PKD1 and PKD2 mRNA cis-inhibition drives polycystic kidney disease progression

Ronak Lakhia; Harini Ramalingam; Chun-Mien Chang; Patricia Cobo-Stark; Laurence Biggers; Andrea Flaten; Jesus Alvarez; Tania Valencia; Darren P. Wallace; Edmund C. Lee; Vishal Patel

doi:10.1038/s41467-022-32543-2

Nature Communications (Aug 2022)

PKD1 and PKD2 mRNA cis-inhibition drives polycystic kidney disease progression

Ronak Lakhia,
Harini Ramalingam,
Chun-Mien Chang,
Patricia Cobo-Stark,
Laurence Biggers,
Andrea Flaten,
Jesus Alvarez,
Tania Valencia,
Darren P. Wallace,
Edmund C. Lee,
Vishal Patel

Affiliations

Ronak Lakhia: Department of Internal Medicine, Nephrology, UT Southwestern Medical Center
Harini Ramalingam: Department of Internal Medicine, Nephrology, UT Southwestern Medical Center
Chun-Mien Chang: Department of Internal Medicine, Nephrology, UT Southwestern Medical Center
Patricia Cobo-Stark: Department of Internal Medicine, Nephrology, UT Southwestern Medical Center
Laurence Biggers: Department of Internal Medicine, Nephrology, UT Southwestern Medical Center
Andrea Flaten: Department of Internal Medicine, Nephrology, UT Southwestern Medical Center
Jesus Alvarez: Department of Internal Medicine, Nephrology, UT Southwestern Medical Center
Tania Valencia: Regulus Therapeutics Inc.
Darren P. Wallace: Department of Internal Medicine and the Jared Grantham Kidney Institute, University of Kansas Medical Center
Edmund C. Lee: Regulus Therapeutics Inc.
Vishal Patel: Department of Internal Medicine, Nephrology, UT Southwestern Medical Center

DOI: https://doi.org/10.1038/s41467-022-32543-2
Journal volume & issue: Vol. 13, no. 1
pp. 1 – 14

Abstract

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ADPKD, a common aetiology of kidney failure, is caused by heterozygous PKD1 or PKD2 mutations. Here the authors show that preventing 3′-UTR cis-inhibition of mRNAs produced by the non-inactivated PKD1/2 alleles ameliorates preclinical ADPKD.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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