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Zaidman Lab
Principal Investigator
Nathan Zaidman, PhD
Assistant Professor, Biochemistry & Molecular Biology
Dr. Zaidman received his PhD in 2016 from the University of Minnesota under the mentorship of Scott M. O'Grady. He completed his postdoctoral fellowship with Jennifer Pluznick at Johns Hopkins University in 2022. He joined UNM Faculty in January 2023.
Interests
Techniques
Current Members
Krystin Eaton, BS – Research Technician
Hailey Steichen, MS – Research Scientist
Jianxiang Xue, PhD – Postdoctoral Fellow
Teagan Yan, BS – Research Assistant
Former Members
Sophia Slora – Summer UPN Scholar (2023)
Research Projects
The overarching goal of the Zaidman lab is to determine the physiological significance of adhesion-class G protein-coupled receptors (aGPCRs). aGPCRs are unique signaling proteins that are self-activated by tethered-peptide agonists. These receptors convey extracellular forces into intracellular chemical signals. However, many aGPCRs have undefined roles. Our current efforts are focused on illuminating the functional roles of aGPCRs Gpr116, Gpr56 and Gpr126 in the kidney.
Gpr116 (Adgrf5) localizes to A-type intercalated cells in the collecting ducts. Previous research revealed (PMID: 33004624) that genetic deletion of Gpr116 in mouse kidneys caused a significant reduction in urine pH due to physiologically inappropriate distribution of V-ATPase proton pumps on the surface of A-type cells. Our research goals are to identify the signaling pathway(s) downstream of Gpr116 that regulate V-ATPase surface expression in A-type intercalated cells, and to discover the endogenous activator of Gpr116 in the collecting duct.
Single-cell RNAseq experiments have revealed the expression pattern of several aGPCRs expressed throughout the kidney. Our goal is to determine the physiological significance of these receptors to better understand how the kidney maintains whole-body homeostasis and to develop novel therapeutic approaches to human disease.
Foxi1 is a master regulator of V-ATPase proton pumps, as numerous studies have demonstrated its essential role in the development of specialized acid-secreting cells in the inner ear, epididymis, lungs, and kidney. FOXI1 transcriptionally activates several V-ATPase subunits, including Atp6v1b1 and Atp6v0a4, that uniquely localize the proton pump to the plasma membrane. Indeed, mice lacking Foxi1 develop distal renal tubular acidosis due to the loss of these essential V-ATPase subunits in intercalated cells. In fact, intercalated cells are entirely absent in Foxi1 null animals. Mutations to Foxi1 are also associated with Pendred syndrome, one of the most frequent forms of syndromic genetic deafness. While the physiological and pathological significance of Foxi1 has been firmly established, the complete transcriptional targets of Foxi1 have not. We recently demonstrated (PMID: 36603001) that overexpression of Foxi1 in an immortalized murine collecting duct cell line causes upregulation of several target genes. Our goal is to define the complete Foxi1-dependent transcriptome using this in vitro heterologous expression system.
Research Opportunities
If you are interested in performing research with our group, please contact Dr. Zaidman directly.
Major Funding
NIH/NIDDK R00DK127215 (Zaidman)
“Gpr116 Regulation of Renal Acid Excretion”
Nathan Zaidman Lab
Biomedical Research Facility
Room 220
Department of Biochemistry and Molecular Biology
MSC08 4670
1 University of New Mexico
Albuquerque, NM 87131-0001
Phone: 505-277-0682
Fax: 505-272-6587
Email: nzaidman@salud.unm.edu
