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February 17, 2026PLoS GeneticsOpen Access

Correction: Lack of ANKMY2 suppresses kidney cystogenesis in embryonic- and adult-onset polycystic kidney disease

The PLOS Genetics Staff

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Key Points

This research aims to correct previous findings regarding the role of ANKMY2 in kidney cystogenesis in both embryonic and adult-onset polycystic kidney disease.
Correction of previously reported data
Analysis of the effects of ANKMY2 absence
Comparison of cyst formation in models of different onset types
Demonstrated that absence of ANKMY2 significantly reduces kidney cyst formation
Highlighted the difference in cystogenesis between embryonic and adult onset conditions

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Implication

This correction reveals that lack of ANKMY2 suppresses kidney cyst formation in polycystic kidney disease, indicating a potential therapeutic target.

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Cite This Study

The PLOS Genetics Staff (2026) studied this question.

synapsesocial.com/papers/6997f984ad1d9b11b3452575 https://doi.org/10.1371/journal.pgen.1012049

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Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Lack of ANKMY2 suppresses kidney cystogenesis in embryonic- and adult-onset polycystic kidney diseaseOriginal Research · 2025 · 5 citations
2Notch2 Inhibition and Kidney Cyst Growth in Autosomal Dominant Polycystic Kidney DiseaseOriginal Research · 2025 · 5 citations
3Anks3 mediates cilia dependent polycystin signaling and is essential for adult kidney homeostasisOriginal Research · 2025 · 4 citations
4Polycystin-1 C-terminal tail suppresses cystic phenotype in autosomal dominant polycystic kidney disease in a Pkd genotype-independent mannerReview · 2026
5Pkd1<sup>RC/RC</sup> mice demonstrate remodeling of purinergic receptors in ADPKD cysts2024

Inhibiting centrosome clustering reduces cystogenesis and improves kidney function in autosomal dominant polycystic kidney disease2024
Time-Dependent Regulation of Cystogenesis and Disease Severity by AMPK in Polycystic Kidney Disease Cells and Mice2024
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