High-throughput screening of mouse gene knockouts identifies established and novel skeletal phenotypes.
The Woodlands, United States. In Bone Res, 2013
Together, these screens identified multiple genes affecting bone mass: 23 previously reported genes (Calcr, Cebpb, Crtap, Dcstamp, Dkk1, Duoxa2, Enpp1, Fgf23, Kiss1/Kiss1r, Kl (Klotho), Lrp5, Mstn, Neo1, Npr2, Ostm1, Postn, Sfrp4, Slc30a5, Slc39a13, Sost, Sumf1, Src, Wnt10b), five novel genes extensively characterized (Cldn18, Fam20c, Lrrk1, Sgpl1, Wnt16), five novel genes with preliminary characterization (Agpat2, Rassf5, Slc10a7, Slc26a7, Slc30a10) and three novel undisclosed genes coding for potential osteoporosis drug targets.
The SLC26 gene family of anion transporters and channels.
Boston, United States. In Mol Aspects Med, 2013
Additional disease phenotypes evident only in mouse knockout models include oxalate urolithiasis for Slc26a6 and Slc26a1, non-syndromic deafness for Slc26a5, gastric hypochlorhydria for Slc26a7 and Slc26a9, distal renal tubular acidosis for Slc26a7, and male infertility for Slc26a8.
Anion transport by the cochlear motor protein prestin.
Hannover, Germany. In J Physiol, 2012
A comparison with a non-mammalian prestin from D. rerio - recently shown to function as Cl(-)/SO(4)(2-) antiporter - and an SLC26 anion channel, human SLC26A7, revealed that SCN(-) transport is conserved in these distinct members of the SLC26 family.
Renal physiology of SLC26 anion exchangers.
Boston, United States. In Curr Opin Nephrol Hypertens, 2007
Slc26a4 (pendrin) and Slc26a7 are expressed in intercalated cells, and are involved in acid-base homeostasis and blood pressure regulation.