CXCL14: C-X-C Motif Chemokine Ligand 14
A chemokine involved in immune regulation, angiogenesis, and tumor suppression.
Gene Information Card
| Symbol | CXCL14 |
|---|---|
| Full Name | C-X-C Motif Chemokine Ligand 14 |
| Gene Type | Protein coding |
| Chromosomal Location | 5q31.1 |
| NCBI Gene ID | 9547 ncbi.nlm.nih.gov/gene/9547 |
| Ensembl ID | ENSG00000145824 |
| UniProt ID | O95715 |
| OMIM ID | 604186 |
| HGNC ID | 10640 |
| Aliases | BRAK, KEC, MIP-2G, SCYB14, bolekine |
Description
CXCL14 (C-X-C Motif Chemokine Ligand 14) is a chemokine gene located on chromosome 5q31.1. It encodes a secreted protein that functions as a chemoattractant for monocytes, dendritic cells, and natural killer cells. CXCL14 is involved in immune surveillance, angiogenesis modulation, and has been implicated in tumor suppression in various cancers. It is constitutively expressed in many normal tissues but often downregulated in tumors.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Breast cancer | Downregulation of CXCL14 may promote tumor growth and metastasis by reducing immune cell infiltration. | PMID: 20629172 |
| Prostate cancer | Loss of CXCL14 expression correlates with aggressive disease and poor prognosis. | PMID: 21573173 |
| Colorectal cancer | CXCL14 methylation and silencing associated with tumor progression. | PMID: 22952447 |
| Head and neck squamous cell carcinoma | Reduced CXCL14 expression linked to immune evasion. | PMID: 23575478 |
| Type 2 diabetes | CXCL14 polymorphisms associated with insulin resistance. | PMID: 20086238 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Skin | 12.5 | Medium |
| Lung | 9.8 | Medium |
| Kidney | 8.2 | Medium |
| Breast | 6.1 | Low |
| Prostate | 4.3 | Low |
| Colon | 3.7 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HEK 293 | 15.2 | High expression in embryonic kidney cells |
| MCF-7 | 2.1 | Low expression in breast cancer cell line |
| PC-3 | 1.8 | Low expression in prostate cancer cell line |
| HCT-116 | 1.5 | Low expression in colorectal cancer cell line |
Data source:Human Protein Atlas(proteinatlas.org)
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1A>G | Missense | <0.1% | Unknown functional effect |
| c.124C>T | Nonsense | <0.1% | Predicted loss of function |
| c.256G>A | Missense | <0.1% | Unknown functional effect |
Mutation functional classification
Loss of Function (LOF)
Nonsense mutations (e.g., c.124C>T) are predicted to cause premature truncation and loss of chemokine activity.
Gain of Function (GOF)
No gain-of-function mutations have been reported in CXCL14.
Dominant Negative (DN)
No dominant-negative mutations have been described for CXCL14.
View complete mutation data:
Gene Ontology (GO)
| • chemokine activity (GO:0008009) | • immune response (GO:0006955) |
| • chemotaxis (GO:0006935) | • extracellular region (GO:0005576) |
| • extracellular space (GO:0005615) |
Pathways
• Chemokine signaling pathway (KEGG: hsa04062)
• Cytokine-cytokine receptor interaction (KEGG: hsa04060)
Protein Summary
CXCL14 is a 111-amino-acid secreted chemokine with a typical C-X-C motif. It is structurally related to other CXC chemokines but lacks the ELR (Glu-Leu-Arg) motif, classifying it as non-angiogenic. The protein binds to an unknown receptor and mediates chemotaxis of immune cells. It is widely expressed in normal tissues but frequently silenced in cancers via promoter methylation. CXCL14 has been proposed as a tumor suppressor and potential therapeutic target.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| CXCL14 Knockout HEK293 Cell Line | EDJ-KQ50879 | Human | 9547 | Details Get a Quote |
| CXCL14 Knockout HeLa Cell Line | EDJ-KQ55192 | Human | 9547 | Details Get a Quote |
| CXCL14 Knockout A-549 Cell Line | EDJ-KQ63674 | Human | 9547 | Details Get a Quote |
| CXCL14 Knockout HCT 116 Cell Line | EDJ-KQ72136 | Human | 9547 | Details Get a Quote |