FBXO31 (F-box protein 31)
2008-06-01 Anthony J Bais AffiliationImmunogene Therapy Surgical Research Division, Boston University School of Medicine, Roger Williams Medical Center, 825 Chalkstone Avenue, Providence, RI 02908, USA
Identity
HGNC
LOCATION
16q24.2
LOCUSID
ALIAS
FBX14,FBXO14,Fbx31,MRT45,pp2386
FUSION GENES
DNA/RNA
Description
FBXO31 encodes one mRNA transcript, published analyses have not reordered alternative five prime transcript or start sequences.
FBXO31 is 3,635-bp in length, composed of 9 exons (1 to 9) spanning approximately 55-kb of genomic DNA, and has an ORF of 1,620-bp encoding a protein of 539 amino acids with a predicted mass of 61-kDa.
Alternative five prime transcripts may exist. Homologous mouse cDNA sequences extending further five prime have been used for RT-PCR to identify putative translation start sites and established that alternatively spliced five prime exons result in short and long isoforms. The short isoform is 3,635-bp in length (i.e. approximately with poly A), and is the predicted primary transcript. The long isoform is 3,725-bp in length, contains an additional five prime exon of 87-bp and has an ORF of 1,707-bp encoding a protein of 568 amino acids. An additional smaller isoform of 3,099-bp with an ORF of 1,104-bp and 367 amino acids was predicted in GenBank.
FBXO31 contains a moderate density C + G rich region (66% G + G with 9% CpG) spanning approximately 2.48-kb located within and five prime to the 350-bp exon 1.
The FBXO31 transcript has and an uncharacteristically short 23-bp five prime untranslated region.
Pseudogene
None identified.
Proteins
Description
FBXO31 contains no significant homology to other known proteins apart from a characteristic 40 amino acid F-box domain at the COOH-terminal end.
FBXO31 forms part of the FBXO class of F-box proteins. Comparison of FBXO31 with the F-box domain of functionally demonstrated F-box proteins (i.e. Fbx1, Fbx2, Fbw1a, Fbw1b and Fbl1 ) indicates that FBXO31 matches the F-box consensus more closely than recognized F-box proteins from each of the three classes. Most F-box proteins notated as FBXO do not have recognizable substrate binding domains. In one instance Fbx7 has been shown to contain a proline-rich region that functions with SCF complexes in regulating Cdk1 - cyclin B - phosphorylated hepatoma up-regulated protein ( HURP ) proteolysis. This proline-rich region has been found in other FBXO proteins. The COOH-terminal end of FBXO31 contains a 175-aa glycine and arginine rich region with possible similar function.
FBXO31 contains six minimal D-box (RxxL) motifs. Proteins with RxxL motifs are often degraded via the APC/C( Cdh1 ) ubiquitin ligase.
Expression
FBXO31 is widely expressed as a 3.6-kb transcript at similar levels in breast, testis, ovary, liver, uterus, prostate, colon, stomach, bladder, spinal cord, pancreas, trachea, kidney and thyroid. High expression is found in brain and low expression in bone marrow. FBXO31 is represented by the unigene cluster Hs.567582. cDNA clones from Hs.567582 express in the adrenal gland, blood, colon, germ cells, heart, kidney, liver, lung, muscle, placenta, synovial membrane, tonsil, cervix, lymph tissue, skin, mammary gland, testis, ovary, uterus, prostate, stomach, bladder, spinal cord, pancreas, thyroid and brain.
Localisation
Co-immunoprecipitation experiments indicate that the carboxy terminal domain of FBXO31 associates with the Skp1, Roc-1 and Cullin-1 proteins. Immuno-localization studies demonstrate that ectopic expression of FBXO31 causes a change of Skp1 localization from the nucleus to the cytoplasm. The Skp1 protein returns to a nuclear localization when co-expressed with a FBXO31 protein with a deleted F-box domain.
Function
FBXO31 is associated with the Skp1, Roc-1 and Cullin-1 proteins through its substrate F-box recognition domain and forms part of an SCF ubiquitination complex.
The ubiquitin-dependant proteasome degradation pathway regulates protein abundance and the function of oncogenes, tumor suppressors, transcription factors and other signaling molecules. Ubiquitination begins with the addition of ubiquitin moieties to target proteins and follows a multi-step process, the end point being proteolysis of polyubiquitinated substrates by a 26S multi-protein complex. Ubiquitination of substrates targeted for degradation requires 3 classes of enzymes; the ubiquitin-activating enzymes (E1), the ubiquitin conjugating enzymes (E2) and the ubiquitin ligases (E3). E3 proteins participate in cell cycle progression. SCF complexes (a class of E3 ligases) regulate the G1-S phase transition. A wide variety of SCF targets include G1 phase cyclins, cyclin-dependant kinase inhibitors, DNA replication factors and transcription factors that promote cell cycle progression.
F-box containing proteins act as substrate recognition components of the SCF ubiquitin-ligase complexes in the ubiquitin-dependant proteasome degradation pathway. These complexes contain four components; Skp1, Cullin, Rbx-Rocl-Hrtl and an F-box protein. The F-box motif tethers the F-box protein to other components of the SCF complex by binding the core SCF component Skp1. This motif is generally found in the amino half of the proteins and is often coupled with other protein domains in the variable carboxy terminus of the protein. The most common carboxy terminal domains include leucine-rich repeats (LRRs) and WD-40 domains. Regions rich in glycine and arginine have also been implicated as protein binding domains, although such domains contain a more definitive repeat region than present in FBXO31.
F-box SCF ubiquitin ligase complexes are involved in proteolysis pathways critical to diverse cellular functions including muscle atrophy, DNA metabolism, ER-associated degradation, desmin-related myopathy, signal transduction, control of G1-S progression and orderly execution of cell cycle. Skp1, Cul1 and Rbx1 are invariant proteins of the SCF complex while the F-box proteins that bind to Skp1 are the components that impart functional specificity. For instance Skp2 specifically binds phosphorylated p27 resulting in its degradation and control of S phase entry in the cell cycle.
The ubiquitin-dependant proteasome degradation pathway regulates protein abundance and the function of oncogenes, tumor suppressors, transcription factors and other signaling molecules. Ubiquitination begins with the addition of ubiquitin moieties to target proteins and follows a multi-step process, the end point being proteolysis of polyubiquitinated substrates by a 26S multi-protein complex. Ubiquitination of substrates targeted for degradation requires 3 classes of enzymes; the ubiquitin-activating enzymes (E1), the ubiquitin conjugating enzymes (E2) and the ubiquitin ligases (E3). E3 proteins participate in cell cycle progression. SCF complexes (a class of E3 ligases) regulate the G1-S phase transition. A wide variety of SCF targets include G1 phase cyclins, cyclin-dependant kinase inhibitors, DNA replication factors and transcription factors that promote cell cycle progression.
F-box containing proteins act as substrate recognition components of the SCF ubiquitin-ligase complexes in the ubiquitin-dependant proteasome degradation pathway. These complexes contain four components; Skp1, Cullin, Rbx-Rocl-Hrtl and an F-box protein. The F-box motif tethers the F-box protein to other components of the SCF complex by binding the core SCF component Skp1. This motif is generally found in the amino half of the proteins and is often coupled with other protein domains in the variable carboxy terminus of the protein. The most common carboxy terminal domains include leucine-rich repeats (LRRs) and WD-40 domains. Regions rich in glycine and arginine have also been implicated as protein binding domains, although such domains contain a more definitive repeat region than present in FBXO31.
F-box SCF ubiquitin ligase complexes are involved in proteolysis pathways critical to diverse cellular functions including muscle atrophy, DNA metabolism, ER-associated degradation, desmin-related myopathy, signal transduction, control of G1-S progression and orderly execution of cell cycle. Skp1, Cul1 and Rbx1 are invariant proteins of the SCF complex while the F-box proteins that bind to Skp1 are the components that impart functional specificity. For instance Skp2 specifically binds phosphorylated p27 resulting in its degradation and control of S phase entry in the cell cycle.
Homology
F-box domain containing no other significant homology.
Mutations
Note
None recorded.
Implicated in
Entity name
Neurodegenerative disorders and cancer
Note
Aberrant ubiquitin-dependant proteasome degradation in neurodegenerative disorders and cancer.
Precedence for disruption in neurodegenerative disorders. The Parkin gene functions as a E3 ubiquitin ligase often mutated in inherited forms of Parkinsons disease. In Alzheimers disease defective ubiquitination of cerebral proteins has been identified. The Von Hippel-Lindau ( VHL ) tumor suppressor protein is part of a complex that functions as a ubiquitin-protein ligase E3. VHL associates the ligase complex to target proteins such as HIF1aand VDU1 (VHL interacting deubiquitinating enzyme 1). HIF-a has been shown to regulate genes involved in tumor angiogenesis; VDU1 has deubiquitinating activity.
Aberrant ubiquitin-dependant proteasome degradation of SCF-FBXO31 complexes has been proposed as a mechanism for tumor progression. FBXO31 would function as a tumor suppressor by mediating generation of SCF-FBXO31 complexes that compete and balance levels of other SCF complexes normally targeted to degradation proteins required to maintain cell proliferation. An example is SCF complexes resulting in SCF-Skp2 E3 ligases that mediate ubiquitination and subsequent degradation of the CDK-inhibitor p27. Ectopic expression of FBXO31 would lower SCF-Skp2 complexes resulting in increased p27 and inhibition of transition from G1-S phase. This model corroborates with studies showing that high levels of Skp2 were associated with reduced levels of p27 in several cancers.
Precedence for disruption in neurodegenerative disorders. The Parkin gene functions as a E3 ubiquitin ligase often mutated in inherited forms of Parkinsons disease. In Alzheimers disease defective ubiquitination of cerebral proteins has been identified. The Von Hippel-Lindau ( VHL ) tumor suppressor protein is part of a complex that functions as a ubiquitin-protein ligase E3. VHL associates the ligase complex to target proteins such as HIF1aand VDU1 (VHL interacting deubiquitinating enzyme 1). HIF-a has been shown to regulate genes involved in tumor angiogenesis; VDU1 has deubiquitinating activity.
Aberrant ubiquitin-dependant proteasome degradation of SCF-FBXO31 complexes has been proposed as a mechanism for tumor progression. FBXO31 would function as a tumor suppressor by mediating generation of SCF-FBXO31 complexes that compete and balance levels of other SCF complexes normally targeted to degradation proteins required to maintain cell proliferation. An example is SCF complexes resulting in SCF-Skp2 E3 ligases that mediate ubiquitination and subsequent degradation of the CDK-inhibitor p27. Ectopic expression of FBXO31 would lower SCF-Skp2 complexes resulting in increased p27 and inhibition of transition from G1-S phase. This model corroborates with studies showing that high levels of Skp2 were associated with reduced levels of p27 in several cancers.
Fusion protein
None recorded
Entity name
Breast cancer, Prostate cancer, and several other cancers
Note
Loss of heterozygosity (LOH) of 16q22-qter in breast cancer, prostate cancer, and several other cancers.
This region is frequently deleted in several human cancers causing loss of heterozygosity. The 16q24.3 region including FBXO31 spans approximately 3-Mb from the marker D16S498 to the telomere and contains at least two smallest regions of overlap (SROs). These SROs are most frequently deleted in early and late stage breast cancer and in prostate cancer. Loss of normal function of FBXO31 may be a key event in the early stage of breast cancer. LOH on the whole 16q22-qter region is frequently detected in breast and prostate cancer. Micro-cell mediated transfer experiments with 16q22-qter fragments (the 360-kb YAC clone 792E1 at D16S476 and D16S498 and the 85-kb BAC clone 346J21 at D16S3048 and D16S3063) have been shown to induce senescence in human and rat breast tumor cell lines. FBXO31 encompasses the 792E1 clone and a partial region of 346J21, has been shown to induce senescence in the breast cancer cell line MCF-7 and is regarded as the cellular senescence gene. FBXO31 is a potential tumor suppressor shown to be down-regulated in breast cancer cell lines relative to normal breast expression and cause G1 phase cell cycle arrest of the MDA-MB-468 cell line.
Quantitative gene expression analysis of 78 genes in the 16q24.3 region demonstrated that FBXO31 was one of two genes including CYBA with a moderately aberrant expression profile. Expression of FBXO31 was reduced 100 to 200-fold in MDA-MB-134 and SK-BR-3 and moderately reduced in the other cell lines. 68 other genes displayed normal expression, one displayed significantly aberrant expression ( CBFA2T3 ), six displayed mildly aberrant expression (DPEP1, CDH15, Hs.17074, Hs.189419, SLC7A5 and AA994450), and one gene displayed excessively reduced expression (CA5A). From microarray analysis FBXO31 was one of the 70-gene classifiers down-regulated in association with tumors of a favorable prognosis. The prognostic association between down-regulated FBXO31 and breast tumors corroborates with other studies demonstrating that LOH of chromosome 16q is associated with tumors of favorable prognosis.
This region is frequently deleted in several human cancers causing loss of heterozygosity. The 16q24.3 region including FBXO31 spans approximately 3-Mb from the marker D16S498 to the telomere and contains at least two smallest regions of overlap (SROs). These SROs are most frequently deleted in early and late stage breast cancer and in prostate cancer. Loss of normal function of FBXO31 may be a key event in the early stage of breast cancer. LOH on the whole 16q22-qter region is frequently detected in breast and prostate cancer. Micro-cell mediated transfer experiments with 16q22-qter fragments (the 360-kb YAC clone 792E1 at D16S476 and D16S498 and the 85-kb BAC clone 346J21 at D16S3048 and D16S3063) have been shown to induce senescence in human and rat breast tumor cell lines. FBXO31 encompasses the 792E1 clone and a partial region of 346J21, has been shown to induce senescence in the breast cancer cell line MCF-7 and is regarded as the cellular senescence gene. FBXO31 is a potential tumor suppressor shown to be down-regulated in breast cancer cell lines relative to normal breast expression and cause G1 phase cell cycle arrest of the MDA-MB-468 cell line.
Quantitative gene expression analysis of 78 genes in the 16q24.3 region demonstrated that FBXO31 was one of two genes including CYBA with a moderately aberrant expression profile. Expression of FBXO31 was reduced 100 to 200-fold in MDA-MB-134 and SK-BR-3 and moderately reduced in the other cell lines. 68 other genes displayed normal expression, one displayed significantly aberrant expression ( CBFA2T3 ), six displayed mildly aberrant expression (DPEP1, CDH15, Hs.17074, Hs.189419, SLC7A5 and AA994450), and one gene displayed excessively reduced expression (CA5A). From microarray analysis FBXO31 was one of the 70-gene classifiers down-regulated in association with tumors of a favorable prognosis. The prognostic association between down-regulated FBXO31 and breast tumors corroborates with other studies demonstrating that LOH of chromosome 16q is associated with tumors of favorable prognosis.
Disease
16q22-qter LOH is detected in bilateral breast cancer and ductal lavage, in rare inflammatory breast cancer, and in several other cancers, including central nervous system neuroectodermal ependymoma and primary ependymomas, colorectal liver metastases, gastric tumor cancer, head and neck squamous cell carcinoma, hepatocellular carcinoma, lung tumor, nasopharyngeal tumor, ovarian tumor, rhabdomyosarcoma, and Wilms tumor. 16q22-qter LOH in ovarian, hepatocellular and particularly breast and prostate cancers, exhibit similar SROs, suggesting common molecular pathways are affected.
Article Bibliography
| Pubmed ID | Last Year | Title | Authors |
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| 10024691 | 1999 | Cervical metastases of head and neck squamous cell carcinoma correlate with loss of heterozygosity on chromosome 16q. | Wang X et al |
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| 11526514 | 2001 | Identification of homozygous deletions at chromosome 16q23 in aflatoxin B1 exposed hepatocellular carcinoma. | Yakicier MC et al |
| 11780468 | 2001 | Novel chromosomal alterations detected in primary nasopharyngeal carcinoma by comparative genomic hybridization. | Yan J et al |
| 15756451 | 2005 | Loss of heterozygosity in ductal lavage for breast tumor and the contralateral breast. | Yonekura Y et al |
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Other Information
Locus ID:
NCBI: 79791
MIM: 609102
HGNC: 16510
Ensembl: ENSG00000103264
Variants:
dbSNP: 79791
ClinVar: 79791
TCGA: ENSG00000103264
COSMIC: FBXO31
RNA/Proteins
| Gene ID | Transcript ID | Uniprot |
|---|---|---|
| ENSG00000103264 | ENST00000311635 | Q5XUX0 |
| ENSG00000103264 | ENST00000565593 | H3BQG7 |
| ENSG00000103264 | ENST00000618298 | A0A0C4DGU8 |
| ENSG00000103264 | ENST00000636077 | A0A1B0GV77 |
Expression (GTEx)
Pathways
Protein levels (Protein atlas)
References
| Pubmed ID | Year | Title | Citations |
|---|---|---|---|
| 37611899 | 2024 | Aberrantly High FBXO31 Impairs Oocyte Quality in Premature Ovarian Insufficiency. | 0 |
| 38216561 | 2024 | FBXO31 is upregulated by METTL3 to promote pancreatic cancer progression via regulating SIRT2 ubiquitination and degradation. | 2 |
| 37611899 | 2024 | Aberrantly High FBXO31 Impairs Oocyte Quality in Premature Ovarian Insufficiency. | 0 |
| 38216561 | 2024 | FBXO31 is upregulated by METTL3 to promote pancreatic cancer progression via regulating SIRT2 ubiquitination and degradation. | 2 |
| 36803542 | 2023 | LincRNA ZNF529-AS1 inhibits hepatocellular carcinoma via FBXO31 and predicts the prognosis of hepatocellular carcinoma patients. | 0 |
| 36803542 | 2023 | LincRNA ZNF529-AS1 inhibits hepatocellular carcinoma via FBXO31 and predicts the prognosis of hepatocellular carcinoma patients. | 0 |
| 34706096 | 2022 | Feedback-regulated transcriptional repression of FBXO31 by c-Myc triggers ovarian cancer tumorigenesis. | 4 |
| 34839191 | 2022 | Effects and mechanisms of FBXO31 on Taxol chemoresistance in esophageal squamous cell carcinoma. | 2 |
| 35019165 | 2022 | Novel variants underlying autosomal recessive neurodevelopmental disorders with intellectual disability in Iranian consanguineous families. | 3 |
| 35940557 | 2022 | FBXO31 suppresses lipogenesis and tumor progression in glioma by promoting ubiquitination and degradation of CD147. | 1 |
| 36269678 | 2022 | FBXO31 sensitizes cancer stem cells-like cells to cisplatin by promoting ferroptosis and facilitating proteasomal degradation of GPX4 in cholangiocarcinoma. | 8 |
| 34706096 | 2022 | Feedback-regulated transcriptional repression of FBXO31 by c-Myc triggers ovarian cancer tumorigenesis. | 4 |
| 34839191 | 2022 | Effects and mechanisms of FBXO31 on Taxol chemoresistance in esophageal squamous cell carcinoma. | 2 |
| 35019165 | 2022 | Novel variants underlying autosomal recessive neurodevelopmental disorders with intellectual disability in Iranian consanguineous families. | 3 |
| 35940557 | 2022 | FBXO31 suppresses lipogenesis and tumor progression in glioma by promoting ubiquitination and degradation of CD147. | 1 |
Citation
Anthony J Bais
FBXO31 (F-box protein 31)
Atlas Genet Cytogenet Oncol Haematol. 2008-06-01
Online version: http://atlasgeneticsoncology.org/gene/44280/fbxo31-(f-box-protein-31)
