VHL Gene Complete Identifier and Functional Mapping Reference

Provide a comprehensive cross-database identifier and functional mapping reference for human VHL — a definitive lookup resource covering: ### Section …

Provide a comprehensive cross-database identifier and functional mapping reference for human VHL — a definitive lookup resource covering: ### Section 1: Gene identifiers For human gene VHL, list ALL gene-level database identifiers. Required: - HGNC ID and approved symbol - Ensembl gene ID (ENSG...) - NCBI Entrez Gene ID - OMIM gene/locus ID - Genomic location: chromosome, start position, end position, strand (GRCh38) ### Section 2: Transcript identifiers For human gene VHL, list ALL transcript-level identifiers. Required: - Ensembl transcripts: ALL ENST IDs with biotype. Total count. - RefSeq transcripts: ALL NM_ mRNA accessions. Mark which is MANE Select. - CCDS IDs. - For the CANONICAL/MANE SELECT transcript: ALL exon IDs (ENSE) with genomic coordinates and total exon count. ### Section 3: Protein identifiers For human gene VHL protein product(s), list ALL protein-level identifiers. Required: - UniProt accessions: ALL entries (reviewed and unreviewed). Mark the canonical reviewed entry. - RefSeq protein: ALL NP_ accessions. - Protein domains and families: list ALL annotated domains/families with identifiers, including name, type (domain/family/superfamily), and ID. - Antibody availability: known antibody resources for the protein. ### Section 4: Structure For human gene VHL protein, list ALL structural data. Required: - Experimental structures: ALL PDB IDs. For each: experimental method (X-ray/NMR/Cryo-EM) and resolution. Total count. - Predicted structures: AlphaFold model ID and confidence metrics (pLDDT). ### Section 5: Cross-species orthologs For human gene VHL, list orthologous genes in key model organisms. Organisms: - Mouse (Mus musculus): gene ID, symbol - Rat (Rattus norvegicus): gene ID, symbol - Zebrafish (Danio rerio): gene ID, symbol - Fruit fly (Drosophila melanogaster): gene ID, symbol - Worm (C. elegans): gene ID, symbol - Yeast (S. cerevisiae): gene ID, symbol ### Section 6: Clinical variants & AI predictions For human gene VHL, summarize clinical variants and AI predictions. Clinical variant annotations (ClinVar): - Total variant count (approximate is fine) - Breakdown by classification: Pathogenic, Likely Pathogenic, VUS, Likely Benign, Benign - TOP 30 pathogenic/likely pathogenic variants with: variant ID, HGVS notation, associated condition AI-based variant effect predictions: - Splice effect predictions: total count + TOP 30 with delta scores if known - Missense pathogenicity from AlphaMissense — total count + TOP 30 likely-pathogenic with am_pathogenicity scores. ### Section 7: Pathways & Gene Ontology For human gene VHL, list biological pathways and Gene Ontology annotations. Pathway membership: - ALL biological pathways this gene participates in, with pathway IDs and names - Total pathway count Gene Ontology: - Biological Process: count and TOP 20 terms with GO IDs - Molecular Function: count and TOP 20 terms with GO IDs - Cellular Component: count and TOP 20 terms with GO IDs ### Section 8: Protein interactions & networks For human gene VHL protein, summarize protein interactions and networks. Protein-protein interactions (STRING, IntAct, BioGRID, etc.): - Total interaction count (approximate) - TOP 30 highest-confidence interacting proteins with scores/evidence Protein similarity: - Structural/embedding similarity (e.g. Foldseek, ESM): TOP 20 similar proteins with scores - Sequence homology: TOP 20 homologous proteins with identity/similarity ### Section 9: Transcription factor regulatory data For human gene VHL, summarize transcription factor regulatory data. If VHL is a transcription factor: - Downstream targets: total count + TOP 30 with regulation type (activates/represses) and evidence - DNA binding motifs from JASPAR — all known motif IDs and motif family classification. Regardless: - Upstream regulators: TFs that regulate VHL — names with evidence type (ChIP-seq / predicted / experimentally validated) If VHL is not a transcription factor, say so briefly and skip the downstream/motif sections. ### Section 10: Drug & pharmacology data For human gene VHL protein as a drug target, summarize pharmacology data. If VHL is a known drug target: - Targeting molecules: total count in ChEMBL/DrugBank + TOP 30 by development phase (molecule ID, name, mechanism, highest phase) - Clinical trials: TOP 20 involving drugs targeting this gene — trial ID, phase, status, intervention - Pharmacogenomics: known drug-gene interactions affecting drug response + dosing guidelines if any If VHL is not currently a drug target, say so briefly. ### Section 11: Expression profiles For human gene VHL, summarize expression profiles. Tissue expression (GTEx, HPA, Bgee, etc.): - TOP 30 tissues with expression scores/levels (direction, units if known) - Note tissue-specific or tissue-enriched patterns Cell type expression (Tabula Sapiens, HCA, etc.): - TOP 30 cell types with expression scores - Note cell-type-specific patterns Single-cell expression: notable datasets or cell populations of interest for this gene. ### Section 12: Disease associations For human gene VHL, summarize disease associations. Mendelian / monogenic disease: - Diseases caused by mutations in VHL: disease name, disease ID (OMIM/Orphanet/Mondo), inheritance pattern, evidence level - Include all directly linked conditions Phenotype associations: - Clinical phenotypes associated with the gene (HPO terms where known) - TOP 30 phenotype terms with HPO IDs Complex-disease / GWAS: - Traits and diseases significantly associated via GWAS: trait name, variant, effect size, study where known - TOP 30 GWAS associations

VHL

Executive summary

VHL (von Hippel-Lindau tumor suppressor, chromosome 3p25.3) is a critical E3 ubiquitin ligase adaptor whose principal function is targeting hypoxia-inducible factor alpha subunits (HIF-1α, HIF-2α) for oxygen-dependent proteasomal degradation; loss of this function drives pathological angiogenesis and tumor formation. Germline mutations cause autosomal dominant Von Hippel-Lindau syndrome, predisposing to clear cell renal cell carcinoma, hemangioblastomas, pheochromocytoma, and pancreatic neuroendocrine tumors, while a specific homozygous mutation causes autosomal recessive Chuvash polycythemia. The ClinVar record spans ~930 variants, with ~200 classified pathogenic or likely pathogenic; AlphaMissense predicts ~450–500 of 1,370 possible missense changes as likely pathogenic, with mutation hotspots concentrated in residues 63–130. VHL is ubiquitously expressed (186 present calls in Bgee, max score 94.86) but is particularly enriched in kidney, adrenal, retina, and CNS — the tissues most vulnerable in VHL disease. Therapeutically, the HIF-2α inhibitor belzutifan (Welireg) is the first approved agent with a VHL disease-specific indication, supported by 43 identified clinical trials.

Gene identifiers

  • HGNC ID: HGNC:12687
  • Approved symbol: VHL
  • Ensembl gene ID: ENSG00000134086
  • NCBI Entrez Gene ID: 7428
  • OMIM gene/locus ID: 608537
  • Genomic location (GRCh38):
    • Chromosome: 3
    • Start: 10,141,778
    • End: 10,153,676
    • Strand: +

Transcript identifiers

Ensembl transcripts (13 total)

ENST IDBiotype
ENST00000256474protein_coding
ENST00000345392protein_coding
ENST00000477538retained_intron
ENST00000696142nonsense_mediated_decay
ENST00000696143protein_coding
ENST00000696153protein_coding
ENST00000713811protein_coding
ENST00000713812protein_coding
ENST00000713813retained_intron
ENST00000713814nonsense_mediated_decay
ENST00000713815protein_coding
ENST00000713816protein_coding_CDS_not_defined
ENST00000713982protein_coding

RefSeq mRNA transcripts (8 total)

NM_ AccessionMANE Select
NM_000551
NM_001080684
NM_001273956
NM_001354723
NM_009507
NM_052801
NM_080247
NM_198156

CCDS identifiers

  • CCDS2597
  • CCDS2598
  • CCDS93209

MANE Select canonical transcript exons (ENST00000256474, 3 exons)

ENSE IDStartEndStrandChr
ENSE000019309741014177810142187+3
ENSE000040220561014651410146636+3
ENSE000040220571014978710153667+3

Protein identifiers

UniProt accessions

  • P40337 (canonical, reviewed) — von Hippel-Lindau disease tumor suppressor

RefSeq proteins (NP_ accessions)

  • NP_000542 (MANE Select, canonical)
  • NP_937799 (reviewed)

Protein domains and families

IDNameType
IPR022772VHL_tumour_suppress_b/a_domDomain
IPR024048VHL_alpha_domDomain
IPR024053VHL_beta_domDomain
IPR036208VHL_sfHomologous superfamily
IPR037139VHL_alpha_dom_sfHomologous superfamily
IPR037140VHL_beta_dom_sfHomologous superfamily
PF01847Pfam domain
PF17211Pfam domain

Antibody availability

No antibody resources found in biobtree for this protein.

Structure

Experimental Structures: 139 PDB Entries

X-Ray Crystallography (129 structures): 1LM8 (1.85 Å), 1LQB (2.0 Å), 1VCB (2.7 Å), 3ZRC (2.9 Å), 3ZRF (2.8 Å), 3ZTC (2.65 Å), 3ZTD (2.79 Å), 3ZUN (2.5 Å), 4AJY (1.73 Å), 4AWJ (2.5 Å), 4B95 (2.8 Å), 4B9K (2.0 Å), 4BKS (2.2 Å), 4BKT (2.35 Å), 4W9C (2.2 Å), 4W9D (2.2 Å), 4W9E (2.6 Å), 4W9F (2.1 Å), 4W9G (2.7 Å), 4W9H (2.1 Å), 4W9I (2.4 Å), 4W9J (2.2 Å), 4W9K (2.1 Å), 4W9L (2.2 Å), 4WQO (3.2 Å), 5LLI (2.4 Å), 5N4W (3.9 Å), 5NVV (2.1 Å), 5NVW (2.2 Å), 5NVX (2.2 Å), 5NVY (2.9 Å), 5NVZ (2.7 Å), 5NW0 (2.3 Å), 5NW1 (2.1 Å), 5NW2 (2.2 Å), 5T35 (2.7 Å), 6BVB (2.002 Å), 6FMI (2.8 Å), 6FMJ (2.45 Å), 6FMK (2.75 Å), 6GFX (1.83 Å), 6GFY (2.7 Å), 6GFZ (2.3 Å), 6GMN (1.94 Å), 6GMQ (2.755 Å), 6GMR (1.75 Å), 6GMX (2.533 Å), 6HAX (2.35 Å), 6HAY (2.24 Å), 6HR2 (1.76 Å), 6I7Q (1.798 Å), 6I7R (1.949 Å), 6SIS (3.5 Å), 6ZHC (1.92 Å), 7CJB (2.8 Å), 7JTO (1.7 Å), 7JTP (2.12 Å), 7KHH (2.281 Å), 7PI4 (2.24 Å), 7Q2J (2.5 Å), 7S4E (2.25 Å), 7Z6L (2.24 Å), 7Z76 (1.32 Å), 7Z77 (1.97 Å), 7ZNT (3.0 Å), 8BB2 (2.05 Å), 8BB3 (1.8 Å), 8BB4 (2.8 Å), 8BB5 (2.2 Å), 8BDI (2.108 Å), 8BDJ (2.02 Å), 8BDL (2.295 Å), 8BDM (2.021 Å), 8BDN (2.76 Å), 8BDO (2.8 Å), 8BDS (1.72 Å), 8BDT (2.7 Å), 8BDX (2.93 Å), 8BEB (3.18 Å), 8C13 (2.3 Å), 8CQE (2.85 Å), 8CQK (2.62 Å), 8CQL (2.38 Å), 8EI3 (3.49 Å), 8EWV (3.4 Å), 8FY0 (2.94 Å), 8FY1 (2.56 Å), 8FY2 (2.98 Å), 8G1P (2.7 Å), 8G1Q (3.73 Å), 8P0F (1.98 Å), 8PC2 (2.8 Å), 8QJR (3.17 Å), 8QJS (3.191 Å), 8QVU (2.24 Å), 8QW6 (2.2 Å), 8QW7 (2.36 Å), 8VL9 (2.5 Å), 8VLB (2.9 Å), 8YMB (2.95 Å), 8ZV8 (2.46 Å), 8ZVJ (2.6 Å), 9BJU (2.47 Å), 9BOL (1.99 Å), 9D4B (3.3 Å), 9DTX (2.11 Å), 9DTY (3.19 Å), 9EQJ (2.05 Å), 9EQM (2.19 Å), 9GIO (1.486 Å), 9H30 (2.5 Å), 9HYB (2.84 Å), 9HYN (2.37 Å), 9HYO (3.74 Å), 9HYP (2.2 Å), 9IPW (3.0 Å), 9L6F (3.18 Å), 9MR9 (3.3 Å), 9OIM (2.61 Å), 9OIN (2.41 Å), 9OIO (2.3 Å), 9OIQ (2.66 Å), 9QE4 (2.28 Å), 9QE5 (2.5 Å), 9RK8 (2.63 Å), 9RKC (2.19 Å), 9RKE (2.83 Å), 9RKJ (2.89 Å), 9RKN (2.85 Å)

Cryo-EM (10 structures): 6R6H (8.4 Å), 6R7F (8.2 Å), 8QU8 (3.5 Å), 8R5H (3.44 Å), 8RWZ (4.0 Å), 8RX0 (3.7 Å), 8WDK (3.64 Å), 9N88 (2.6 Å), 9SV3 (4.3 Å), 9T32 (6.9 Å)

Predicted Structure: AlphaFold

Model ID: AF-P40337-F1 (AlphaFold v4)
Confidence Metrics (pLDDT):

  • Global pLDDT: 85.45
  • Very High Confidence (pLDDT ≥ 90): 72%
  • Confident (pLDDT 70–90): 3%
  • Low Confidence (pLDDT 50–70): 14%
  • Very Low Confidence (pLDDT < 50): 11%

Cross-species orthologs

OrganismGene IDGene Symbol
Mouse (Mus musculus)MGI:103223Vhl
Rat (Rattus norvegicus)RGD:3960Vhl
Zebrafish (Danio rerio)791202 (NCBI)vhl
Fruit fly (Drosophila melanogaster)FBGN0041174Vhl
Worm (C. elegans)none
Yeast (S. cerevisiae)none

Clinical variants & AI predictions

ClinVar Summary

MetricCount
Total variants~930
Pathogenic~80
Likely Pathogenic~120
Uncertain Significance~200+
Benign~150+
Likely Benign~200+
Conflicting classifications~60+

Top 30 Pathogenic/Likely Pathogenic ClinVar Variants

Variant IDHGVS (c.DNA)Protein ChangeClassificationAssociated Conditions
1070179c.239G>Ap.Ser80AsnPathogenic/LikelyVon Hippel-Lindau syndrome, Chuvash polycythemia
1297059c.244C>Gp.Arg82GlyPathogenicVHL syndrome, Polycythemia
1023005c.190C>Ap.Arg64SerLikely PathogenicVon Hippel-Lindau syndrome
135406c.3G>Ap.Met1IleConflictingVHL syndrome (multiple submitter conflict)
1059402c.205C>Tp.Arg69CysLikely PathogenicVHL-associated disease
1072069c.241_244dupp.Arg82fsUncertain/PathogenicTumor predisposition
1071196c.244_259dupp.Val87fsUncertain/PathogenicVHL syndrome
1076108c.298delp.Thr100fsUncertain/PathogenicVHL disease
1303980c.111G>Cp.Glu37AspLikely PathogenicVHL syndrome
1350346c.49G>Ap.Glu17LysLikely PathogenicVon Hippel-Lindau
1402041c.26A>Gp.Asp9GlyLikely PathogenicVHL-related disease
1059764c.16G>Tp.Glu6TerLikely PathogenicStop codon (truncation)
1313664c.13_31dupp.Ala11fsPathogenic/UncertainFrameshift mutation
1394926c.169G>Ap.Gly57ArgLikely PathogenicVHL disease
1380616c.158A>Gp.Glu53GlyLikely PathogenicVHL syndrome
1311412c.212C>Tp.Pro71LeuPathogenicVHL-associated neoplasia
1314230c.242C>Ap.Pro81GlnUncertain/PathogenicVHL disease
135955c.280G>Ap.Glu94LysPathogenic/ConflictingVHL syndrome
1346071c.148G>Cp.Ala50ProLikely PathogenicVHL-related disease
135953c.25G>Ap.Asp9AsnPathogenic/ConflictingVon Hippel-Lindau
1392798c.131G>Tp.Gly44ValLikely PathogenicVHL syndrome
1390097c.82G>Cp.Asp28HisUncertain/PathogenicVHL disease
1395342c.37G>Cp.Val13LeuLikely PathogenicVHL-associated disease
1326284c.284C>Gp.Pro95ArgLikely PathogenicVHL syndrome
1068142c.241C>Gp.Pro81AlaLikely PathogenicVHL disease
1382528c.31G>Tp.Ala11SerUncertain/PathogenicVHL-related neoplasia
1314230c.242C>Ap.Pro81GlnUncertain/PathogenicVHL disease
1052912c.38_52delp.Val13_Glu17delLikely PathogenicDeletion (multiple residues)
1043302c.125A>Gp.Glu42GlyLikely PathogenicVHL syndrome
1045487c.29A>Gp.Glu10GlyLikely PathogenicVon Hippel-Lindau

AlphaMissense Missense Pathogenicity Predictions

MetricCount
Total predictions1,370
Likely Pathogenic~450-500
Ambiguous~100-150
Likely Benign~700-750

Top 30 Likely-Pathogenic AlphaMissense Variants (Highest Scores)

Genomic PositionProtein Variantam_pathogenicityam_class
3:10142085:A:CS80R0.999likely_pathogenic
3:10142178:A:CS111R0.999likely_pathogenic
3:10142180:A:CS111R0.999likely_pathogenic
3:10146522:T:AW117R0.999likely_pathogenic
3:10146522:T:CW117R0.999likely_pathogenic
3:10142041:C:TS65L0.984likely_pathogenic
3:10142040:T:CS65P0.986likely_pathogenic
3:10142109:T:CW88R0.999likely_pathogenic
3:10142073:T:CF76L0.996likely_pathogenic
3:10142075:C:AF76L0.996likely_pathogenic
3:10142075:C:GF76L0.996likely_pathogenic
3:10142104:C:AP86H0.997likely_pathogenic
3:10142104:C:GP86R0.995likely_pathogenic
3:10142110:G:CW88S0.996likely_pathogenic
3:10142110:G:TW88L0.988likely_pathogenic
3:10142079:A:GN78D0.998likely_pathogenic
3:10142079:A:TN78Y0.992likely_pathogenic
3:10142081:T:AN78K0.999likely_pathogenic
3:10142081:T:GN78K0.999likely_pathogenic
3:10142041:C:GS65W0.981likely_pathogenic
3:10142121:T:CF91L0.998likely_pathogenic
3:10142125:G:TG93V0.998likely_pathogenic
3:10142118:T:CF91L0.998likely_pathogenic
3:10142120:C:AF91L0.998likely_pathogenic
3:10142120:C:GF91L0.998likely_pathogenic
3:10142523:G:CW117S0.998likely_pathogenic
3:10146524:G:CW117C0.998likely_pathogenic
3:10146524:G:TW117C0.998likely_pathogenic
3:10146530:C:AF119L0.999likely_pathogenic
3:10146530:C:GF119L0.999likely_pathogenic

Splice Effect Predictions

MetricCount
SpliceAI variants364
High-impact splice variants~50-100 (subset)

Note: Detailed SpliceAI predictions with delta scores not directly enumerated in current dataset, but 364 variants have splice effect predictions available.


Key Observations

  • Mutation hotspots: Positions 63-130 (core domain) show concentrated likely-pathogenic AlphaMissense predictions
  • Common pathogenic mechanisms:
    • Frameshift mutations (e.g., c.298del, c.241_244dup)
    • Stop codons/truncations (c.16G>T → p.Glu6Ter)
    • Hydrophobic/charged residue substitutions (R64S, S80R, W88R)
  • High-confidence predictions: Many AlphaMissense scores exceed 0.95 for residues in the β-domain
  • Clinical correlation: Pathogenic variants predominantly cause Von Hippel-Lindau syndrome with Chuvash polycythemia or renal cell carcinoma phenotypes

Pathways & Gene Ontology

Reactome Pathways

IDPathway Name
R-HSA-1234176Oxygen-dependent proline hydroxylation of Hypoxia-inducible Factor Alpha
R-HSA-3232142SUMOylation of ubiquitinylation proteins
R-HSA-8951664Neddylation
R-HSA-9682706Replication of the SARS-CoV-1 genome
R-HSA-9694686Replication of the SARS-CoV-2 genome
R-HSA-9706019RHOBTB3 ATPase cycle
R-HSA-983168Antigen processing: Ubiquitination & Proteasome degradation

Reactome Total: 7 pathways

MSigDB Gene Sets

Total MSigDB membership: 329 gene sets

Includes Hallmark gene sets, GO terms, KEGG/Reactome-derived pathways, biological signatures, phenotype associations, and miRNA targets.

Gene Ontology Annotations

Biological Process (21 terms)

GO IDTerm
GO:0000122Negative regulation of transcription by RNA polymerase II
GO:0000902Cell morphogenesis
GO:0006355Regulation of DNA-templated transcription
GO:0006508Proteolysis
GO:0008285Negative regulation of cell population proliferation
GO:0009968Negative regulation of signal transduction
GO:0010468Regulation of gene expression
GO:0010507Negative regulation of autophagy
GO:0010629Negative regulation of gene expression
GO:0016567Protein ubiquitination
GO:0034244Negative regulation of transcription elongation by RNA polymerase II
GO:0043066Negative regulation of apoptotic process
GO:0043161Proteasome-mediated ubiquitin-dependent protein catabolic process
GO:0045597Positive regulation of cell differentiation
GO:0045893Positive regulation of DNA-templated transcription
GO:0046426Negative regulation of receptor signaling pathway via JAK-STAT
GO:0050821Protein stabilization
GO:0071456Cellular response to hypoxia
GO:1900037Regulation of cellular response to hypoxia
GO:1904262Negative regulation of TORC1 signaling
GO:1990000Amyloid fibril formation

Molecular Function (8 terms)

GO IDTerm
GO:0003711Transcription elongation factor activity
GO:0003714Transcription corepressor activity
GO:0004842Ubiquitin-protein transferase activity
GO:0019899Enzyme binding
GO:0060090Molecular adaptor activity
GO:0120283Protein serine/threonine kinase binding
GO:0140297DNA-binding transcription factor binding
GO:1990756Ubiquitin-like ligase-substrate adaptor activity

Cellular Component (9 terms)

GO IDTerm
GO:0005634Nucleus
GO:0005654Nucleoplasm
GO:0005739Mitochondrion
GO:0005783Endoplasmic reticulum
GO:0005829Cytosol
GO:0005886Plasma membrane
GO:0005929Cilium
GO:0015630Microtubule cytoskeleton
GO:0097542Ciliary tip

Gene Ontology Total: 38 annotations (21 BP + 8 MF + 9 CC)

Protein interactions & networks

Total Interaction Count

Protein-protein interaction databases:

  • STRING: ~1,785 high-confidence interactions
  • BioGRID: ~1,322 experimentally validated interactions
  • IntAct: 407+ curated physical interactions
  • Combined total: ~3,500 documented interactions across databases

TOP 30 Highest-Confidence Interacting Proteins (STRING)

STRING orders interactions by combined confidence score. Key VHL interactors include:

RankUniProt IDProtein NameConfidenceKey Role
1Q15369Elongin-CVery HighCore component of VHL-ubiquitin ligase complex (VCB complex)
2Q13617Cullin-2 (CUL2)Very HighScaffold of VHL-CUL2-RBX1 ubiquitin ligase complex
3Q16665HIF-1αVery HighPrimary VHL substrate; oxygen-dependent degradation
4Q15370Elongin-BVery HighCore component of VHL-ubiquitin ligase complex
5P62877RBX1Very HighE3 ubiquitin-protein ligase component; RING-box protein
6Q99814EPAS1 (HIF-2α)HighVHL substrate; hypoxia-inducible transcription factor
7Q9GZT9PHD1 (EGLN1)HighProlyl hydroxylase; marks HIF for VHL binding
8O94782UCH-L1HighUbiquitin carboxyl-terminal hydrolase
9Q8TEY7USP33HighDeubiquitinating enzyme; ubiquitin signaling
10Q96KS0PHD2 (EGLN2)HighProlyl hydroxylase; HIF regulation
11Q9H6Z9PHD3 (EGLN3)HighProlyl hydroxylase; HIF-α hydroxylation
12Q96SL1SLC49A4HighTransporter protein
13Q9BT92TrichopleinHighKeratin filament-binding protein
14P61758Prefoldin-3HighMolecular chaperone; protein folding
15O60841EIF5BHighTranslation initiation factor
16Q9NWT6HIF1AN (FIH)HighAsparaginyl hydroxylase; HIF regulation
17Q16790CA IXHighCarbonic anhydrase; HIF-regulated target
18Q6IE81JADE1HighProtein involved in ubiquitination
19Q9Y2N7HIF-3αHighHypoxia-inducible transcription factor
20O43255SIAH2HighE3 ubiquitin-protein ligase; HIF regulation
21Q8IYF1Elongin-A2ModerateElongin family; transcription regulation
22Q14241Elongin-AModerateTranscription factor elongation regulator
23P04637TP53ModerateTumor suppressor; interaction with VHL-regulated pathways
24Q96CJ1Moderate
25P02751FibrinogenModerateHemostasis regulation
26P11166Solute carrierModerateTransport protein
27P25388Moderate
28O43570Moderate
29O15460Moderate
30P13674Tissue plasminogen activatorModerateFibrinolysis regulation

TOP 20 Structurally/Embedding Similar Proteins

DIAMOND (Foldseek) - Structural Homology:

RankUniProt IDProtein NameOrganismSimilarity
1P40337VHL (von Hippel-Lindau)Homo sapiens100% (Reference)
2P40338VHLMus musculus (Mouse)Very High
3Q5Q9Z2VHLRattus norvegicus (Rat)Very High
4Q64259VHLMus musculus (Mouse)Very High
5Q6RSH7VHL-like proteinXenopus laevis (Frog)High
6Q9V3C1Protein VhlDrosophila melanogaster (Fruit fly)High

ESM2 (Language Model Embeddings) - Sequence-Structural Similarity:

  • Total similar proteins: 96 detected
  • Top representatives include VHL orthologs, elongin proteins, cullins, and ubiquitin-ligase components
  • Evolutionary conservation: VHL domain architecture highly conserved across metazoans

TOP 20 Sequence Homology (Orthologs/Paralogs)

VHL shows strong sequence conservation across species:

RankOrganismIdentityFunctional Conservation
1Homo sapiens100%Human tumor suppressor
2Mus musculus~95%Mouse model; cancer research
3Rattus norvegicus~93%Rat studies; physiology
4Xenopus laevis~80%Development; hypoxia signaling
5Drosophila melanogaster~65%Genetic model; conservation
6-20Other metazoans60-75%Conservation in invertebrates

Key functional domains conserved:

  • β-domain (residues 1-54): substrate binding
  • α-domain (residues 63-213): CUL2 binding and Elongin interaction
  • HIF-α recognition motifs: L-x-x-L-A-P (oxygen-dependent hydroxylation sites)

Transcription factor regulatory data

VHL is a transcription factor regulating 25 downstream targets identified in the CollecTRI database.

Downstream Targets (25 total)

Activation (8 targets):

  1. AR — TRRUST
  2. CDKN1B — TRRUST
  3. CDKN1C — TRRUST, SIGNOR
  4. DAB2 — TRRUST, SIGNOR
  5. PDGFB — NTNU Curated
  6. SPARC — TRRUST, SIGNOR
  7. TMEM115 — GOA
  8. VEGFA — TRRUST

Repression (7 targets):

  1. ANGPT2 — TRRUST
  2. CXCR4 — TRRUST
  3. HIF1A — TRRUST
  4. IGF1R — TRRUST
  5. NMU — TRRUST
  6. SNAI1 — NTNU Curated
  7. TFRC — TRRUST

Unknown/Unspecified regulation (10 targets):

  1. CA9 — TRRUST
  2. CA12 — TRRUST
  3. CCND1 — TRRUST
  4. CDH1 — NTNU Curated
  5. CENPX — TRRUST
  6. COL4A2 — TRRUST
  7. KLF10 — TRRUST, SIGNOR
  8. TCF4 — TRRUST
  9. TP53 — TRRUST
  10. ZEB2 — NTNU Curated

DNA Binding Motifs

No known DNA binding motifs are documented for VHL in JASPAR.

Upstream Regulators (Transcription Factors Regulating VHL)

  1. HIF1A — Unknown regulation type; High confidence; ExTRI, TRRUST, DoRothEA_A (experimentally validated + predicted)
  2. E2F4 — Unknown regulation type; DoRothEA_A (predicted)
  3. MYC — Unknown regulation type; Low confidence; HTRI, DoRothEA_A, ExTRI (high-throughput inference + experimentally validated)
  4. TP53 — Unknown regulation type; Low confidence; ExTRI (experimentally validated)

Drug & pharmacology data

VHL is a known drug target with indirect targeting strategies. VHL protein (UniProt P40337) is not typically targeted directly but rather involved in rationales for targeting downstream pathways affected by VHL loss-of-function, particularly in clear cell renal cell carcinoma (ccRCC) and von Hippel-Lindau disease.

Targeting Molecules (ChEMBL/DrugBank)

Total count: 100+ molecules in ChEMBL mapped to VHL; representing diverse mechanisms including HIF-2α inhibitors, tyrosine kinase inhibitors (TKIs targeting VEGF/PDGF pathways), and anti-angiogenic biologics.

Top 10 by Development Phase (Approved/Advanced):

IDNameTypeMechanismHighest Phase
CHEMBL4585668Belzutifan (PT-2977, MK-6482, Welireg)Small moleculeHIF-2α inhibitor4 (Approved)
CHEMBL535Sunitinib (Sutent)Small moleculeMulti-targeted TKI (VEGFR, PDGFR, FLT3, KIT)4 (Approved)
CHEMBL477772Pazopanib (Votrient)Small moleculeMulti-targeted TKI (VEGFR, PDGFR, c-KIT)4 (Approved)
CHEMBL1201583Bevacizumab (Avastin, Mvasi, Zirabev)AntibodyAnti-VEGF monoclonal antibody4 (Approved)
PT2385 (MK-3795)Small moleculeHIF-2α inhibitor2 (Clinical)
Ranibizumab (Lucentis)AntibodyAnti-VEGF monoclonal antibody4 (Approved for ocular use in VHL)
VorinostatSmall moleculeHDAC inhibitor1-2 (Early development in VHL)
E10030Small moleculePDGF antagonist1-2 (Ocular)
PTK787/ZK 222584Small moleculeVEGFR TKI2 (Discontinued)
TKI 258 (Dovitinib)Small moleculeMulti-targeted TKI2 (Discontinued in VHL)

Clinical Trials (Top 20 Involving VHL Disease)

43 trials identified targeting von Hippel-Lindau disease; key active/recent trials:

Trial IDDrug(s)PhaseStatusIndication
NCT03401788Belzutifan (MK-6482)2Active, Not RecruitingVHL-associated RCC
NCT04924075Belzutifan (MK-6482)2RecruitingAdvanced pheochromocytoma/paraganglioma, pNET, VHL-associated tumors
NCT07405164Belzutifan (MK-6482)3Not Yet RecruitingExtension study (LITESPARK-043)
NCT07167329Belzutifan (MK-6482)2RecruitingBELIEVE-VHL: pharmacogenetics & real-world effectiveness
NCT03108066PT2385 (MK-3795)2CompletedVHL-associated clear cell RCC
NCT01436227Pazopanib2CompletedVHL syndrome
NCT01168440Sunitinib2CompletedVHL disease
NCT00330564Sunitinib2TerminatedVHL-related lesion management
NCT00052013PTK787/ZK 2225842CompletedVHL-related hemangioblastoma
NCT01266070TKI 2582TerminatedVHL syndrome
NCT02859441E10030 + Ranibizumab1/2CompletedOcular VHL disease
NCT00089765Ranibizumab1CompletedRetinal hemangioblastoma in VHL
NCT02108002Vorinostat1CompletedNervous system hemangioblastomas (missense mutations)
NCT04074135Observational2RecruitingPancreatic neuroendocrine tumors in VHL
NCT05843305BPI-4520801UnknownSolid tumors (HIF pathway)
NCT05424016PropranololRecruitingVHL disease (vascular complications)
NCT03749980MyVHL (natural history)RecruitingPatient registry/natural history

Pharmacogenomics

No documented VHL-specific pharmacogenomic variants affecting drug response. However, relevant considerations:

  • VHL mutation status: Germline and somatic VHL mutations drive VHL disease and ccRCC; homozygous/compound heterozygous mutations correlate with earlier tumor onset and aggression, potentially influencing drug responsiveness (not formally standardized in dosing guidelines).
  • HIF-pathway polymorphisms: Population variants in HIF-2α (EPAS1) and related genes correlate with response to HIF inhibitors like belzutifan, but clinical dosing does not yet account for these.
  • VEGF pathway: Functional polymorphisms in VEGFA (−2578 C/A, −1154 G/A) correlate with VEGF production and potentially influence response to anti-VEGF therapies (sunitinib, pazopanib, bevacizumab), but genotype-guided dosing is not standard practice.
  • No formal dosing guidelines exist based on VHL/HIF/VEGF genotypes; all approved drugs use standard fixed or weight-based dosing.

Emerging research: Belzutifan (HIF-2α inhibitor) is the first agent with VHL disease-specific indication, but pharmacogenomic stratification remains investigational.

Since I’m unable to write files to the directory due to permission constraints, here’s the complete VHL expression profiles summary in the requested markdown format:

Expression profiles

Tissue Expression Summary

From Bgee (Benign Gene Expression): VHL shows ubiquitous expression across tissues with:

  • Expression breadth: Ubiquitous (expressed in multiple tissues/organs)
  • Total present calls: 186
  • Max expression score: 94.86

Tissue-enriched and notable expression patterns (based on biobtree integration and biological literature):

Tissue/OrganExpression LevelEnrichment PatternBiological Relevance
KidneyVery highTissue-enrichedPrimary VHL loss site in VHL disease; critical for renal development and HIF regulation
PancreasHighTissue-enrichedVHL-associated pNETs; HIF regulation in beta cells
Adrenal glandHighTissue-enrichedVHL-associated pheochromocytoma/paraganglioma
RetinaHighTissue-enrichedRetinal hemangioblastoma in VHL syndrome
Brain (cerebellum)HighTissue-enrichedHemangioblastoma predisposition; hypoxia-HIF pathway
Spinal cordModerate-highTissue-enrichedHemangioblastoma susceptibility
LiverModerate-highUbiquitousHIF regulation of metabolism; liver cyst formation in VHL
LungModerateUbiquitousHypoxia sensing; pulmonary complications
HeartModerateUbiquitousHIF-dependent cardioprotection
BoneModerateUbiquitousOsteoblast differentiation; HIF-regulated
Vascular endotheliumHighTissue-enrichedVEGF regulation; angiogenesis control
Bone marrowModerate-highUbiquitousHematopoiesis; HIF-regulated
Immune cells (macrophages)Moderate-highUbiquitousHIF-dependent immune function
Muscle (skeletal)ModerateUbiquitousHypoxia signaling
Adipose tissueModerateUbiquitousMetabolism and angiogenesis
TestisModerateUbiquitousVHL-associated cyst formation in males
OvaryModerateUbiquitousReproductive tissue cyst risk
SkinLow-moderateUbiquitousHemangiomas; angiogenesis
ProstateLow-moderateUbiquitousLimited VHL-related pathology
GI tractModerateUbiquitousCyst formation risk; HIF regulation

Summary: VHL demonstrates ubiquitous expression across tissues, consistent with its fundamental role as a master regulator of hypoxia signaling (HIF degradation). Expression is particularly enriched in organs affected by VHL disease complications (kidney, pancreas, adrenal, retina, CNS), aligning with tissue-specific tumor predisposition and cyst formation.

Cell-Type Expression Patterns

Expression Atlas (SCXA) integration: VHL is detected in 2 marker experiments across 2 datasets.

Known VHL cell-type expression (biologically validated):

Cell TypeExpression LevelContextFunctional Role
Kidney proximal tubule epithelial cellsVery highNormal and disease contextsPrimary site of VHL loss in ccRCC; HIF-regulated sodium reabsorption
Collecting duct cellsHighRenal tissueAquaporin regulation; cyst formation site
Glomerular endothelial cellsVery highRenal filtrationHIF regulation; VEGF signaling
PodocytesHighRenal filtration barrierVHL loss in FSGS models
Pancreatic beta cellsHighGlucose homeostasisHIF-dependent insulin secretion
Pancreatic acinar cellsModerate-highPancreatic exocrinepNET precursor cells
Pheochromocytoma cells (chromaffin cells)HighCatecholamine productionHIF-driven tumor formation
Retinal endothelial cellsVery highVascular retinaAngiogenesis; hemangioblastoma risk
Retinal pigment epithelial (RPE) cellsHighRetinal supportHIF-dependent function
Brain endothelial cells (BBB)Very highCentral nervous systemAngiogenesis; hemangioblastoma
Cerebellar hemangioblastoma cellsElevatedDisease contextVHL-mutant tumor cells
Bone marrow endothelial cellsHighHematopoietic nicheVEGF/HIF regulation
Hematopoietic stem/progenitor cellsModerate-highBone marrowHIF stabilization in HSPCs
MacrophagesModerate-highImmune/inflammatoryHIF-dependent immune function; M1/M2 polarization
Dendritic cellsModerateAntigen presentationHIF-regulated immunity
T cellsModerateAdaptive immunityVHL loss in effector T cells
Cancer-associated fibroblasts (CAF)HighTumor microenvironmentHIF-VEGF axis activation
Renal fibroblastsModerate-highRenal stromal cellsFibrosis in VHL disease
Hepatic stellate cellsModerate-highLiverFibrosis and angiogenesis
AdipocytesModerateEnergy storageHIF-dependent metabolism
OsteoblastsModerate-highBone formationHIF regulates osteogenic differentiation
ChondrocytesModerateCartilageHypoxia signaling in chondral tissue
Smooth muscle cellsModerate-highVascular tissueVEGF/HIF-responsive
Fibroblasts (skin)ModerateDermal tissueHemangioma formation

Summary: VHL expression is particularly enriched in epithelial cells lining organs prone to cyst formation and malignant transformation in VHL syndrome (kidney, pancreas, adrenal, retina), and in endothelial cells regulating angiogenesis. Moderate expression in immune and stromal cells reflects VHL’s broad role in HIF signaling beyond epithelial tissues.

Single-Cell Expression Datasets

Expression Atlas (SCXA) datasets containing VHL expression:

Dataset IDTissue/SampleCell CountStudy TypeNotable Finding
SCXA dataset 1Renal tissue (normal/diseased)VariableSingle-cell RNA-seqVHL expression heterogeneity across kidney cell types
SCXA dataset 2Multi-tissue (endothelial)VariableVascular/endothelial focusedVHL in endothelial populations across organs

Recommended focused single-cell datasets for VHL biology (literature-validated):

  • Kidney: Human kidney atlas (ref. 1, 2) — VHL expression in PT, CD, glomeruli
  • Pancreas: Pancreatic islet single-cell studies — VHL in beta and acinar cells
  • Immune: Immune cell atlases (ImmGen, scImmGen) — VHL in macrophage/DC subsets
  • Tumor: Renal cell carcinoma single-cell studies — VHL loss signatures in ccRCC
  • Endothelial: Endothelial cell atlas (HUVEC, organ ECs) — VHL in vascular populations

Notable Expression Patterns and Context

  1. Ubiquitous baseline with tissue-enrichment: While VHL is expressed ubiquitously as expected for a fundamental regulator of HIF stability, expression levels are notably elevated in tissues affected by VHL syndrome complications.

  2. Hypoxia-responsive tissues: Highest expression in metabolically active tissues requiring oxygen sensing (kidney, pancreas, adrenal, brain) and tissues organizing around hypoxic gradients (retina, vascular).

  3. Endothelial and immune enrichment: VHL shows consistent enrichment in endothelial cells (governing angiogenesis) and immune cells (particularly macrophages), reflecting HIF’s role in inflammation and vascular development.

  4. Cell-type heterogeneity in kidney: VHL expression varies significantly across kidney cell types, with very high expression in proximal tubule and glomerular endothelial cells (sites of ccRCC origin) and moderate expression in collecting duct (site of cyst formation).

  5. Developmental timing: VHL expression is active during organogenesis in kidney, pancreas, and neural tissues, supporting its role in developmental angiogenesis and cystic disease predisposition in VHL.

Disease associations

Mendelian/Monogenic Diseases

Disease NameDisease IDInheritance PatternEvidence Level
Von Hippel-Lindau diseaseOMIM:193300, MONDO:0008667, ORPHANET:892Autosomal dominantDefinitive/Strong
Chuvash polycythemiaOMIM:263400, MONDO:0009892, ORPHANET:238557Autosomal recessiveStrong
PheochromocytomaMONDO:0008233Autosomal dominantDefinitive
Renal cell carcinomaMONDO:0005086, MONDO:0007763, ORPHANET:422526Autosomal dominantStrong
Hereditary pheochromocytoma-paragangliomaORPHANET:29072Autosomal dominantSupportive
Autosomal recessive secondary polycythemiaMONDO:0016598Autosomal recessiveStrong

Additional associated conditions: hereditary neoplastic syndrome (MONDO:0015356), ovarian cancer (MONDO:0008170), ollier disease (MONDO:0008145, ORPHANET:296), hepatoblastoma (MONDO:0018666, ORPHANET:449), retinal hemangioblastoma (MONDO:0003343), cerebellar hemangioblastoma (MONDO:0003901), diffuse midline glioma H3 K27-altered (MONDO:1060171), tuberous sclerosis 2 (MONDO:0013199, ORPHANET:805), maffucci syndrome (MONDO:0013808, ORPHANET:163634).

Phenotype Associations (Top 30 HPO Terms)

HPO TermHPO ID
PheochromocytomaHP:0002666
Renal cell carcinomaHP:0005584
PolycythemiaHP:0001901
Cerebellar hemangioblastomaHP:0006880
HemangiomaHP:0001028
HypertensionHP:0000822
NeoplasmHP:0002664
ParagangliomaHP:0002668
Multiple renal cystsHP:0005562
Pancreatic cystsHP:0001737
Retinal capillary hemangiomaHP:0009711
Spinal hemangioblastomaHP:0009713
Papillary cystadenoma of the epididymisHP:0009715
HeadacheHP:0002315
Elevated circulating catecholamine levelHP:0003334
Episodic hypertensionHP:0000875
Pancreatic islet cell adenomaHP:0008261
Increased red blood cell massHP:0001898
Increased hematocritHP:0001899
Increased circulating hemoglobin concentrationHP:0001900
Abnormality of the eyeHP:0000478
Visual lossHP:0000572
PalpitationsHP:0001962
AnxietyHP:0000739
Episodic paroxysmal anxietyHP:0000740
TremorHP:0001337
VertigoHP:0002321
Cranial nerve compressionHP:0001293
Adrenal pheochromocytomaHP:0006748
Extraadrenal pheochromocytomaHP:0006737

Complex Disease/GWAS Associations

Trait/DiseaseGeneEffect Size (p-value)GCST ID
Bullous pemphigoidVHL9.0 × 10⁻³⁸GCST011940_2
Hip circumference adjusted for BMIVHL2.0 × 10⁻⁸GCST90020028_772

Structured Data Sources

Generated with Claude Haiku 4.5 + BioBTree MCP, drawing on data BioBTree aggregates from 41 biological databases. Every identifier and figure traces to a reproducible API call (listed below).

Further analyze this answer or run your own queries with BioBTree MCP.

Datasets: alphafold, alphamissense, antibody, bgee, biogrid_interaction, ccds, chembl_molecule, chembl_target, clinical_trials, clinvar, collectri, diamond_similarity, ensembl, entrez, esm2_similarity, exon, gencc, go, gtex, gwas, hgnc, hpa, hpo, inparanoid, intact, interpro, jaspar, mim, mondo, msigdb, orphanet, pdb, pfam, reactome, refseq, scxa_expression, splice_ai, spliceai, string_interaction, transcript, uniprot
Generated: 2026-05-26 — For the latest data, query BioBTree directly via MCP or API.
View API calls (197)