PTTG1IP

Chr 21

PTTG1 interacting protein

Also known as: C21orf1, C21orf3, PBF, PTTG1IP1

The protein facilitates nuclear translocation of pituitary tumor-transforming 1 protein (PTTG1) and induces transcriptional activation of basic fibroblast growth factor. Mutations cause autosomal recessive pituitary hormone deficiency, dwarfism, and cortisol deficiency, affecting the endocrine system. The gene shows tolerance to loss-of-function variants with low constraint metrics.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
6
Pubs (1 yr)
92
P/LP submissions
0%
P/LP missense
1.08
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryPTTG1IP
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
87 unique Pathogenic / Likely Pathogenic· 40 VUS of 143 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.08LOEUF
pLI 0.005
Z-score 1.40
OE 0.51 (0.271.08)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.05Z-score
OE missense 0.98 (0.831.17)
96 obs / 97.5 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.51 (0.271.08)
00.351.4
Missense OE0.98 (0.831.17)
00.61.4
Synonymous OE1.15
01.21.6
LoF obs/exp: 5 / 9.7Missense obs/exp: 96 / 97.5Syn Z: -0.73
DN
0.79top 25%
GOF
0.76top 25%
LOF
0.2287th %ile

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

DNprediction above median
GOFprediction 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

143 submitted variants in ClinVar

Classification Summary

Pathogenic83
Likely Pathogenic4
VUS40
Likely Benign2
Benign1
Conflicting1
83
Pathogenic
4
Likely Pathogenic
40
VUS
2
Likely Benign
1
Benign
1
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
83
0
83
Likely Pathogenic
0
0
4
0
4
VUS
0
24
16
0
40
Likely Benign
0
1
1
0
2
Benign
0
1
0
0
1
Conflicting
1
Total0261040131

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

View in ClinVar →

Protein Context — Lollipop Plot

PTTG1IP · 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
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