Cloning and Characterization of a Na+-driven Anion Exchanger (NDAE1)

Romero, Michael F.; Henry, Darin; Nelson, Stephanie; Harte, Peter J.; Dillon, Alison K.; Sciortino, Christopher M.

doi:10.1074/jbc.m003476200

Cited by 113 publications

(118 citation statements)

References 38 publications

(43 reference statements)

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“…These properties are similar to those of the Na ϩ -driven Cl Ϫ /HCO 3 Ϫ exchanger described in native cells (14,16,(27)(28)(29), indicating that the cloned NCBE is a Na ϩ -driven Cl Ϫ / HCO 3 Ϫ exchanger. The functional properties of NCBE are different from those of the recently identified Drosophila NDAE1, which does not require HCO 3 Ϫ for transport activity (30). Expression of NCBE mRNA in insulin-secreting cell line MIN6 and pancreatic islets implies its physiological relevance.…”

Section: Namentioning

confidence: 87%

The Na+-driven Cl−/HCO3−Exchanger

Wang¹,

Yano

Nagashima³

et al. 2000

Journal of Biological Chemistry

131

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Section: Namentioning

confidence: 87%

The Na+-driven Cl−/HCO3−Exchanger

Wang¹,

Yano

Nagashima³

et al. 2000

Journal of Biological Chemistry

131

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“…studied 3-6 days after injection. Oocyte expression of SLC5A8 was verified by immunolocalization of the V5-tag , and oocyte electrophysiology experiments were carried out as described (12) and as detailed in Supporting Materials and Methods.…”

Section: Methodsmentioning

confidence: 99%

SLC5A8 , a sodium transporter, is a tumor suppressor gene silenced by methylation in human colon aberrant crypt foci and cancers

Myeroff

Smiraglia

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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268

254

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We identify a gene, SLC5A8, and show it is a candidate tumor suppressor gene whose silencing by aberrant methylation is a common and early event in human colon neoplasia. Aberrant DNA methylation has been implicated as a component of an epigenetic mechanism that silences genes in human cancers. Using restriction landmark genome scanning, we performed a global search to identify genes that would be aberrantly methylated at high frequency in human colon cancer. From among 1,231 genomic NotI sites assayed, site 3D41 was identified as methylated in 11 of 12 colon cancers profiled. Site 3D41 mapped to exon 1 of SLC5A8, a transcript that we assembled. In normal colon mucosa we found that SLC5A8 exon 1 is unmethylated and SLC5A8 transcript is expressed. In contrast, SLC5A8 exon 1 proved to be aberrantly methylated in 59% of primary colon cancers and 52% of colon cancer cell lines. SLC5A8 exon 1 methylated cells were uniformly silenced for SLC5A8 expression, but reactivated expression on treatment with a demethylating drug, 5-azacytidine. Transfection of SLC5A8 suppressed colony growth in each of three SLC5A8-deficient cell lines, but showed no suppressive effect in any of three SLC5A8-proficient cell lines. SLC5A8 exon 1 methylation is an early event, detectable in colon adenomas, and in even earlier microscopic colonic aberrant crypt foci. Structural homology and functional testing demonstrated that SLC5A8 is a member of the family of sodium solute symporters, which are now added as a class of candidate colon cancer suppressor genes.colon cancer

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“…Because Slc4a8 appeared to be broadly expressed in neurons, and sodium-dependent chloride-bicarbonate exchangers had repeatedly been proposed to be key regulators of neuronal pH i (Russell and Boron, 1976;Schwiening and Boron, 1994;Bevensee et al, 1996;Romero et al, 2000), we investigated the role of Slc4a8 in neuronal pH homeostasis by BCECF fluorescence imaging of cultured hippocampal neurons from KO and WT mice. In bicarbonate-buffered solutions, the resting pH i of KO neurons was significantly lower compared with WT ( Fig.…”

Section: Slc4a8 Is Important For the Regulation Of Ph I In Hippocampamentioning

confidence: 99%

Synaptic Glutamate Release Is Modulated by the Na⁺-Driven Cl⁻/HCO₃⁻Exchanger Slc4a8

Sinning

Liebmann²,

Kougioumtzes³

et al. 2011

J. Neurosci.

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On the one hand, neuronal activity can cause changes in pH; on the other hand, changes in pH can modulate neuronal activity. Consequently, the pH of the brain is regulated at various levels. Here we show that steady-state pH and acid extrusion were diminished in cultured hippocampal neurons of mice with a targeted disruption of the Na ϩ -driven Cl Ϫ /HCO 3 Ϫ exchanger Slc4a8. Because Slc4a8 was found to predominantly localize to presynaptic nerve endings, we hypothesize that Slc4a8 is a key regulator of presynaptic pH. Supporting this hypothesis, spontaneous glutamate release in the CA1 pyramidal layer was reduced but could be rescued by increasing the intracellular pH. The reduced excitability in vitro correlated with an increased seizure threshold in vivo. Together with the altered kinetics of stimulated synaptic vesicle release, these data suggest that Slc4a8 modulates glutamate release in a pH-dependent manner.

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Cloning and Characterization of a Na+-driven Anion Exchanger (NDAE1)

Abstract: Regulation of intra-and extracellular ion activities

Cited by 113 publications

References 38 publications

The Na+-driven Cl−/HCO3−Exchanger

The Na+-driven Cl−/HCO3−Exchanger

SLC5A8 , a sodium transporter, is a tumor suppressor gene silenced by methylation in human colon aberrant crypt foci and cancers

Synaptic Glutamate Release Is Modulated by the Na⁺-Driven Cl⁻/HCO₃⁻Exchanger Slc4a8

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Cloning and Characterization of a Na+-driven Anion Exchanger (NDAE1)

Abstract: Regulation of intra-and extracellular ion activities

Cited by 113 publications

References 38 publications

The Na+-driven Cl−/HCO3−Exchanger

The Na+-driven Cl−/HCO3−Exchanger

SLC5A8 , a sodium transporter, is a tumor suppressor gene silenced by methylation in human colon aberrant crypt foci and cancers

Synaptic Glutamate Release Is Modulated by the Na+-Driven Cl−/HCO3−Exchanger Slc4a8

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Synaptic Glutamate Release Is Modulated by the Na⁺-Driven Cl⁻/HCO₃⁻Exchanger Slc4a8