CCL3
C-C motif chemokine 3
Also known as: CCL3_HUMAN, G0S19-1, LD78ALPHA, MIP-1-alpha, SCYA3
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P10147
- Gene
- CCL3
- Ensembl
- ENSG00000277632
- Chromosome
- 17
- Canonical length
- 92 aa
- Protein class
- Cancer-related genes, Predicted secreted proteins
- Secretome location
- Secreted to blood
OverviewNCBI Gene
This locus represents a small inducible cytokine. The encoded protein, also known as macrophage inflammatory protein 1 alpha, plays a role in inflammatory responses through binding to the receptors CCR1, CCR4 and CCR5. Polymorphisms at this locus may be associated with both resistance and susceptibility to infection by human immunodeficiency virus type 1.[provided by RefSeq, Sep 2010]
Canonical amino-acid sequenceUniProt
92 residues, UniProt reviewed canonical sequence.
>P10147|CCL3
1 MQVSTAALAV LLCTMALCNQ FSASLAADTP TACCFSYTSR QIPQNFIADY FETSSQCSKP
61 GVIFLTKRSR QVCADPSEEW VQKYVSDLEL SALocalizationUniProt · AlphaFold · HPA
Whether an antibody against CCL3 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Secreted
- Secreted
- Yes
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.44
- Highest tissue expression
- 73 nTPM
Expression across tissuesHPA
Tissue
- bone marrow: 73 nTPM
- spleen: 49 nTPM
- lung: 35 nTPM
- adipose tissue: 17 nTPM
- cerebral cortex: 16 nTPM
- adrenal gland: 15 nTPM
Single-cell type
- hofbauer cells: 94 nCPM
- nk-cells: 63 nCPM
- macrophages: 48 nCPM
- kupffer cells: 45 nCPM
- microglia: 35 nCPM
- monocytes: 31 nCPM
Immune cell
- gdT-cell: 24 nTPM
- total PBMC: 12 nTPM
- eosinophil: 11 nTPM
- neutrophil: 11 nTPM
- naive B-cell: 10 nTPM
- naive CD8 T-cell: 6.8 nTPM
Brain region
- cerebral cortex: 2.7 nTPM
- white matter: 2.7 nTPM
- basal ganglia: 1.5 nTPM
- medulla oblongata: 1.4 nTPM
- thalamus: 1 nTPM
- amygdala: 0 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about CCL3.
Disease | ImmuneIEDB
Conditions an epitope on CCL3 was assayed in.
- berylliosis T cell
- chronic lymphocytic leukemia T cell
ReferencesPubMed · IEDB
Publications for CCL3 from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.
Reference: AutoantibodyPubMed
2 publications
- Autoantibodies to CCL3 are of low sensitivity and specificity for the diagnosis of type 1 diabetes.
2012 · Acta Diabetol · RCR 0.1 · 3 citations - Anti-CCL3 autoantibodies are not markers of type 1 diabetes when measured by a commercial ELISA method.
2011 · Diabetologia · RCR 0.1 · 2 citations
Reference: T cellIEDB
2 publications
- Beryllium-specific CD4+ T cells induced by chemokine neoantigens perpetuate inflammation.
2021 · J Clin Invest · RCR 0.8 · 16 citations - Naturally processed cytokine-derived peptide bound to HLA-class II molecules.
1993 · J Immunol · RCR 0.2 · 12 citations
Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. IEDB — curated epitope assays from the Immune Epitope Database (Vita et al., Nucleic Acids Research 2019). Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.04
- gnomAD pLI
- 0.35
- gnomAD missense Z
- 0.12
- DepMap mean gene effect
- -0.03
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- antimicrobial humoral immune response mediated by antimicrobial peptide
- astrocyte cell migration
- calcium ion transport
- calcium-mediated signaling
- cell activation
- cell chemotaxis
- cell-cell signaling
- cellular response to interleukin-1
- cellular response to tumor necrosis factor
- cellular response to type II interferon
- chemokine-mediated signaling pathway
- chemotaxis
- cytoskeleton organization
- eosinophil chemotaxis
- eosinophil degranulation
- exocytosis
- granulocyte chemotaxis
- host-mediated suppression of viral transcription
- inflammatory response
- intracellular calcium ion homeostasis
- lymphocyte chemotaxis
- macrophage chemotaxis
- MAPK cascade
- monocyte chemotaxis
- negative regulation of bone mineralization
- negative regulation of gene expression
- negative regulation of osteoclast differentiation
- neutrophil chemotaxis
- osteoblast differentiation
- positive regulation of calcium ion import
- positive regulation of calcium ion transport
- positive regulation of calcium-mediated signaling
- positive regulation of cell migration
- positive regulation of ERK1 and ERK2 cascade
- positive regulation of gene expression
- positive regulation of inflammatory response
- positive regulation of interleukin-1 beta production
- positive regulation of microglial cell activation
- positive regulation of microglial cell migration
- positive regulation of natural killer cell chemotaxis
- positive regulation of neuron apoptotic process
- positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction
- positive regulation of tumor necrosis factor production
- regulation of behavior
- regulation of cell shape
- regulation of sensory perception of pain
- release of sequestered calcium ion into cytosol by sarcoplasmic reticulum
- response to cholesterol
- response to toxic substance
- signaling
- T cell chemotaxis
Molecular functions
- CCR chemokine receptor binding
- CCR1 chemokine receptor binding
- CCR5 chemokine receptor binding
- chemoattractant activity
- chemokine activity
- identical protein binding
- kinase activity
- phospholipase activator activity
- protein kinase activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of CCL3 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads CCL3 as an antibody target. Whether an autoantibody or antibody against CCL3 could matter depends on whether native CCL3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
CCL3 is annotated as secreted, so native CCL3 circulates and is directly accessible to antibodies. Secreted and cell-surface proteins are the autoantibody targets most likely to act like drugs, blocking or depleting the native protein.
Annotation status
The present source text does not explicitly label CCL3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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