCAUGGG… | 2566 nt | 0.5511 | |
| GUCCUAUUCGGGCUCCCGCCUCUGUUCAGGACACUGGGUCCCCUUGGAG… | 2242 nt | 0.5482 | |
| GAGGGAGCAGAAAAAACCCAACUCAGCAGAUCUGGGAACUGUGAGAGCG… | 2199 nt | 0.5384 | |
| GUCCUAUUCGGGCUCCCGCCUCUGUUCAGGACACUGGGUCCCCUUGGAG… | 2312 nt | 0.5420 |
This gene regulates glucose-6-phosphate transport from the cytoplasm to the lumen of the endoplasmic reticulum, in order to maintain glucose homeostasis. It also plays a role in ATP-mediated calcium sequestration in the lumen of the endoplasmic reticulum. Mutations in this gene have been associated with various forms of glycogen storage disease. Alternative splicing in this gene results in multiple transcript variants.[provided by RefSeq, Aug 2009]
A study in mice demonstrated that in vivo α-particle irradiation of Kupffer or endothelial liver cells via boron neutron capture induced a characteristic inflammatory gene expression profile, with the SLC37A4 being under-expressed in Kupffer cell, endothelial cell, and neutron exposures [Roudkenar et al. DOI:10.1269/jrr.07078]. In a separate mouse model of hind limb burn injury, the SLC37A4 was also found to be down-regulated in skeletal muscle at three days post-burn, as part of a broader suppression of genes involved in glucose transport and mitochondrial energy metabolism [Padfield et al. DOI:10.01211102].