FBXO5 Antibody
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Description
Applications in Research
The FBXO5 antibody is widely employed in cancer biology studies to investigate:
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Prognostic biomarker potential: Elevated FBXO5 expression correlates with poor clinical outcomes in cancers like breast, colon, and cervical tumors .
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Immune microenvironment analysis: FBXO5 modulates tumor-infiltrating immune cells (e.g., Treg/CD8+ T cell ratios) and immune checkpoints, making it a candidate for immunotherapy research .
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Cell cycle regulation: Studies use this antibody to track FBXO5’s role in mitotic progression and its interaction with APC/C .
Example experimental workflows include:
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IHC: Staining tumor sections to localize FBXO5 expression.
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WB: Quantifying FBXO5 levels in lysates from cancer cell lines (e.g., LOVO, SiHa) .
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ICC: Visualizing nuclear/cytoplasmic FBXO5 distribution in fixed cells .
Cancer Prognosis
Pan-cancer analyses reveal that high FBXO5 expression is associated with aggressive tumor phenotypes, including enhanced proliferation and metastasis . For instance:
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In cervical cancer, FBXO5 overexpression promotes autophagy and cell cycle progression (G2/M phase arrest) .
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In colon cancer, FBXO5 silencing reduces tumor growth in vivo, suggesting therapeutic potential .
Immunotherapy Implications
FBXO5’s correlation with immune suppressive markers (e.g., Treg cells) and checkpoint proteins (e.g., PD-1/PD-L1) highlights its role in immune evasion . This makes FBXO5 a candidate for stratifying patients for checkpoint inhibitor therapies.
Mechanistic Insights
The antibody has enabled studies linking FBXO5 to pathways like:
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DNA damage response: FBXO5 stabilizes RAD51, influencing PARP inhibitor sensitivity .
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PI3K/Akt signaling: FBXO5 promotes cell proliferation via this pathway .
Technical Considerations
Product Specs
Buffer
PBS with 0.1% Sodium Azide, 50% Glycerol, pH 7.3. Store at -20°C. Avoid freeze/thaw cycles.
Lead Time
Typically, we can ship your orders within 1-3 business days after receiving them. Delivery time may vary depending on the purchase method or location. Please consult your local distributors for specific delivery timeframes.
Synonyms
Early mitotic inhibitor 1 antibody; Emi 1 antibody; EMI1 antibody; F box only protein 5 antibody; F box protein 5 antibody; F box protein Fbx 5 antibody; F box protein Fbx5 antibody; F-box only protein 5 antibody; FBX5 antibody; FBX5_HUMAN antibody; Fbxo31 antibody; fbxo5 antibody
Target Names
FBXO5
Uniprot No.
Target Background
Function
FBXO5 is a regulator of Anaphase-Promoting Complex (APC) activity during both mitotic and meiotic cell cycles. In the mitotic cell cycle, it acts as both a substrate and an inhibitor of the APC-FZR1 complex. During the G1 phase, it serves as a substrate for the APC-FZR1 complex E3 ligase. Subsequently, it transitions to an inhibitor of the APC-FZR1 complex during S and G2 phases, promoting cell cycle commitment. As an APC inhibitor, FBXO5 prevents the degradation of APC substrates at multiple levels: by interacting with APC and blocking access of APC substrates to the D-box coreceptor (formed by FZR1 and ANAPC10); by suppressing ubiquitin ligation and chain elongation by APC by inhibiting the activities of UBE2C and UBE2S. FBXO5 contributes to genome integrity preservation by coordinating DNA replication with mitosis. Through its APC inhibitory function during interphase, it stabilizes CCNA2 and GMNN, promoting mitosis and preventing rereplication and DNA damage-induced cellular senescence. During oocyte maturation, FBXO5 plays a role in meiosis by inactivating the APC-FZR1 complex. It inhibits APC through its interaction with RPS6KA2, which increases FBXO5 affinity for CDC20, leading to the metaphase arrest of the second meiotic division before fertilization. FBXO5 controls entry into the first meiotic division by inactivating the APC-FZR1 complex. Additionally, FBXO5 promotes migration and osteogenic differentiation of mesenchymal stem cells.
Gene References Into Functions
- Studies using human cell models demonstrate that cell-cycle commitment is mediated by an EMI1-APC/C(CDH1) dual-negative feedback switch, where EMI1 acts as both a substrate and an inhibitor of APC/C(CDH1). (PMID: 29875408)
- Both isoforms of FBXO5 have been shown to enhance the migration and osteogenic differentiation potential of human periodontal ligament stem cells. (PMID: 29850565)
- A study analyzing gene variability markers in early-stage human embryos identified FBXO5 as a putative variability marker for the 3-day, 8-cell embryo stage. (PMID: 26288249)
- Overexpression of Emi1 has been found to promote chromosome instability (CIN) and the development of solid cancers in vivo, suggesting a direct role in solid tumorigenesis. These findings have significant clinical implications. (PMID: 27065322)
- An investigation into the relationship between Emi1 and Skp2 expression in breast cancer revealed a positive correlation between the two. Emi1 expression was also significantly associated with histologic grade, with Skp2 expression exhibiting similar results. (PMID: 24277465)
- Human papillomavirus type 16 E7 expression has been shown to increase EMI1 mRNA expression and inhibit its degradation. (PMID: 24074588)
- The C-terminal domain of Emi1 inhibits multiple functions of APC/C(CDH1). The intrinsically disordered D-box, linker & tail elements, and a structured Zn-binding domain synergistically block the substrate-binding site and inhibit ubiquitin-chain elongation. (PMID: 23708605)
- Depletion of Emi1 has been found to increase the sensitivity of cancer cells to doxorubicin and x-ray irradiation. (PMID: 23645673)
- Emi1 expression (>5%) was observed in 23.3% of ovarian clear cell carcinoma and was associated with high FIGO grades and poor overall survival. (PMID: 23202783)
- Emi1 participates in human hepatocellular carcinoma (HCC) cell proliferation, and its progression is regulated by anaphase-promoting complex/cyclosome (APC/C) inhibition. This inhibition stabilizes Skp2 and enables p27(kip1) degradation. (PMID: 22995332)
- The inhibitory ability of Emi1 on APC/C is negatively regulated by CDKs. (PMID: 21454540)
- Research suggests that Bcr-Abl increases Emi1 phosphorylation and stability, preventing Skp2 protein degradation via APC/Cdh1-induced ubiquitination and promoting proliferation of CML cells. (PMID: 20717963)
- These data indicate that E2F can activate both transcription of cyclin A and the hEmi1-dependent stabilization of APC(Cdh1) targets, such as cyclin A, to facilitate S phase entry. (PMID: 11988738)
- Plk1 activates the anaphase promoting complex by directing the SCF-dependent destruction of Emi1 in prophase. (PMID: 15469984)
- Loss of pRb repression of E2F-mediated transcription leads to misregulation of Emi1 and APC/C substrates, resulting in the generation of tetraploidy and proliferation of genomically unstable cells in the absence of normal p53 function. (PMID: 16861914)
- Emi1 associates with the anaphase-promoting complex/cyclosome (APC/C) and Cdh1 in a complex. Emi1 binds to the APC/C via a conserved C-terminal destruction (D)-box and can compete for APC/C-substrate interaction. (PMID: 16921029)
- Observations reveal a novel mechanism for the control of entry into the first meiotic division: an Emi1-dependent inhibition of APC(Cdh1). (PMID: 17190794)
- These findings suggest that Emi1 plays a critical role in preserving genome integrity by blocking rereplication, highlighting a previously unrecognized function of this inhibitor of anaphase-promoting complex/cyclosome. (PMID: 17234884)
- Emi1 is essential for cell cycle progression, coupling DNA replication with mitosis. (PMID: 17485488)
- A critical spindle pole-associated mechanism, known as the END (Emi1/NuMA/dynein-dynactin) network, spatially restricts APC/C activity in early mitosis. (PMID: 17609108)
- Emi1 protein expression was investigated in ovarian neoplasms. (PMID: 18204430)
- Downregulation of Emi1 and activation of APC leads to stable p21-dependent G2 arrest after DNA damage. (PMID: 19211842)
- Research underscores the crucial role of cyclin A2-CDK2 in regulating the PLK1-SCF(beta-TrCP1)-EMI1-APC/C axis and CDC6 to trigger genome reduplication after suppression of CDK1 activity. (PMID: 19822658)
Database Links
Subcellular Location
Nucleus. Cytoplasm. Cytoplasm, cytoskeleton, spindle.
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