Gabriel Loeb, MD, PhD is a physician-scientist whose research and patient-care focuses on genetic kidney diseases.
The Loeb laboratory uses genetics to understand the mechanisms underlying common and rare forms of kidney disease. Our research focuses on two major areas: 1) using human common genetic variation to identify cellular and molecular drivers of chronic kidney disease and 2) identifying the molecular mediators of Autosomal Dominant Polycystic Kidney Disease. By integrating human genetics, novel kidney disease models, and genomics we are discovering essential regulators of kidney health to enable new therapies for people suffering from kidney disease.
In the UCSF Nephrology Faculty Practice, Dr. Loeb specializes in the care of individuals with familial and genetic forms of kidney disease.
Publications
ADPKD-Causing Missense Variants in Polycystin-1 Disrupt Cell Surface Localization or Polycystin Channel Function.
Deconvolution of Human Urine across the Transcriptome and Metabolome.
Variants in tubule epithelial regulatory elements mediate most heritable differences in human kidney function.
Current genomic deep learning models display decreased performance in cell type-specific accessible regions.
Cilia-enriched oxysterol 7β,27-DHC is required for polycystin ion channel activation.
Current genomic deep learning models display decreased performance in cell type specific accessible regions.
Variants in tubule epithelial regulatory elements mediate most heritable differences in human kidney function.
Multiomics characterization of cell type repertoires for urine liquid biopsies.
The Tabula Sapiens: A multiple-organ, single-cell transcriptomic atlas of humans.
The effect of cellular context on miR-155-mediated gene regulation in four major immune cell types.
Stage-specific regulation of natural killer cell homeostasis and response against viral infection by microRNA-155.
Transcriptome-wide miR-155 binding map reveals widespread noncanonical microRNA targeting.
Up-regulation of miR-21 by HER2/neu signaling promotes cell invasion.
Dicer loss in striatal neurons produces behavioral and neuroanatomical phenotypes in the absence of neurodegeneration.
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