PROK2

Chr 3ADAR

prokineticin 2

Also known as: BV8, HH4, KAL4, MIT1, PK2

This gene encodes prokineticin 2, a secreted protein that functions as an output molecule from the suprachiasmatic nucleus to transmit circadian behavioral rhythms and also contracts gastrointestinal smooth muscle. Mutations cause hypogonadotropic hypogonadism with or without anosmia (Kallmann syndrome), involving defective puberty and often absent sense of smell. The condition shows both autosomal dominant and autosomal recessive inheritance patterns.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

Hypogonadotropic hypogonadism 4 with or without anosmiaMIM #610628
ADAR
0
Active trials
25
Pubs (1 yr)
38
P/LP submissions
16%
P/LP missense
1.65
LOEUF
DN
Mechanism· predicted
Clinical SummaryPROK2
🧬
Gene-Disease Validity (ClinGen)
hypogonadotropic hypogonadism 4 with or without anosmia · SDDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.01) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
25 unique Pathogenic / Likely Pathogenic· 47 VUS of 114 total submissions
📖
GeneReview available — PROK2
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.65LOEUF
pLI 0.014
Z-score 0.59
OE 0.69 (0.311.65)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.26Z-score
OE missense 1.10 (0.901.35)
64 obs / 58.4 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.69 (0.311.65)
00.351.4
Missense OE1.10 (0.901.35)
00.61.4
Synonymous OE0.69
01.21.6
LoF obs/exp: 3 / 4.3Missense obs/exp: 64 / 58.4Syn Z: 1.05
DN
0.75top 25%
GOF
0.5857th %ile
LOF
0.3260th %ile

The highest-scoring mechanism for this gene is dominant-negative.

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

114 submitted variants in ClinVar

Classification Summary

Pathogenic17
Likely Pathogenic8
VUS47
Likely Benign24
Benign10
Conflicting5
17
Pathogenic
8
Likely Pathogenic
47
VUS
24
Likely Benign
10
Benign
5
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
1
15
0
17
Likely Pathogenic
4
3
1
0
8
VUS
2
33
11
1
47
Likely Benign
0
2
15
7
24
Benign
0
1
9
0
10
Conflicting
5
Total740518111

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

View in ClinVar →

Protein Context — Lollipop Plot

PROK2 · protein map & ClinVar variants

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

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗