SLC4A11 Membrane Protein Introduction

Introduction of SLC4A11

SLC4A11 is an integral membrane protein that in humans is encoded by the SLC4A11 gene. It belongs to the SLC4 family of bicarbonate transporters and is widely expressed in kidney, testis, salivary gland, thyroid, trachea and corneal endothelium, but not detected in retina and lymphocytes. SLC4A11 possesses active borate transmembrane transporter activity involved in the transport of borate across a membrane against the concentration gradient.

Function of SLC4A11 Membrane Protein

SLC4A11 is a voltage-regulated, electrogenic sodium-coupled borate cotransporter that plays an important role in sodium-mediated fluid transport in different organs. SLC4A11 has been revealed to inhibit severe corneal morphological changes caused by increased sodium chloride concentrations in the stroma. In the inner ear, it regulates the transport of potassium to pass the fibrocyte layer to the stria vascularis and is vital for the production of the endocochlear potential. However, it is not responsible for the regulation of potassium concentrations in the endolymph. In the kidney, it mediates a sodium flux into the thin descending limb of Henle loop to allow countercurrent multiplication by osmotic equilibration, involved in regulation for urinary concentration. Moreover, SLC4A11 is also associated with borate homeostasis. It functions as a Na⁺ and OH^-(H⁺) channel in case of borate absence. It also functions as an electrogenic Na⁺ coupled borate cotransporter in the presence of borate. Mutations in SLC4A11 gene are associated with many endothelial corneal dystrophies including recessive corneal endothelial dystrophy 2, Fuchs endothelial corneal dystrophy, and corneal dystrophy and perceptive deafness.

Fig.1 Cartoon of SLC4A11 protein topology showing the location of CHED-linked missense mutations. (Patel, 2015)

Application of SLC4A11 Membrane Protein in Literature

1. Qin L., et al. High SLC4A11 expression is an independent predictor for poor overall survival in grade 3/4 serous ovarian cancer. Plos One. 2017, 12(11):e0187385. PubMed ID: 29091960
   
   

   The article implicates that high SLC4A11 expression caused by DNA amplification and hypomethylation is an independent predictor for poor overall survival in grade 3/4 serous ovarian cancer.

2. Hand C.K., et al. Homozygous SLC4A11 mutation in a large Irish CHED2 pedigree. Ophthalmic Paediatrics & Genetics. 2016, 38(2):148-151. PubMed ID: 27057589
   
   

   This study first reports homozygous SLC4A11 mutation (Leu843Pro) is associated with congenital hereditary endothelial dystrophy (CHED) in Irish.

3. Lal K.B., et al. Delayed onset of congenital hereditary endothelial dystrophy due to compound heterozygous SLC4A11 mutations. Indian Journal of Ophthalmology. 2016, 64(7):492-495. PubMed ID: 27609159
   
   

   In this study, authors reveal that compound heterozygous SLC4A11 mutations impair protein function resulting in the delayed onset of congenital hereditary endothelial dystrophy.

4. Mei R., et al. Sustained viral response and treatment-induced cytopenia correlate with SLCs and KLF12 genotypes in interferon/ribavirin-treated Chinese chronic hepatitis C patients. Journal of Gastroenterology & Hepatology. 2016, 31(8):1489-1497. PubMed ID: 26750805
   
   

   The genotyped results indicate that rs3810560 polymorphism in SLC4A11 independently affects the sustained viral response rates in patients with chronic hepatitis C, whereas SLC29A1 rs760370 and KLF12 rs9543524 are associated with treatment-induced adverse events.

5. Hui T., et al. Analysis of SLC4A11, ZEB1, LOXHD1, COL8A2 and TCF4 gene sequences in a multi-generational family with late-onset Fuchs corneal dystrophy. International Journal of Molecular Medicine. 2016, 37(6):1487-1500. PubMed ID: 27121161
   
   

   The work analyzes SLC4A11, ZEB1, LOXHD1, COL8A2 and TCF4 gene sequences in a multi-generational family with late-onset Fuchs corneal dystrophy and finds no evidence for found polymorphisms causing the disease in this specific pedigree.

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Reference

1. Patel S P and Parker M D. (2015). SLC4A11 and the pathophysiology of congenital hereditary endothelial dystrophy. Biomed Res Int. 2015, 475392.

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