Anti-SLC9A1 monoclonal antibody (DCABH-1851)


Host Species
Antibody Isotype
Species Reactivity
Synthetic peptide, corresponding to residues in the extracellular domain of Human Sodium/ Hydrogen Exchanger 1 (UniProt P19634).


Application Notes
WB: 1/1000 - 1/10000.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
SLC9A1; solute carrier family 9, subfamily A (NHE1, cation proton antiporter 1), member 1; APNH, NHE1, solute carrier family 9 (sodium/hydrogen exchanger), isoform 1 (antiporter, Na+/H+, amiloride sensitive) , solute carrier family 9 (sodium/hydrogen ex
Entrez Gene ID
UniProt ID

Product Background

Bile secretion, organism-specific biosystem; Bile secretion, conserved biosystem; Cardiac muscle contraction, organism-specific biosystem; Cardiac muscle contraction, conserved biosystem; Endothelins, organism-specific biosystem; ErbB1 downstream signaling, organism-specific biosystem; G Protein Signaling Pathways, organism-specific biosystem;


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Custom Antibody Labeling

We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Contribution of Na+,HCO3--cotransport to cellular pH control in human breast cancer: A role for the breast cancer susceptibility locus NBCn1 (SLC4A7)


Authors: Boedtkjer, Ebbe; Moreira, Jose M. A.; Mele, Marco; Vahl, Pernille; Wielenga, Vera T.; Christiansen, Peer M.; Jensen, Vibeke E. D.; Pedersen, Stine F.; Aalkjaer, Christian

Genome-wide association studies recently linked the locus for Na+,HCO3--cotransporter NBCn1 (SLC4A7) to breast cancer susceptibility, yet functional insights have been lacking. To determine whether NBCn1, by transporting HCO3- into cells, may dispose of acid produced during high metabolic activity, we studied the expression of NBCn1 and the functional impact of Na+,HCO3--cotransport in human breast cancer. We found that the plasmalemmal density of NBCn1 was 2030% higher in primary breast carcinomas and metastases compared to matched normal breast tissue. The increase in NBCn1 density was similar in magnitude to that observed for Na+/H+-exchanger NHE1 (SLC9A1), a transporter previously implicated in cell migration, proliferation and malignancy. In primary breast carcinomas, the apparent molecular weight for NBCn1 was increased compared to normal tissue. Using pH-sensitive fluorophores, we showed that Na+,HCO3--cotransport is the predominant mechanism of acid extrusion and is inhibited 34 +/- 9% by 200 mu M 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid in human primary breast carcinomas. At intracellular pH (pHi) levels >6.6, CO2/HCO3--dependent mechanisms accounted for >90% of total net acid extrusion. Na+/H+-exchange activity was prominent only at lower pHi-values. Furthermore, steady-state pHi was 0.35 +/- 0.06 units lower in the absence than in the presence of CO2/HCO3-. In conclusion, expression of NBCn1 is upregulated in human primary breast carcinomas and metastases compared to normal breast tissue. Na+,HCO3--cotransport is a major determinant of pHi in breast cancer and the modest DIDS-sensitivity is consistent with NBCn1 being predominantly responsible. Hence, our results suggest a major pathophysiological role for NBCn1 that may be clinically relevant.

NHE1 deficiency in liver: Implications for non-alcoholic fatty liver disease


Authors: Prasad, Vikram; Chirra, Shivani; Kohli, Rohit; Shull, Gary E.

Non-alcoholic fatty liver disease NAFLD is closely associated with the dysregulation of lipid homeostasis. Diet-induced hepatic steatosis, which can initiate NAFLD progression, has been shown to be dramatically reduced in mice lacking the electroneutral Na+/H+ exchanger NHE1 (Slc9a1). In this study, we investigated if NHE1 deficiency had effects in liver that could contribute to the apparent protection against aberrant lipid accumulation. RT-PCR and immunoblot analyses of wild-type and NHE1-null livers revealed an expression profile that strongly suggested attenuation of both de nova lipogenesis and hepatic stellate cell activation, which is implicated in liver fibrosis. This included upregulation of the farnesoid X receptor FXR, peroxisome proliferator-activated receptor PPAR gamma, its co-activator PGC1 alpha, and sestrin 2, an antioxidant protein involved in hepatic metabolic homeostasis. Furthermore, expression levels of the pro-lipogenic liver X receptor LXR alpha, and acetyl CoA carboxylases 1 and 2 were downregulated. These changes were associated with evidence of reduced cellular stress, which persisted even upon exposure to a high-fat diet, and the better preservation of insulin signaling, as evidenced by protein kinase B/Akt phosphorylation (Ser473). These results indicate that NHE1 deficiency may protect against NAFLD pathogenesis, which is significant given the availability of highly specific NHE1 inhibitors. (C) 2014 Elsevier Inc. All rights reserved.

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