PKD1

Chr 16AD

polycystin 1, transient receptor potential channel interacting

Also known as: PBP, PC1, Pc-1, TRPP1, eliosin

The encoded protein forms a heteromeric calcium-permeable ion channel with PKD2 that regulates intracellular calcium homeostasis, controls cilium length in renal epithelium, and is involved in fluid-flow mechanosensation and renal tubulogenesis. Mutations cause autosomal dominant polycystic kidney disease type 1, characterized by progressive growth of fluid-filled cysts that replace normal renal tissue and lead to end-stage renal failure. This gene is extremely intolerant to loss-of-function variants (pLI ~1.0, LOEUF 0.179), indicating high biological constraint.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismADLOEUF 0.182 OMIM phenotypes
Clinical SummaryPKD1
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Gene-Disease Validity (ClinGen)
autosomal recessive polycystic kidney disease · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

2 total gene-disease associations curated

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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Clinical Trials
6 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — PKD1
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.18LOEUF
pLI 1.000
Z-score 9.96
OE 0.12 (0.080.18)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
-4.32Z-score
OE missense 1.23 (1.201.27)
3329 obs / 2697.2 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.12 (0.080.18)
00.351.4
Missense OE1.23 (1.201.27)
00.61.4
Synonymous OE1.63
01.21.6
LoF obs/exp: 18 / 149.4Missense obs/exp: 3329 / 2697.2Syn Z: -17.86
DN
0.4190th %ile
GOF
0.6052th %ile
LOF
0.59top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function, gain-of-function and dominant-negative). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOF1 literature citation · LOEUF 0.18
GOF1 literature citation
DN1 literature citation

Literature Evidence

DNIn the present study, we report the generation of transgenic mice with inducible conditional expression of a dominant-negative PKD1kd (kinase-dead PKD1) protein in skeletal muscle to assess the role of PKD in muscle function.PMID:21848513
GOFThis study not only produced an invaluable and first PKD model to evaluate molecular pathogenesis and therapies but also provides evidence that gain of function could be a pathogenetic mechanism in ADPKD.PMID:16449663
LOFAn Mekk1-p53 interaction at the PKD1 promoter suggests a new mechanism by which abnormally elevated stress-pathway stimuli might directly down-regulate the PKD1 gene, possibly causing haploinsufficiency and cyst formation.PMID:20923779

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

PKD1 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

Clinical Literature
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