RGS19

Chr 20

regulator of G protein signaling 19

Also known as: GAIP, RGSGAIP

The protein functions as a regulator of G-protein signaling by increasing GTPase activity of G protein alpha subunits, thereby terminating G protein-mediated cellular signaling pathways. Mutations cause autosomal dominant neurodevelopmental disorders with intellectual disability and developmental delay. This gene is highly constrained against loss-of-function variants (pLI 0.96, LOEUF 0.30), indicating that complete protein loss is likely incompatible with normal development.

Summary from RefSeq, UniProt
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0
Active trials
4
Pubs (1 yr)
0
P/LP submissions
P/LP missense
0.29
LOEUF· LoF intol.
Mechanism
Clinical SummaryRGS19
Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 0.96). One damaged copy is likely sufficient to cause disease.

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.29LOEUF
pLI 0.961
Z-score 2.95
OE 0.00 (0.000.29)
Highly constrained

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

Missense Constraint
1.06Z-score
OE missense 0.76 (0.650.88)
114 obs / 150.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.00 (0.000.29)
00.351.4
Missense OE0.76 (0.650.88)
00.61.4
Synonymous OE1.14
01.21.6
LoF obs/exp: 0 / 10.1Missense obs/exp: 114 / 150.7Syn Z: -0.88

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

RGS19 · 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.

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Clinical Literature
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