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Renal reabsorptive and orphan transporters in the SLC22 family

Award Number: R35GM163909
ORGANIZATION: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/01/2026
PERIOD OF PERFORMANCE END DATE: 03/31/2031

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Renal reabsorptive and orphan transporters in the SLC22 family - SUMMARY/ ABSTRACT: Renal Reabsorptive and Orphan Transporters in the SLC22 Family Membrane transporters in the SoLute Carrier family 22 (SLC22, the Organic Ion Transporter family) are known to play critical roles in pharmacology and physiology. Notably, many of the 30 transporters in the SLC22 family are expressed in the kidney, and appear to play a role in renal handling of organic solutes. Reabsorption of drugs in the kidney is thought to occur primarily through passive mechanisms and in particular, nonionic diffusion driven by a drug’s concentration gradient from renal tubule to plasma.11 Few studies have focused on transporter-mediated reabsorption of drugs via SLC22 family members 11-13. In this MIRA research proposal, we will continue our highly recognized research efforts focused on the SLC22 family including our successful research deorphaning SLC22 family members. In particular, we will study four poorly studied renal transporters in the family: SLC22A11, SLC22A17, SLC22A18 and SLC22A24. Two of these transporters, SLC22A17 and SLC22A18 are orphan transporters, with no known substrates. The remaining two transporters (SLC22A11 and SLC22A24) have been localized to the apical membrane of the renal tubule and appear to play a role in reabsorption of their substrates. The overall goal of studies in this MIRA proposal is to continue our highly successful research program exploring transporters in the SLC22 family. In particular, we will elucidate the substrate specificities and the functional roles of SLC22 family transporters in the kidney with a particular focus on the poorly studied transporters, SLC22A11, SLC22A17, SLC22A18 and SLC22A24. Three key questions will be addressed: (1) Do OAT4 and SLC22A24 play key roles in the renal reabsorption and recycling of sulfate and glucuronide conjugates of steroids? (2) What are the molecular determinants of substrate recognition, binding and release of OAT4 and SLC22A24? (3) What are the substrates, inhibitors and biological roles of the orphan transporters, SLC22A17 and SLC22A18, in the kidney? To address these questions, we will use a variety of experimental and computational methods. These include: (i) analyzing publicly available metabolomic-genomewide association data; (ii) a host of functional genomic assays including metabolomic and kinetic studies in cells recombinantly expressing human SLC22 family members, and confocal microscopy of GFP-chimera transporters; and (iii) phylogenetic analysis and comparative structural modeling to uncover new ligands for orphan transporters. These comprehensive genomic, metabolomic and functional studies will serve as a blueprint for the systematic evaluation of the physiological and pharmacological roles of poorly explored transporters in the SLC22 family in the kidney.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $495,280 )
2026	2026	REGENTS OF THE UNIVERSITY OF CALIFORNIA, SAN FRANCISCO, THE	1855 FOLSOM ST STE 425	SAN FRANCISCO	CA	94103	SAN FRANCISCO	USA	Biomedical Research and Research Training	000	1	6/24/2026	NEW	$495,280
														Subtotal = $495,280

Grand Total All Awards = $495,280

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Renal reabsorptive and orphan transporters in the SLC22 family

Award Number: R35GM163909

ORGANIZATION: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 07/01/2026

PERIOD OF PERFORMANCE END DATE: 03/31/2031

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