Pulmonary hypertension, neonatal, susceptibility to: genes and variants

Pulmonary hypertension, neonatal, susceptibility to is linked to 1 analyzed protein (CPS1). 29 DNA variants are known to cause it; 27 more are uncertain, and 3 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Genes linked to Pulmonary hypertension, neonatal, susceptibility to

Known disease-causing variants in Pulmonary hypertension, neonatal, susceptibility to

VariantPositionProtein partClinical label
CPS1 R587H587ATP-grasp 1Disease-causing (★★)
CPS1 R587C587ATP-grasp 1Disease-causing (★★)
CPS1 R850H850Disease-causing (★★)
CPS1 R587L587ATP-grasp 1Disease-causing (★★)
CPS1 R803G803Disease-causing (★★)
CPS1 R850C850Disease-causing (★★)
CPS1 P265L265Glutamine amidotransferase type-1Disease-causing (★★)
CPS1 A438P438Disease-causing (★★)
CPS1 V457G457Disease-causing (★★)
CPS1 S913L913Disease-causing (★★)
CPS1 D914H914Disease-causing (★★)
CPS1 G987C987Disease-causing (★★)
CPS1 R1453Q1453MGS-likeDisease-causing (★★)
CPS1 T544M544Disease-causing (★★)
CPS1 Y959C959Disease-causing (★★)
CPS1 S1203P1203ATP-grasp 2Disease-causing (★★)
CPS1 R1453W1453MGS-likeDisease-causing (★★)
CPS1 R814W814Disease-causing (★★)
CPS1 V1187F1187ATP-grasp 2Disease-causing (★★)
CPS1 G301E301Glutamine amidotransferase type-1Disease-causing (★★)
CPS1 N716K716ATP-grasp 1Disease-causing (★★)
CPS1 R780H780Disease-causing (★★)
CPS1 K280N280Glutamine amidotransferase type-1Disease-causing (★★)
CPS1 P382L382Glutamine amidotransferase type-1Disease-causing (★★)
CPS1 R803H803Disease-causing (★)
CPS1 G79E79Anthranilate phosphoribosyltransferase homologDisease-causing (★)
CPS1 R174W174Anthranilate phosphoribosyltransferase homologDisease-causing (★)
CPS1 S918P918Disease-causing (★)
CPS1 A1378T1378MGS-likeDisease-causing (★)

Uncertain variants in Pulmonary hypertension, neonatal, susceptibility to that look disease-causing

VariantPositionProtein partClinical labelEvidence
CPS1 S1203L1203ATP-grasp 2Conflicting reports (★)+7: S1203P at the same position is pathogenic; seen in 6.8e-06 of gnomAD DNA copies; REVEL 0.966
CPS1 R803C803Conflicting reports (★)+6: 2 other pathogenic changes within 3 positions; R803H at the same position is pathogenic; REVEL 0.942
CPS1 R803S803Conflicting reports (★)+6: 2 other pathogenic changes within 3 positions; R803H at the same position is pathogenic; REVEL 0.930

Which prediction tools work for Pulmonary hypertension, neonatal, susceptibility to

How often each tool ranks a disease-causing variant above a harmless one (AUROC × 100).

Diseases related to Pulmonary hypertension, neonatal, susceptibility to

Frequently asked questions

Which genes are linked to Pulmonary hypertension, neonatal, susceptibility to?

In CATVariant, Pulmonary hypertension, neonatal, susceptibility to is linked to 1 analyzed protein: CPS1 (Carbamoyl-phosphate synthase [ammonia], mitochondrial).

How many genetic variants are linked to Pulmonary hypertension, neonatal, susceptibility to?

59 variants: 29 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 27 are of uncertain significance or have conflicting reports.

Which uncertain variants in Pulmonary hypertension, neonatal, susceptibility to look disease-causing?

3 uncertain variants reach the likely-pathogenic range of the ACMG/AMP points scale on computable evidence, for example CPS1 S1203L, CPS1 R803C and CPS1 R803S. These are leads for expert review, not diagnoses.

Which variant effect predictor works best for Pulmonary hypertension, neonatal, susceptibility to?

Among tools not trained on clinical labels, CADD separates this disease's known disease-causing variants from harmless ones best (AUROC 0.95, based on 28 disease-causing and 41 harmless variants).

About this data

Variant–disease links come from ClinVar, Open Targets and UniProt, pooled from the latest public CATVariant analysis of each human protein. Evidence scores use the ACMG/AMP Bayesian points scale with computable criteria only (position among known disease variants, rarity in gnomAD, calibrated predictors, deep mutational scanning); there is no family or patient data, so they prioritise variants for expert review and never classify them.

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