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2.A.1.1.72
The kidney basolateral urate efflux transporter (SLC2A9, URATv1 or GLUT9) (orthologue of 2.A.1.1.47) (Anzai et al., 2008). Human SLC2A9a and SLC2A9b isoforms mediate electrogenic transport of urate with different characteristics in the presence of hexoses (Witkowska et al., 2012).  It transports hexoses as well as urate, the latter by a uniport mechanism, thus catalyzing uptake as well as efflux. The ITM2B protein Q9Y287; 266 aas and 1 TMS) inhibits urate uptake and stimulates efflux (Mandal and Mount 2019). GLUT9's transcription is regulated by a hepatocyte nuclear factor, HNF4α (Prestin et al. 2014). Residues involved in urate transport have been identified (Long et al. 2017). Pathogenic variants of SLC22A12 (URAT1) and SLC2A9 (GLUT9) can give rise to renal hypouricemia (Perdomo-Ramirez et al. 2023).

Accession Number:Q9NRM0
Protein Name:Solute carrier family 2, facilitated glucose transporter member 9
Length:540
Molecular Weight:58817.00
Species:Homo sapiens (Human) [9606]
Number of TMSs:12
Location1 / Topology2 / Orientation3: Membrane1 / Multi-pass membrane protein2
Substrate 7,9-dihydro-1H-purine-2,6,8(3H)-trione

Cross database links:

RefSeq: NP_001001290.1    NP_064425.2   
Entrez Gene ID: 56606   
Pfam: PF00083   
OMIM: 606142  gene
612076  phenotype
KEGG: hsa:56606    hsa:56606   

Gene Ontology

GO:0005351 F:sugar:hydrogen symporter activity
GO:0015758 P:glucose transport
GO:0055085 P:transmembrane transport
GO:0016021 C:integral to membrane
GO:0005887 C:integral to plasma membrane
GO:0005635 C:nuclear envelope
GO:0005886 C:plasma membrane
GO:0005355 F:glucose transmembrane transporter activity
GO:0046415 P:urate metabolic process

References (17)

[1] “Cloning and expression analysis of a novel member of the facilitative glucose transporter family, SLC2A9 (GLUT9).”  Phay J.E.et.al.   10860667
[2] “Generation and annotation of the DNA sequences of human chromosomes 2 and 4.”  Hillier L.W.et.al.   15815621
[3] “The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).”  The MGC Project Teamet.al.   15489334
[4] “Human articular chondrocytes express three facilitative glucose transporter isoforms: GLUT1, GLUT3 and GLUT9.”  Mobasheri A.et.al.   11991658
[5] “Identification and characterization of human glucose transporter-like protein-9 (GLUT9): alternative splicing alters trafficking.”  Augustin R.et.al.   14739288
[6] “SLC2A9 influences uric acid concentrations with pronounced sex-specific effects.”  Doering A.et.al.   18327256
[7] “SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout.”  Vitart V.et.al.   18327257
[8] “Cloning and expression analysis of a novel member of the facilitative glucose transporter family, SLC2A9 (GLUT9).”  Phay J.E.et.al.   10860667
[9] “Generation and annotation of the DNA sequences of human chromosomes 2 and 4.”  Hillier L.W.et.al.   15815621
[10] “The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).”  The MGC Project Teamet.al.   15489334
[11] “Human articular chondrocytes express three facilitative glucose transporter isoforms: GLUT1, GLUT3 and GLUT9.”  Mobasheri A.et.al.   11991658
[12] “Identification and characterization of human glucose transporter-like protein-9 (GLUT9): alternative splicing alters trafficking.”  Augustin R.et.al.   14739288
[13] “SLC2A9 influences uric acid concentrations with pronounced sex-specific effects.”  Doering A.et.al.   18327256
[14] “SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout.”  Vitart V.et.al.   18327257
[15] “Mutations in glucose transporter 9 gene SLC2A9 cause renal hypouricemia.”  Matsuo H.et.al.   19026395
[16] “Homozygous SLC2A9 mutations cause severe renal hypouricemia.”  Dinour D.et.al.   19926891
[17] “Two novel homozygous SLC2A9 mutations cause renal hypouricemia type 2.”  Dinour D.et.al.   21810765

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Predict TMSs (Predict number of transmembrane segments)
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FASTA formatted sequence 
1:	MARKQNRNSK ELGLVPLTDD TSHARPPGPG RALLECDHLR SGVPGGRRRK DWSCSLLVAS 
61:	LAGAFGSSFL YGYNLSVVNA PTPYIKAFYN ESWERRHGRP IDPDTLTLLW SVTVSIFAIG 
121:	GLVGTLIVKM IGKVLGRKHT LLANNGFAIS AALLMACSLQ AGAFEMLIVG RFIMGIDGGV 
181:	ALSVLPMYLS EISPKEIRGS LGQVTAIFIC IGVFTGQLLG LPELLGKEST WPYLFGVIVV 
241:	PAVVQLLSLP FLPDSPRYLL LEKHNEARAV KAFQTFLGKA DVSQEVEEVL AESRVQRSIR 
301:	LVSVLELLRA PYVRWQVVTV IVTMACYQLC GLNAIWFYTN SIFGKAGIPL AKIPYVTLST 
361:	GGIETLAAVF SGLVIEHLGR RPLLIGGFGL MGLFFGTLTI TLTLQDHAPW VPYLSIVGIL 
421:	AIIASFCSGP GGIPFILTGE FFQQSQRPAA FIIAGTVNWL SNFAVGLLFP FIQKSLDTYC 
481:	FLVFATICIT GAIYLYFVLP ETKNRTYAEI SQAFSKRNKA YPPEEKIDSA VTDGKINGRP