ALG9-associated autosomal dominant polycystic kidney disease

disease
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Also known as ALG9 autosomal dominant polycystic kidney diseaseALG9 related autosomal dominant polycystic kidney diseaseALG9-associated ADPKDAutosomal Dominant Polycystic Kidney Disease - ALG9autosomal dominant polycystic kidney disease caused by mutation in ALG9

Summary

ALG9-associated autosomal dominant polycystic kidney disease (MONDO:0700000) is a disease caused by ALG9 (GenCC Strong), with 1 cohort gene.

At a glance

  • Causal gene: ALG9 (GenCC Strong)
  • Cohort genes: 1
  • ClinVar variants: 9

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

FieldValue
Canonical nameALG9-associated autosomal dominant polycystic kidney disease
Mondo IDMONDO:0700000
GARD0026304
Is cancer (heuristic)no

Also known as: ALG9 autosomal dominant polycystic kidney disease · ALG9 related autosomal dominant polycystic kidney disease · ALG9-associated ADPKD · ALG9-associated autosomal dominant polycystic kidney disease · Autosomal Dominant Polycystic Kidney Disease - ALG9 · autosomal dominant polycystic kidney disease caused by mutation in ALG9

Data availability: 9 ClinVar variants · 1 GenCC gene-disease record.

Disease family

Classification path: disease › human disease › disease by etiologic mechanism › disease of genetic or genomic mechanism › hereditary disease › autosomal genetic disease › autosomal dominant disease › autosomal dominant polycystic kidney diseaseALG9-associated autosomal dominant polycystic kidney disease

Related subtypes (6): polycystic kidney disease 1, polycystic kidney disease 3 with or without polycystic liver disease, polycystic kidney disease 2, polycystic kidney disease 7, polycystic kidney disease 6 with or without polycystic liver disease, polycystic kidney disease 8

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

ClinVar germline variants

9 retrieved; paginated sample, class counts are floors:

2 pathogenic/likely pathogenic, 2 likely pathogenic, 2 pathogenic, 2 uncertain significance, 1 conflicting classifications of pathogenicity

ClinVarVariant (HGVS)GeneClassificationReview
2443122NM_024740.2(ALG9):c.1225del (p.Arg409fs)ALG9Pathogenic/Likely pathogeniccriteria provided, multiple submitters, no conflicts
3345062NM_024740.2(ALG9):c.1163_1164del (p.Ser388fs)ALG9Pathogeniccriteria provided, single submitter
4531701NM_024740.2(ALG9):c.1534G>T (p.Gly512Ter)ALG9Pathogeniccriteria provided, single submitter
4705323NM_024740.2(ALG9):c.427C>T (p.Arg143Ter)ALG9Pathogenic/Likely pathogeniccriteria provided, multiple submitters, no conflicts
2633266NM_024740.2(ALG9):c.522del (p.Ala175fs)ALG9Likely pathogeniccriteria provided, single submitter
4531721NM_024740.2(ALG9):c.213T>A (p.Cys71Ter)ALG9Likely pathogeniccriteria provided, single submitter
1314309NM_024740.2(ALG9):c.1363C>T (p.Arg455Ter)ALG9Conflicting classifications of pathogenicitycriteria provided, conflicting classifications
4531711NM_024740.2(ALG9):c.1109G>T (p.Arg370Ile)ALG9Uncertain significancecriteria provided, single submitter
523889NM_024740.2(ALG9):c.1780C>T (p.Gln594Ter)ALG9Uncertain significancecriteria provided, multiple submitters, no conflicts

Genes & proteins

Mendelian disease overlap and somatic drivers

GenCC: 10 · Orphanet: 2 · OMIM-shared: 0 · Dual-evidence (GWAS+Mendelian): 0

GenCC gene–disease validity (cohort genes)

the Disease column is the GenCC-asserted condition — a cohort gene’s strongest validity may be for a related predisposition syndrome.

GeneClassificationInheritanceDiseaseRecords
ALG9StrongAutosomal recessiveALG9-congenital disorder of glycosylation10

Orphanet rare-disease linkage (cohort genes)

GeneOrphanet IDRare disease
ALG9Orphanet:730Autosomal dominant polycystic kidney disease
ALG9Orphanet:79328ALG9-CDG

Cohort genes → proteins

1 cohort genes, 1 distinct canonical proteins.

Evidence partition

SubsetGenes
multi_evidence1

Cohort genes (full)

SymbolHGNCEnsemblUniProtNameEvidence
ALG9HGNC:15672ENSG00000086848Q9H6U8Alpha-1,2-mannosyltransferase ALG9gencc,clinvar

Cohort function summary

Lead sentence per gene, UniProt-curated.

SymbolProtein nameFunction (lead sentence)
ALG9Alpha-1,2-mannosyltransferase ALG9Mannosyltransferase that operates in the biosynthetic pathway of dolichol-linked oligosaccharides, the glycan precursors employed in protein asparagine (N)-glycosylation.

Protein-family classification

Druggable: 1 · Difficult: 0 · Unknown: 0 · Druggable fraction: 1.0

Family distribution

Cohort families vs a genome-wide background (hypergeometric, BH-FDR; fold = observed/expected). Counts kept; sorted by enrichment, so the catch-all Other/Unknown bucket no longer leads.

FamilyGenesFoldFDR
Enzyme (other)112.0×0.083

Per-gene assignment

SymbolFamilyDruggable?ECInterPro (top 3)
ALG9Enzyme (other)yes2.4.1.259GPI_mannosylTrfase

Expression context

Cohort genes with no expression data: 0.

1 cohort gene are a single-cell marker in ≥1 SCXA experiment.

Breadth distribution (Bgee present_calls)

BucketGenes
narrow (1-5 tissues)0
moderate (6-20)0
broad (>20)1
unknown0

Top tissues across cohort

TissueCohort genes
body of pancreas1
endothelial cell1
ganglionic eminence1

Per-gene tissue summary (top 30)

SymbolBgee breadthFANTOM5 breadthSCXATop tissues
ALG9240ubiquitousmarkerendothelial cell, body of pancreas, ganglionic eminence

Protein interactions among cohort

Intra-cohort edges: 0.

Hub genes (top 10 by interactor count)

SymbolInteractor count
ALG91,167

Structural data

PDB: 1 · AlphaFold-only: 0 · No structure: 0

Cohort genes with PDB structures (top 30)

SymbolUniProtPDB entries
ALG9Q9H6U82

Function

Pathway analysis

Distinct Reactome pathways touched by cohort: 9. Enrichment computed across 1 evidence-associated genes (1 with Reactome annotation).

Pathways by enrichment

Over-representation of cohort genes vs the genome-wide background (hypergeometric test, Benjamini-Hochberg FDR; fold = observed/expected over 1 annotated cohort genes). Counts and members are kept as ground-truth; sorted by enrichment.

PathwayCohort genesFoldFDRSample cohort genes
Defective ALG9 causes CDG-1l111420.0×8e-04ALG9
Diseases associated with N-glycosylation of proteins1634.4×0.007ALG9
Biosynthesis of the N-glycan precursor (dolichol lipid-linked oligosaccharide, LLO) and transfer to a nascent protein1207.6×0.014ALG9
Diseases of glycosylation1131.3×0.017ALG9
Diseases of metabolism180.4×0.022ALG9
Asparagine N-linked glycosylation160.1×0.025ALG9
Post-translational protein modification119.2×0.067ALG9
Disease113.1×0.081ALG9
Metabolism of proteins112.4×0.081ALG9

GO biological processes by enrichment

Over-representation of cohort genes vs the genome-wide background (hypergeometric test, Benjamini-Hochberg FDR; fold = observed/expected over 1 annotated cohort genes). Counts and members are kept as ground-truth; sorted by enrichment.

GO termCohort genesFoldFDRSample cohort genes
dolichol-linked oligosaccharide biosynthetic process1842.6×0.002ALG9
protein N-linked glycosylation1263.3×0.004ALG9

Therapeutics

Drug target analysis

Approved (phase 4): 0 · Phase ≥3: 0 · Phased (≥1): 0 · Undrugged: 1

Druggability breadth: 0 of 1 evidence-associated genes (0%) have a ChEMBL target (buckets above are over the deeply-mined display cohort).

Top cohort targets by molecule count

SymbolMoleculesMax phase
ALG900

Bioactivity and enzyme data

Enzyme cohort genes (≥1 EC): 1.

Cohort enzymes (BRENDA EC)

SymbolEC numbersNames
ALG92.4.1.259, 2.4.1.261dolichyl-P-Man:Man6GlcNAc2-PP-dolichol alpha-1,2-mannosyltransferase, dolichyl-P-Man:Man8GlcNAc2-PP-dolichol alpha-1,2-mannosyltransferase

Pharmacogenomics

Cohort genes with a PharmGKB record: 1; with CPIC/DPWG dosing guidelines: 0.

No cohort gene has a CPIC/DPWG genotype-guided dosing guideline (PharmGKB).

Chemical tractability of cohort targets

0 approved/phased compounds have measured bioactivity against a cohort gene (and aren’t yet in disease-level trials). This is a research / tractability signal, NOT a therapeutic recommendation — a bioactivity row often reflects off-target or screening binding (e.g. promiscuous kinase inhibitors against a cohort kinase), implying no disease mechanism.

Druggability pyramid

Cohort genes binned by druggability tier (high → low):

TierDefinitionGenesSymbols
AApproved (phase 4 drug)0
BPhased (≥1) drug, not yet approved0
CDruggable family + PDB, no drug1ALG9
DDruggable family + AlphaFold only, no drug0
EDifficult family or no structure, no drug0

Undrugged target profiles

1 cohort genes are undrugged. Ranked by ‘starting-point quality’ (assay depth + drugged-partner adjacency).

SymbolChEMBL assaysDrugged partners (top 3)
ALG90

Clinical trials & evidence

Clinical trials

Clinical trials: 0.