Introduction of SLC29A3
Solute carrier family 29 member 3 (SLC29A3), also known as Equilibrative nucleoside transporter 3 (ENT3), is a protein that in humans is encoded by the SLC29A3 gene. SLC29A3 protein also contains 11 characteristic transmembrane domains of the ENT family, but they are preceded by a long cytoplasmic N-terminal region not found in SLC29A1 or SLC29A2. The unique N-terminal domain of SLC29A3 contains a conserved putative dileucine-based endosomal/lysosomal targeting motif. SLC29A3 is widely expressed in a range of tissues, including kidney, placenta, breast, colon, testis, fetal liver, fetal spleen, and several neoplastic tissues.
|Basic Information of SLC29A3|
|Protein Name||Equilibrative nucleoside transporter 3|
|Aliases||Solute carrier family 29 member 3, SLC29A3, ENT3|
|Organism||Homo sapiens (Human)|
Function of SLC29A3 Membrane Protein
SLC29A3 can function as an equilibrative transporter to mediate both influx and efflux of nucleosides across the membrane, which is essential for nucleotide synthesis by salvage pathways in cells that lack de novo biosynthetic pathways. In addition, it can also mediate transport of adenine, adenosine, and uridine, as well as several nucleoside analog drugs, such as anticancer and antiviral agents, including cladribine, cordycepin, tubercidin and 3′-azido-3′-deoxythymidine (AZT). SLC29A3 mutations have been linked to a group of heterogeneous hereditary diseases in humans, including H syndrome, Faisalabad histiocytosis, pigmentary hypertrichosis, and non-autoimmune insulin-dependent diabetes mellitus syndromes, and Rosai-Dorfman disease. Unlike other ENT family members with localization on the plasma membrane, SLC29A3 has been reported to be expressed in organelle membranes, including endosomal/lysosomal and mitochondrial membrane.
Fig.1 SLC29A3 deficiency leads to an enlarged and disturbed lysosomal compartment, resulting in accumulation of surplus mitochondria, elevation of intracellular reactive oxygen species, and DNA damage in T cells. (Wei, 2018)
Application SLC29A3 of Membrane Protein in Literature
This article indicates that SLC29A3 mutations are associated with dysosteosclerosis. In addition, intermediate autosomal recessive osteopetrosis due to TCIRG1 splice site mutations increases the molecular heterogeneity of dysosteosclerosis-like sclerosing bone dysplasias.
This article reveals that ENT3 functions as a vital metabolite transporter to support T cell homeostasis and activation by regulating lysosomal integrity and the availability of nucleosides.
This study finds that apical hCNT3 and basolateral hENT2 are involved in proximal tubular reabsorption of adenosine and some nucleoside drugs. In addition, this article also reveals that apical hENT1 and basolateral hOATs are involved in proximal tubular secretion of 2'-deoxyadenosine.
This article reveals that the N-terminal half of hENT3 is primarily responsible for the hENT3-3'-deoxynucleoside analog interaction and 225D and 231L in the N-terminal half of hENT3 partially contribute to the ability of hENT3 to transport AZT and DDI.
This article demonstrates that tocilizumab should be the first choice when considering treatment of the autoinflammatory or cutaneous manifestations of pigmentary hypertrichosis and non-autoimmune insulin-dependent diabetes mellitus (PHID), which is associated with recessive mutations in SLC29A3.
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