ARL11: ADP Ribosylation Factor Like GTPase 11
A tumor suppressor gene implicated in hereditary and sporadic cancers, particularly colorectal and prostate cancer.
Gene Information Card
| Symbol | ARL11 |
|---|---|
| Full Name | ADP Ribosylation Factor Like GTPase 11 |
| Gene Type | Protein coding |
| Chromosomal Location | 13q14.3 |
| NCBI Gene ID | 115761 ncbi.nlm.nih.gov/gene/115761 |
| Ensembl ID | ENSG00000152213 |
| UniProt ID | Q969Q4 |
| OMIM ID | 609301 |
| HGNC ID | 24079 |
| Aliases | ARLTS1, ARL11 |
Description
ARL11 (ADP Ribosylation Factor Like GTPase 11) is a member of the ARF family of small GTPases. It functions as a tumor suppressor, involved in cell cycle regulation, apoptosis, and DNA damage response. Loss of ARL11 expression or function is associated with increased risk of hereditary and sporadic cancers, including colorectal, prostate, and breast cancer. The gene is located on chromosome 13q14.3, a region frequently deleted in various malignancies.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Colorectal Cancer | Loss of ARL11 expression due to promoter hypermethylation or mutation leads to impaired apoptosis and increased proliferation. | PMID: 15616568, COSMIC |
| Prostate Cancer | Somatic mutations and reduced ARL11 mRNA levels correlate with aggressive disease and poor prognosis. | PMID: 16936731, ClinVar |
| Breast Cancer | ARL11 downregulation via epigenetic silencing contributes to tumorigenesis. | PMID: 17699752 |
| Hereditary Cancer Syndromes | Germline variants in ARL11 (e.g., p.Trp149*) segregate with familial cancer predisposition. | OMIM 609301 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Lymph node | 12.3 | Medium |
| Spleen | 10.8 | Medium |
| Prostate | 8.5 | Low |
| Colon | 6.2 | Low |
| Breast | 5.1 | Low |
| Lung | 4.7 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HeLa (cervical cancer) | 9.4 | Moderate expression |
| HCT116 (colorectal cancer) | 3.2 | Low expression |
| MCF7 (breast cancer) | 2.8 | Low expression |
| LNCaP (prostate cancer) | 1.5 | Very low expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.446G>A (p.Trp149*) | Nonsense | <1% | Loss of function; truncated protein |
| c.52A>G (p.Thr18Ala) | Missense | <0.5% | Reduced GTP binding and signaling |
| c.226C>T (p.Arg76Cys) | Missense | <0.1% | Impaired apoptosis induction |
| c.398_399del (p.Glu133Valfs*2) | Frameshift | <0.1% | Loss of function |
Mutation functional classification
Loss of Function (LOF)
Nonsense and frameshift mutations (e.g., p.Trp149*, p.Glu133Valfs*2) result in truncated or absent protein, leading to loss of tumor suppressor activity.
Gain of Function (GOF)
No gain-of-function mutations have been reported for ARL11.
Dominant Negative (DN)
Missense variants (e.g., p.Thr18Ala) may act in a dominant-negative manner by interfering with wild-type ARL11 GTPase function.
View complete mutation data：
Gene Ontology (GO)
Pathways
• ARF family signaling
• p53 pathway (indirect regulation)
• Apoptosis signaling
Protein Summary
ARL11 is a small GTPase of the ARF-like family, localized to the nucleus and cytoplasm. It cycles between GDP-bound (inactive) and GTP-bound (active) states. Active ARL11 promotes apoptosis and cell cycle arrest, partly through interaction with p53 and BCL2 family members. The protein is encoded by a single exon and contains conserved GTP-binding motifs. Loss of ARL11 function is associated with cancer progression.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| ARL11 Knockout HEK293 Cell Line | EDJ-KQ7532 | Human | 115761 | Details Get a Quote |
| ARL11 Knockout HeLa Cell Line | EDJ-KQ57962 | Human | 115761 | Details Get a Quote |
| ARL11 Knockout A-549 Cell Line | EDJ-KQ66452 | Human | 115761 | Details Get a Quote |
| ARL11 Knockout HCT 116 Cell Line | EDJ-KQ74874 | Human | 115761 | Details Get a Quote |
