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SLC26A8 Membrane Protein Introduction

Introduction of SLC26A8

SLC26A8 is encoded by the SLC26A8 gene and is also known as Testis anion transporter 1, TAT1, Anion exchange transporter, and Solute carrier family 26 member 8. It belongs to the solute carrier 26 (SLC26) family, which is a transmembrane protein located at the plasma membrane of the cells and transporting a variety of monovalent and divalent anions, including chloride, bicarbonate, sulfate, and oxalate. SLC26A8 displays a SO42- transport activity at least partly through a SO42-/Cl- exchange mechanism.

Basic Information of SLC26A8
Protein Name Testis anion transporter 1
Gene Name SLC26A8
Aliases Anion exchange transporter, Solute carrier family 26 member 8
Organism Homo sapiens (Human)
UniProt ID Q96RN1
Transmembrane Times 14
Length (aa) 970
Sequence MAQLERSAISGFSSKSRRNSFAYDVKREVYNEETFQQEHKRKASSSGNMNINITTFRHHVQCRCSWHRFLRCVLTIFPFLEWMCMYRLKDWLLGDLLAGISVGLVQVPQGLTLSLLARQLIPPLNIAYAAFCSSVIYVIFGSCHQMSIGSFFLVSALLINVLKVSPFNNGQLVMGSFVKNEFSAPSYLMGYNKSLSVVATTTFLTGIIQLIMGVLGLGFIATYLPESAMSAYLAAVALHIMLSQLTFIFGIMISFHAGPISFFYDIINYCVALPKANSTSILVFLTVVVALRINKCIRISFNQYPIEFPMELFLIIGFTVIANKISMATETSQTLIDMIPYSFLLPVTPDFSLLPKIILQAFSLSLVSSFLLIFLGKKIASLHNYSVNSNQDLIAIGLCNVVSSFFRSCVFTGAIARTIIQDKSGGRQQFASLVGAGVMLLLMVKMGHFFYTLPNAVLAGIILSNVIPYLETISNLPSLWRQDQYDCALWMMTFSSSIFLGLDIGLIISVVSAFFITTVRSHRAKILLLGQIPNTNIYRSINDYREIITIPGVKIFQCCSSITFVNVYYLKHKLLKEVDMVKVPLKEEEIFSLFNSSDTNLQGGKICRCFCNCDDLEPLPRILYTERFENKLDPEASSINLIHCSHFESMNTSQTASEDQVPYTVSSVSQKNQGQQYEEVEEVWLPNNSSRNSSPGLPDVAESQGRRSLIPYSDASLLPSVHTIILDFSMVHYVDSRGLVVLRQICNAFQNANILILIAGCHSSIVRAFERNDFFDAGITKTQLFLSVHDAVLFALSRKVIGSSELSIDESETVIRETYSETDKNDNSRYKMSSSFLGSQKNVSPGFIKIQQPVEEESELDLELESEQEAGLGLDLDLDRELEPEMEPKAETETKTQTEMEPQPETEPEMEPNPKSRPRAHTFPQQRYWPMYHPSMASTQSQTQTRTWSVERRRHPMDSYSPEGNSNEDV

Function of SLC26A8 Membrane Protein

The functional studies performed so far indicate that SLC26A8 displays a SO42- transport activity at least partly through a SO42-/Cl- exchange mechanism. SLC26A8 transport activity toward the C2O42- but not the I- was also demonstrated. Deletion of SLC26A8 in the mouse was shown to induce a male sterility phenotype due to the lack of sperm motility and impaired capacitation but also to severe structural defects of the flagellum. SLC26A8 anion transport activity was essential for these processes and in human, SLC26A8 mutations could lead to male infertility. Meanwhile, physical interaction and co-localization of SLC26A8 and CFTR in the sperm is demonstrated by co-immunoprecipitation experiments in heterologous cells transiently transfected with plasmids encoding SLC26A8 and CFTR proteins. The interaction between CFTR and SLC26A8 might cooperate in both the sperm head and flagellum to regulate ion fluxes upon capacitation, which are required for the acrosomal reaction and the flagellum hyperactivation, respectively. Physical interaction of SLC26A8 with CFTR results in CFTR stimulation, which is involved in the regulation of the Cl- and/or HCO3- fluxes that are required to switch on the PKA-dependent downstream phosphorylation cascades during sperm motility and capacitation.

Model of the physical interaction between SLC26A8 and CFTR channel. Fig.1 Model of the physical interaction between SLC26A8 and CFTR channel. (El, 2014)

Application of SLC26A8 Membrane Protein in Literature

  1. El Khouri E & Touré A. Functional interaction of the cystic fibrosis transmembrane conductance regulator with members of the SLC26 family of anion transporters (SLC26A8 and SLC26A9): Physiological and pathophysiological relevance. The International Journal of Biochemistry & Cell Biology. 2014, 52: 58-67. PubMed ID: 24530837

    This article focuses on the functional interaction of SLC26A8 with the CFTR channel. This article summarizes the newly published studies, which indicate the mutations in SLC26A8 are associated with a deregulation of the CFTR anion transport activity in the pathophysiological context of the sperm and the pulmonary cells. These findings in this article confirm the physiological relevance of SLC26 and CFTR cross-regulation, opening new gates for the treatment of cystic fibrosis.

  2. Touré A., et al. The Testis Anion Transporter 1 (Slc26a8) is required for sperm terminal differentiation and male fertility in the mouse. Hum. Mol. Genet. 2007, 16(15): 1783-1793. PubMed ID: 17517695

    This article reveals that SLC26A8 as a new family member (Slc26A8), very specifically expressed in male germ cells in both the human and the mouse. Meanwhile, SLC26A8 is essential for proper sperm tail differentiation and motility and is a critical component of the sperm annulus.

  3. Dirami T., et al. Missense Mutations in SLC26A8, Encoding a Sperm-Specific Activator of CFTR, Are Associated with Human Asthenozoospermia. The American Journal of Human Genetics. 2013, 92(5): 760-766. PubMed ID: 23582645

    This article reports that the identification and characterization of heterozygous SLC26A8 missense mutations, which would abolish the functional interaction with the CFTR channel and potentially contribute to subfertility in men by impairing sperm motility and capacitation.

  4. Touré A., et al. Tat1, a Novel Sulfate Transporter Specifically Expressed in Human Male Germ Cells and Potentially Linked to RhoGTPase Signaling. J. Biol. Chem. 2001, 276(23): 20309-20315. PubMed ID: 11278976

    This article suggests that Tat1 (SLC26A8) is a novel sulfate transporter, which can interact with MgcRacGAP in spermatocytes specifically. These observations raise the possibility of a new regulatory pathway linking sulfate transport to Rho signaling in male germ cells.

  5. Mäkelä S., et al. Mutational analysis of the human SLC26A8 gene: exclusion as a candidate for male infertility due to primary spermatogenic failure. MHR: Basic science of reproductive medicin. 2005, 11(2): 129-132. PubMed ID: 15579655

    The authors in this article apply mutational analysis in the coding region of the SLC26A8 gene in 83 male infertility patients and two groups of controls using single-strand conformational polymorphism and direct sequencing methods, and the results of this article suggest that the SLC26A8 mutations are not a common cause of male infertility.

SLC26A8 Preparation Options

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Reference

  1. El Khouri E & Touré A. (2014) Functional interaction of the cystic fibrosis transmembrane conductance regulator with members of the SLC26 family of anion transporters (SLC26A8 and SLC26A9): Physiological and pathophysiological relevance. The International Journal of Biochemistry & Cell Biology. 52: 58-67.

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