C3 Gene

HGNC Family	Complement system, Endogenous ligands
Name	complement component 3
Description	Complement component C3 plays a central role in the activation of complement system. Its activation is required for both classical and alternative complement activation pathways. The encoded preproprotein is proteolytically processed to generate alpha and beta subunits that form the mature protein, which is then further processed to generate numerous peptide products. The C3a peptide, also known as the C3a anaphylatoxin, modulates inflammation and possesses antimicrobial activity. Mutations in this gene are associated with atypical hemolytic uremic syndrome and age-related macular degeneration in human patients. [provided by RefSeq, Nov 2015]
Summary	{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Complement component C3 is a central effector of the innate immune system whose proteolytic activation into C3a and C3b orchestrates a wide range of inflammatory and homeostatic processes. The anaphylatoxin C3a acts as a potent chemoattractant and signaling molecule, while C3b covalently tags pathogens, damaged cells, and debris for clearance by phagocytes. Genetic variation in the C3 gene has been linked to chronic inflammatory diseases such as age‐related macular degeneration (AMD), where specific alleles predispose to excessive complement activation and local inflammation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In atypical hemolytic uremic syndrome (aHUS), gain‐of‐function mutations in C3 increase disease susceptibility by promoting uncontrolled complement activity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " In parallel, studies in autoimmune settings such as the antiphospholipid syndrome reveal that a functional complement cascade—including C3—is required for mediating tissue injury, as deficiency in C3 confers resistance to antibody‐induced fetal loss."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond host defense, C3 influences tissue homeostasis and repair. Structural studies show that the conversion from native C3 to its activated form C3b involves pronounced conformational rearrangements that expose regulatory and opsonic domains, facilitating its interaction with receptors such as CRIg on Kupffer cells for efficient clearance of opsonized targets."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " Moreover, the C3a fragment has been implicated in non‐immune functions; for example, adipsin‐mediated generation of C3a enhances insulin secretion by pancreatic β‐cells"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": ", and C3 activation products contribute to the early priming of hepatocytes during liver regeneration."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In neurodegenerative disorders, dysregulated complement activity is emerging as a double‐edged sword. In Alzheimer’s disease (AD), elevated C3 levels are associated with microglia‐mediated synaptic pruning and neuroinflammation, which contribute to synapse loss and cognitive decline."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "13"}]}, {"type": "t", "text": " Conversely, some experimental evidence suggests that loss of C3 may impair the clearance of amyloid‐β, thereby exacerbating plaque accumulation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Complement activation is also implicated in other inflammatory conditions. In COVID‐19, for instance, enhanced C3 activation fuels immunothrombosis by promoting tissue factor expression on neutrophils, a process that can be attenuated by targeted C3 inhibition."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": " In the vasculature, increased deposition of C3 in atherosclerotic lesions is associated with heightened local inflammation and remodeling"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "16"}]}, {"type": "t", "text": ", while photooxidation of retinal pigments may trigger complement activation and production of C3 split products, thereby linking oxidative stress to chronic retinal inflammation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "17"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these diverse studies highlight that C3 is not only essential for pathogen elimination and clearance of cellular debris but also finely tunes inflammatory responses and tissue repair. Dysregulation of C3—whether through genetic mutations, altered processing, or imbalanced regulatory control—can thus contribute to a spectrum of pathologies ranging from autoimmune and thrombotic disorders to neurodegeneration and metabolic dysfunction."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}, {"type": "fg_f", "ref": "10"}, {"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " \n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "John R W Yates, Tiina Sepp, Baljinder K Matharu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Complement C3 variant and the risk of age-related macular degeneration."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "N Engl J Med (2007)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1056/NEJMoa072618"}], "href": "https://doi.org/10.1056/NEJMoa072618"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17634448"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17634448"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Johanna M Seddon, Yi Yu, Elizabeth C Miller, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Rare variants in CFI, C3 and C9 are associated with high risk of advanced age-related macular degeneration."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Genet (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ng.2741"}], "href": "https://doi.org/10.1038/ng.2741"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24036952"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24036952"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Veronique Frémeaux-Bacchi, Elizabeth C Miller, M Kathryn Liszewski, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Mutations in complement C3 predispose to development of atypical hemolytic uremic syndrome."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Blood (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1182/blood-2008-01-133702"}], "href": "https://doi.org/10.1182/blood-2008-01-133702"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18796626"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18796626"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Tara K Maga, Carla J Nishimura, Amy E Weaver, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Mutations in alternative pathway complement proteins in American patients with atypical hemolytic uremic syndrome."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Mutat (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/humu.21256"}], "href": "https://doi.org/10.1002/humu.21256"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20513133"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20513133"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "V Michael Holers, Guillermina Girardi, Lian Mo, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Complement C3 activation is required for antiphospholipid antibody-induced fetal loss."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Exp Med (2002)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1084/jem.200116116"}], "href": "https://doi.org/10.1084/jem.200116116"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "11805148"}], "href": "https://pubmed.ncbi.nlm.nih.gov/11805148"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Bert J C Janssen, Agni Christodoulidou, Andrew McCarthy, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Structure of C3b reveals conformational changes that underlie complement activity."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nature (2006)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/nature05172"}], "href": "https://doi.org/10.1038/nature05172"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17051160"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17051160"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Karim Y Helmy, Kenneth J Katschke, Nick N Gorgani, et al. "}, {"type": "b", "children": [{"type": "t", "text": "CRIg: a macrophage complement receptor required for phagocytosis of circulating pathogens."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell (2006)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.cell.2005.12.039"}], "href": "https://doi.org/10.1016/j.cell.2005.12.039"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "16530040"}], "href": "https://pubmed.ncbi.nlm.nih.gov/16530040"}]}, {"type": "r", "ref": 8, "children": [{"type": "t", "text": "James C Lo, Sanda Ljubicic, Barbara Leibiger, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Adipsin is an adipokine that improves β cell function in diabetes."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.cell.2014.06.005"}], "href": "https://doi.org/10.1016/j.cell.2014.06.005"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24995977"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24995977"}]}, {"type": "r", "ref": 9, "children": [{"type": "t", "text": "Christoph W Strey, Maciej Markiewski, Dimitrios Mastellos, et al. "}, {"type": "b", "children": [{"type": "t", "text": "The proinflammatory mediators C3a and C5a are essential for liver regeneration."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Exp Med (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1084/jem.20030374"}], "href": "https://doi.org/10.1084/jem.20030374"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12975457"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12975457"}]}, {"type": "r", "ref": 10, "children": [{"type": "t", "text": "Qiaoqiao Shi, Saba Chowdhury, Rong Ma, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Sci Transl Med (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1126/scitranslmed.aaf6295"}], "href": "https://doi.org/10.1126/scitranslmed.aaf6295"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28566429"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28566429"}]}, {"type": "r", "ref": 11, "children": [{"type": "t", "text": "Alexandra Litvinchuk, Ying-Wooi Wan, Dan B Swartzlander, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer's Disease."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neuron (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.neuron.2018.10.031"}], "href": "https://doi.org/10.1016/j.neuron.2018.10.031"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30415998"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30415998"}]}, {"type": "r", "ref": 12, "children": [{"type": "t", "text": "Qiaoqiao Shi, Kenneth J Colodner, Sarah B Matousek, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Complement C3-Deficient Mice Fail to Display Age-Related Hippocampal Decline."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Neurosci (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1523/JNEUROSCI.1698-15.2015"}], "href": "https://doi.org/10.1523/JNEUROSCI.1698-15.2015"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26400934"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26400934"}]}, {"type": "r", "ref": 13, "children": [{"type": "t", "text": "Tiffany Wu, Borislav Dejanovic, Vineela D Gandham, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Rep (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.celrep.2019.07.060"}], "href": "https://doi.org/10.1016/j.celrep.2019.07.060"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31433986"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31433986"}]}, {"type": "r", "ref": 14, "children": [{"type": "t", "text": "Marcel Maier, Ying Peng, Liying Jiang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Complement C3 deficiency leads to accelerated amyloid beta plaque deposition and neurodegeneration and modulation of the microglia/macrophage phenotype in amyloid precursor protein transgenic mice."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Neurosci (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1523/JNEUROSCI.0829-08.2008"}], "href": "https://doi.org/10.1523/JNEUROSCI.0829-08.2008"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18562603"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18562603"}]}, {"type": "r", "ref": 15, "children": [{"type": "t", "text": "Panagiotis Skendros, Alexandros Mitsios, Akrivi Chrysanthopoulou, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Circulation (2004)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1161/01.CIR.0000114526.50618.24"}], "href": "https://doi.org/10.1161/01.CIR.0000114526.50618.24"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "14744975"}], "href": "https://pubmed.ncbi.nlm.nih.gov/14744975"}]}, {"type": "r", "ref": 17, "children": [{"type": "t", "text": "Jilin Zhou, Young Pyo Jang, So Ra Kim, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Complement activation by photooxidation products of A2E, a lipofuscin constituent of the retinal pigment epithelium."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Proc Natl Acad Sci U S A (2006)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1073/pnas.0604255103"}], "href": "https://doi.org/10.1073/pnas.0604255103"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17060630"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17060630"}]}]}]}
Synonyms	C3B, ARMD9, C3A, AHUS5, HEL-S-62P, CPAMD1
Proteins	CO3_HUMAN
NCBI Gene ID	718
API
Download Associations
Predicted Functions
Co-expressed Genes
Expression in Tissues and Cell Lines

Functional Associations

C3 has 19,635 functional associations with biological entities spanning 8 categories (molecular profile, organism, functional term, phrase or reference, chemical, disease, phenotype or trait, structural feature, cell line, cell type or tissue, gene, protein or microRNA) extracted from 141 datasets.

Click the + buttons to view associations for C3 from the datasets below.

If available, associations are ranked by standardized value

Harmonizome 3.0

C3 Gene

Functional Associations

Please acknowledge the Harmonizome in your publications by citing the following reference(s):

	Dataset	Summary
	Allen Brain Atlas Adult Human Brain Tissue Gene Expression Profiles	tissues with high or low expression of C3 gene relative to other tissues from the Allen Brain Atlas Adult Human Brain Tissue Gene Expression Profiles dataset.
	Allen Brain Atlas Adult Mouse Brain Tissue Gene Expression Profiles	tissues with high or low expression of C3 gene relative to other tissues from the Allen Brain Atlas Adult Mouse Brain Tissue Gene Expression Profiles dataset.
	Allen Brain Atlas Aging Dementia and Traumatic Brain Injury Tissue Sample Gene Expression Profiles	tissue samples with high or low expression of C3 gene relative to other tissue samples from the Allen Brain Atlas Aging Dementia and Traumatic Brain Injury Tissue Sample Gene Expression Profiles dataset.
	Allen Brain Atlas Developing Human Brain Tissue Gene Expression Profiles by Microarray	tissue samples with high or low expression of C3 gene relative to other tissue samples from the Allen Brain Atlas Developing Human Brain Tissue Gene Expression Profiles by Microarray dataset.
	Allen Brain Atlas Developing Human Brain Tissue Gene Expression Profiles by RNA-seq	tissue samples with high or low expression of C3 gene relative to other tissue samples from the Allen Brain Atlas Developing Human Brain Tissue Gene Expression Profiles by RNA-seq dataset.
	Allen Brain Atlas Prenatal Human Brain Tissue Gene Expression Profiles	tissues with high or low expression of C3 gene relative to other tissues from the Allen Brain Atlas Prenatal Human Brain Tissue Gene Expression Profiles dataset.
	Biocarta Pathways	pathways involving C3 protein from the Biocarta Pathways dataset.
	BioGPS Cell Line Gene Expression Profiles	cell lines with high or low expression of C3 gene relative to other cell lines from the BioGPS Cell Line Gene Expression Profiles dataset.
	BioGPS Human Cell Type and Tissue Gene Expression Profiles	cell types and tissues with high or low expression of C3 gene relative to other cell types and tissues from the BioGPS Human Cell Type and Tissue Gene Expression Profiles dataset.
	BioGPS Mouse Cell Type and Tissue Gene Expression Profiles	cell types and tissues with high or low expression of C3 gene relative to other cell types and tissues from the BioGPS Mouse Cell Type and Tissue Gene Expression Profiles dataset.
	Carcinogenome Chemical Perturbation Carcinogenicity Signatures	small molecule perturbations changing expression of C3 gene from the Carcinogenome Chemical Perturbation Carcinogenicity Signatures dataset.
	CCLE Cell Line Gene CNV Profiles	cell lines with high or low copy number of C3 gene relative to other cell lines from the CCLE Cell Line Gene CNV Profiles dataset.
	CCLE Cell Line Gene Expression Profiles	cell lines with high or low expression of C3 gene relative to other cell lines from the CCLE Cell Line Gene Expression Profiles dataset.
	CCLE Cell Line Proteomics	Cell lines associated with C3 protein from the CCLE Cell Line Proteomics dataset.
	CellMarker Gene-Cell Type Associations	cell types associated with C3 gene from the CellMarker Gene-Cell Type Associations dataset.
	ChEA Transcription Factor Binding Site Profiles	transcription factor binding site profiles with transcription factor binding evidence at the promoter of C3 gene from the CHEA Transcription Factor Binding Site Profiles dataset.
	ChEA Transcription Factor Targets	transcription factors binding the promoter of C3 gene in low- or high-throughput transcription factor functional studies from the CHEA Transcription Factor Targets dataset.
	ChEA Transcription Factor Targets 2022	transcription factors binding the promoter of C3 gene in low- or high-throughput transcription factor functional studies from the CHEA Transcription Factor Targets 2022 dataset.
	ClinVar Gene-Phenotype Associations 2025	phenotypes associated with C3 gene from the curated ClinVar Gene-Phenotype Associations 2025 dataset.
	CM4AI KOLF21J CRISPRi Gene Perturbation Atlas	gene perturbations changing expression of C3 gene from the CM4AI KOLF21J CRISPRi Gene Perturbation Atlas dataset.
	CMAP Signatures of Differentially Expressed Genes for Small Molecules	small molecule perturbations changing expression of C3 gene from the CMAP Signatures of Differentially Expressed Genes for Small Molecules dataset.
	COMPARTMENTS Curated Protein Localization Evidence Scores	cellular components containing C3 protein from the COMPARTMENTS Curated Protein Localization Evidence Scores dataset.
	COMPARTMENTS Curated Protein Localization Evidence Scores 2025	cellular components containing C3 protein from the COMPARTMENTS Curated Protein Localization Evidence Scores 2025 dataset.
	COMPARTMENTS Experimental Protein Localization Evidence Scores	cellular components containing C3 protein in low- or high-throughput protein localization assays from the COMPARTMENTS Experimental Protein Localization Evidence Scores dataset.
	COMPARTMENTS Text-mining Protein Localization Evidence Scores	cellular components co-occuring with C3 protein in abstracts of biomedical publications from the COMPARTMENTS Text-mining Protein Localization Evidence Scores dataset.
	COMPARTMENTS Text-mining Protein Localization Evidence Scores 2025	cellular components co-occuring with C3 protein in abstracts of biomedical publications from the COMPARTMENTS Text-mining Protein Localization Evidence Scores 2025 dataset.
	COSMIC Cell Line Gene Mutation Profiles	cell lines with C3 gene mutations from the COSMIC Cell Line Gene Mutation Profiles dataset.
	CTD Gene-Chemical Interactions	chemicals interacting with C3 gene/protein from the curated CTD Gene-Chemical Interactions dataset.
	CTD Gene-Disease Associations	diseases associated with C3 gene/protein from the curated CTD Gene-Disease Associations dataset.
	dbGAP Gene-Trait Associations	traits associated with C3 gene in GWAS and other genetic association datasets from the dbGAP Gene-Trait Associations dataset.
	DepMap CRISPR Gene Dependency	cell lines with fitness changed by C3 gene knockdown relative to other cell lines from the DepMap CRISPR Gene Dependency dataset.
	DGIdb Drug Targets 2026	interacting drugs for C3 protein from the DGIdb Drug Targets 2026 dataset.
	DISEASES Curated Gene-Disease Association Evidence Scores	diseases involving C3 gene from the DISEASES Curated Gene-Disease Assocation Evidence Scores dataset.
	DISEASES Curated Gene-Disease Association Evidence Scores 2025	diseases involving C3 gene from the DISEASES Curated Gene-Disease Association Evidence Scores 2025 dataset.
	DISEASES Experimental Gene-Disease Association Evidence Scores	diseases associated with C3 gene in GWAS datasets from the DISEASES Experimental Gene-Disease Assocation Evidence Scores dataset.
	DISEASES Experimental Gene-Disease Association Evidence Scores 2025	diseases associated with C3 gene in GWAS datasets from the DISEASES Experimental Gene-Disease Assocation Evidence Scores 2025 dataset.
	DISEASES Text-mining Gene-Disease Association Evidence Scores	diseases co-occuring with C3 gene in abstracts of biomedical publications from the DISEASES Text-mining Gene-Disease Assocation Evidence Scores dataset.
	DISEASES Text-mining Gene-Disease Association Evidence Scores 2025	diseases co-occuring with C3 gene in abstracts of biomedical publications from the DISEASES Text-mining Gene-Disease Assocation Evidence Scores 2025 dataset.
	DisGeNET Gene-Disease Associations	diseases associated with C3 gene in GWAS and other genetic association datasets from the DisGeNET Gene-Disease Associations dataset.
	DisGeNET Gene-Phenotype Associations	phenotypes associated with C3 gene in GWAS and other genetic association datasets from the DisGeNET Gene-Phenoptype Associations dataset.