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In the late 1980s, I expanded my studies of coupled ion transport to include the regulation of cation-chloride cotransporters, especially the K+/Cl– cotransporter (SLC12) in connection with red blood cell volume control. This work was supported by NIH R01 HL037479 for 10 years.
More recently I have focused on coupled ion transporters in relation to human disease, including the diastrophic dysplasia SO4= transporter DTDST (SLC26A2) and related SO4= transporters in S. cerevisiae. The yeast studies led to work on the sole S. cerevisiae SLC4 family member, which is a boric acid transporter. The boron transport work led to an R21 grant with Mark Parker of Case Western Reserve University on SLC4A11, which was reported to be a boron transporter. Mutations in SLC4A11 cause clouding of the cornea. Mark Parker and I were co-PI’s of the R21 but we agreed that he would continue the project as independent investigator, which he is now doing as a tenured faculty member at the University of Buffalo.
More recently I have focused on coupled ion transporters in relation to human disease, including the diastrophic dysplasia SO4= transporter DTDST (SLC26A2) and related SO4= transporters in S. cerevisiae. The yeast studies led to work on the sole S. cerevisiae SLC4 family member, which is a boric acid transporter. The boron transport work led to an R21 grant with Mark Parker of Case Western Reserve University on SLC4A11, which was reported to be a boron transporter. Mutations in SLC4A11 cause clouding of the cornea. Mark Parker and I were co-PI’s of the R21 but we agreed that he would continue the project as independent investigator, which he is now doing as a tenured faculty member at the University of Buffalo.
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