PLEKHF1

Chr 19

pleckstrin homology and FYVE domain containing 1

Also known as: APPD, LAPF, PHAFIN1, ZFYVE15

The protein binds phosphatidylinositol phosphates and regulates endosome organization, autophagy, and protein trafficking to the plasma membrane, while also participating in lysosomal-mitochondrial apoptotic pathways. Mutations cause autosomal recessive spastic paraplegia with intellectual disability and seizures, typically presenting in early childhood. The gene shows tolerance to loss-of-function variants (low constraint), which is consistent with its recessive inheritance pattern.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
5
Pubs (1 yr)
13
P/LP submissions
0%
P/LP missense
1.16
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryPLEKHF1
Population Constraint (gnomAD)
Low constraint (pLI 0.01) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
13 unique Pathogenic / Likely Pathogenic· 53 VUS of 78 total submissions
Some data sources returned errors (1)

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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.16LOEUF
pLI 0.013
Z-score 1.28
OE 0.51 (0.251.16)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.19Z-score
OE missense 0.96 (0.851.08)
193 obs / 200.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.51 (0.251.16)
00.351.4
Missense OE0.96 (0.851.08)
00.61.4
Synonymous OE0.84
01.21.6
LoF obs/exp: 4 / 7.9Missense obs/exp: 193 / 200.5Syn Z: 1.28
DN
0.6745th %ile
GOF
0.7028th %ile
LOF
0.3067th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median
DNprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

78 submitted variants in ClinVar

Classification Summary

Pathogenic10
Likely Pathogenic3
VUS53
Likely Benign3
Benign3
Conflicting1
10
Pathogenic
3
Likely Pathogenic
53
VUS
3
Likely Benign
3
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
10
0
10
Likely Pathogenic
0
0
3
0
3
VUS
0
49
4
0
53
Likely Benign
0
2
0
1
3
Benign
0
0
0
3
3
Conflicting
1
Total05117473

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

PLEKHF1 · 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

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
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