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PCSK9 and obesity are reported together in 2 articles.

Gene

PCSK9

HGNC
HGNC:20001
66articles
66mentions
9variants with confirmed gene link
Most co-reported phenotypes (articles)
Reported variants (articles · ClinVar status)
Phenotype

Obesity

HPO
HP:0001513
856articles
856mentions
12co-reported genes shown
Most co-reported genes (articles)

Counts are literature co-mentions in SaudiVarKB, not clinical or causal assertions. Gene details: HGNC; variant status: ClinVar via dbSNP.

Publications

2 records shown · first 60

The omics revolution in obesity: from molecularsignatures to clinical solutions.

PMID 41133487 | DOI 10.1039/d5mo00074b · Molecular omics · 2025 · 5 validated mentions
TypeEntitySource evidenceConfidenceExtractor
genePCSK9“Proteomic markers like proprotein convertase subtilisin/kexin type 9 (PCSK9) and retinol binding protein 4 (RBP4) are being evaluated for cardiovascular risk stratification independent of body mass index (BMI).”0.98hgnc_dict_v1
phenotypeobesity“The omics revolution in obesity: from molecularsignatures to clinical solutions.”0.98phenotype_alias_lexicon_v2
geneCPT1A“Epigenomic profiling, particularly deoxy ribose nucleic acid (DNA) methylation signatures such as those at carnitine palmitoyl transferase 1A (CPT1A) and hypoxia inducible factor 3 subunit alpha (HIF3A), has uncovered modifiable pathways linked to adiposity and metabolic dysfunction.”0.98hgnc_dict_v1
geneHIF3A“Epigenomic profiling, particularly deoxy ribose nucleic acid (DNA) methylation signatures such as those at carnitine palmitoyl transferase 1A (CPT1A) and hypoxia inducible factor 3 subunit alpha (HIF3A), has uncovered modifiable pathways linked to adiposity and metabolic dysfunction.”0.98hgnc_dict_v1

The Spectrum of Familial Hypercholesterolemia (FH) in Saudi Arabia: Prime Time for Patient FH Registry.

PMID 28868092 | PMCID PMC5564019 | DOI 10.2174/1874192401711010066 · The open cardiovascular medicine journal · 2017 · 7 validated mentions
TypeEntitySource evidenceConfidenceExtractor
genePCSK9“The underlying molecular basis of FH is the presence of mutations in one or more genes in the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB) or proprotein convertase subtilisin/kexin 9 (PCSK9).”0.98hgnc_dict_v1
phenotypeobesity“Furthermore, the high prevalence of obesity and diabetes mellitus in Saudi Arabia increases the vascular disease burden in FH cases by adding additional CVD risk factors.”0.98phenotype_alias_lexicon_v2
geneLDLR“The underlying molecular basis of FH is the presence of mutations in one or more genes in the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB) or proprotein convertase subtilisin/kexin 9 (PCSK9).”0.98hgnc_dict_v1
geneAPOB“The underlying molecular basis of FH is the presence of mutations in one or more genes in the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB) or proprotein convertase subtilisin/kexin 9 (PCSK9).”0.98hgnc_dict_v1