RIT1

Chr 1AD

Ras like without CAAX 1

Also known as: NS8, RIBB, RIT, ROC1

The protein functions as a Ras-related GTPase that regulates p38 MAPK signaling cascades, promotes neuronal development and regeneration with nerve growth factor, and controls T-lymphocyte differentiation and survival during thymocyte development. Mutations cause Noonan syndrome 8, a multisystem disorder typically presenting in infancy with characteristic facial features, short stature, and cardiac abnormalities. Inheritance is autosomal dominant.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
GOFmechanismADLOEUF 0.651 OMIM phenotype
VCEP Guidelines: RASopathyReleased
View SpecificationsClinGen Panel
Clinical SummaryRIT1
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Gene-Disease Validity (ClinGen)
Noonan syndrome · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.28) despite low pLI — interpret in context.
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ClinVar Variants
37 unique Pathogenic / Likely Pathogenic· 117 VUS of 240 total submissions
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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — RIT1
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
0.65LOEUF
pLI 0.133
Z-score 2.51
OE 0.28 (0.140.65)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
2.08Z-score
OE missense 0.52 (0.430.63)
75 obs / 145.4 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.28 (0.140.65)
00.351.4
Missense OE0.52 (0.430.63)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 4 / 14.2Missense obs/exp: 75 / 145.4Syn Z: 0.09
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveRIT1-related Noonan syndromeGOFAD
DN
0.81top 10%
GOF
0.72top 25%
LOF
0.3261th %ile

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

GOFprediction above median · 1 literature citation · 73% of P/LP are missense
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.

Literature Evidence

GOFGain-of-function mutations in RIT1 cause Noonan syndrome, a RAS/MAPK pathway syndromePMID:23791108

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

240 submitted variants in ClinVar

Classification Summary

Pathogenic21
Likely Pathogenic16
VUS117
Likely Benign74
Benign4
Conflicting4
21
Pathogenic
16
Likely Pathogenic
117
VUS
74
Likely Benign
4
Benign
4
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
12
9
0
21
Likely Pathogenic
0
15
1
0
16
VUS
6
101
9
1
117
Likely Benign
0
0
29
45
74
Benign
0
1
2
1
4
Conflicting
4
Total61295047236

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

View in ClinVar →

Protein Context — Lollipop Plot

RIT1 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →