RIPK4

Chr 21AR

receptor interacting serine/threonine kinase 4

Also known as: ANKK2, ANKRD3, CHANDS, DIK, NKRD3, PKK, PPS2, RIP4

RIPK4 encodes a serine/threonine protein kinase that phosphorylates plakophilin-1 to promote keratinocyte differentiation and cell adhesion, playing an essential role in embryonic skin development and adult skin homeostasis. Autosomal recessive mutations cause CHAND syndrome and Bartsocas-Papas type 1 popliteal pterygium syndrome, both severe developmental disorders affecting skin, limbs, and other organ systems. The gene is highly intolerant to loss-of-function variants (LOEUF 0.594), reflecting its critical developmental role.

Summary from RefSeq, OMIM, UniProt
Research Assistant →

Primary Disease Associations & Inheritance

CHAND syndromeMIM #214350
AR
Popliteal pterygium syndrome, Bartsocas-Papas type 1MIM #263650
AR
UniProtBartsocas-Papas syndrome
0
Active trials
12
Pubs (1 yr)
90
P/LP submissions
5%
P/LP missense
0.59
LOEUF
LOF
Mechanism· G2P
Clinical SummaryRIPK4
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.34) despite low pLI — interpret in context.
📋
ClinVar Variants
85 unique Pathogenic / Likely Pathogenic· 189 VUS of 412 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.59LOEUF
pLI 0.004
Z-score 3.15
OE 0.34 (0.200.59)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
1.89Z-score
OE missense 0.77 (0.710.83)
409 obs / 531.6 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.34 (0.200.59)
00.351.4
Missense OE0.77 (0.710.83)
00.61.4
Synonymous OE1.11
01.21.6
LoF obs/exp: 9 / 26.5Missense obs/exp: 409 / 531.6Syn Z: -1.31
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveRIPK4-related popliteal pterygium syndrome, lethal typeLOFAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.6842th %ile
GOF
0.74top 25%
LOF
0.3356th %ile

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

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

ClinVar Variant Classifications

412 submitted variants in ClinVar

Classification Summary

Pathogenic81
Likely Pathogenic4
VUS189
Likely Benign80
Benign41
Conflicting10
81
Pathogenic
4
Likely Pathogenic
189
VUS
80
Likely Benign
41
Benign
10
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
1
3
77
0
81
Likely Pathogenic
1
1
2
0
4
VUS
0
138
43
8
189
Likely Benign
0
14
24
42
80
Benign
0
2
27
12
41
Conflicting
10
Total215817362405

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

View in ClinVar →

Protein Context — Lollipop Plot

RIPK4 · 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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