CTNNB1 Antibodies
Background
CTNNB1 is a hub protein with dual functions. It not only participates in the structural maintenance of intercellular adhesion junctions but also serves as a core effector molecule in the Wnt signaling pathway to regulate gene transcription. This protein plays a key role in embryonic development, tissue homeostasis and trauma repair by coordinating cadherin-mediated cellular mechanical junctions with the activation of nuclear target genes. In 1993, scientists first discovered that its abnormal activation could lead to colorectal cancer. This breakthrough revealed the core position of the Wnt/β-catenin pathway in tumorigenesis, and related research has led to the development of multiple targeted therapeutic strategies. The dynamic balance of CTNNB1 is strictly regulated by the phosphorylation-degradation complex. Its mutations are closely related to malignant tumors such as liver cancer and endometrial cancer, and have become an important biomarker for cancer diagnosis and treatment.
Structure of CTNNB1
CTNNB1 (β -catenin) is a key signal transduction protein with a molecular weight of approximately 88 kDa, and its precise molecular weight varies slightly among different species:
Species | Human | Mice | Zebrafish | Fruit flies |
Molecular Weight (kDa) | 88.0 | 87.8 | 87.5 | 86.3 |
Primary Structural Differences | Contains 12 Armadillo repeat domains | Phosphorylation sites are highly conserved | Retain the core function of the Wnt signal | Homologous genes for the armadillo |
CTNNB1 is composed of 781 amino acids, and its molecular structure contains 12 repetitive Armadillo domains, forming a superhelical conformation to mediate protein interactions. This protein regulates its stability through the N-terminal phosphorylated degradation motif (DSGXXS). When the Wnt signal is activated, its β-TrCP recognition site is protected, thereby avoiding proteasome degradation. The central Armadillo domain of CTNNB1 has a dual function: the C-terminal region binds to E-cadherin to maintain intercellular connections, while the N-terminal region forms a complex with TCF/LEF transcription factors to initiate target gene expression. The phosphorylation status of serine at position 45 determines its cytoplasmic localization or nuclear translocation ability, a characteristic that makes it a core regulatory node in developmental biology and tumor research.
Fig. 1 Dual roles of CTNNB1/β-catenin: Molecular mechanisms from cell adhesion to Wnt signaling regulation.1
Fig. 2 CTNNB1 mutation map analysis: A newly discovered exon 3 mutation site in craniopharyngioma. 2
Key structural properties of CTNNB1:
- Armadillo repeats the domain
- Phosphorylation regulatory region
- Dual-function combined domain
- Verified location signal
- Key phosphorylation site
Functions of CTNNB1
The core function of CTNNB1 is to coordinate intercellular connections and gene transcription regulation, while also participating in multiple pathophysiological processes:
Function | Description |
Wnt signal transmission | As a core effector molecule of the pathway, it escapes and degrades when Wnt is activated and is transcribed into nuclear initiation target genes (such as c-Myc, Cyclin D1). |
Regulation of cell adhesion | By bridging E-cadherin and α -catenin through the Armadillo domain, the mechanical connections and polarity between epithelial cells are maintained. |
Embryonic development | Regulation of gastrulation, body axis establish key developmental events, such as conditional knockout mice model shows that embryonic death phenotype. |
Tissue regeneration | Activate the stem cell proliferation program to drive tissue reconstruction in hepatectomy and intestinal epithelial injury repair. |
Tumorigenesis | Mutations lead to protein stabilization and are closely related to the occurrence of malignant tumors such as colorectal cancer (APC mutation) and liver cancer (CTNNB1 mutation). |
The activity of CTNNB1 exhibits bistable characteristics: it is strictly controlled by the phosphorylation-degradation complex in rest cells, while rapid nuclear accumulation occurs when Wnt is activated. This "all or none" dynamic regulatory mode is significantly different from the gradient response characteristics of other signaling proteins.
Applications of CTNNB1 and CTNNB1 Antibody in Literature
1. Zhuang, Wenting, et al. "CTNNB1 in neurodevelopmental disorders." Frontiers in psychiatry 14 (2023): 1143328. https://doi.org/10.3389/fpsyt.2023.1143328
The article shows that the CTNNB1 gene encodes β -catenin and is a key molecule in the Wnt signaling pathway. Besides being involved in cancer, recent studies have found that its mutations can lead to neurodevelopmental disorders such as intellectual disability and autism (NDDs) by affecting mechanisms like synaptic plasticity and neurogenesis, and it may be a high-risk gene and therapeutic target for NDDs.
2. He, Juan, et al. "Characterization of novel CTNNB1 mutation in Craniopharyngioma by whole-genome sequencing." Molecular cancer 20.1 (2021): 168.https://doi.org/10.1186/s12943-021-01468-7
The article shows that whole-genome sequencing of craniopharyngioma (CP) reveals that 68.75% of the aminogenic type (ACP) cases have CTNNB1 mutations, which are mutually exclusive to the BRAF V600E mutation of PCP. Research has found that a novel mutation in exon 3 of CTNNB1 enhances its stability by inhibiting the ubiquitination of β -catenin, activates the Wnt pathway and promotes cell proliferation.
3. Chen, Lin, et al. "CTNNB1 alternation is a potential biomarker for immunotherapy prognosis in patients with hepatocellular carcinoma." Frontiers in Immunology 12 (2021): 759565. https://doi.org/10.3389/fimmu.2021.759565
Research has found that CTNNB1 mutation (CTnNB1-MUT) can serve as a potential negative predictive marker for immunotherapy of hepatocellular carcinoma (HCC). Patients carrying this mutation have a reduced number of activated immune cells and an activated immunosuppressive pathway in the immune microenvironment, resulting in a poor response to immune checkpoint inhibitor (ICIs) treatment and a shortened progression-free survival period.
4. Ledinek, Živa, Monika Sobočan, and Jure Knez. "The role of CTNNB1 in endometrial cancer." Disease markers 2022.1 (2022): 1442441.https://doi.org/10.1155/2022/1442441
Research has found that CTNNB1 gene mutations are highly prevalent in endometrial cancer, mainly affecting the phosphorylation site of β-catenin, leading to abnormal activation of the Wnt/β-catenin signaling pathway. Although such tumors often present with low-risk characteristics, they are associated with higher recurrence rates and lower overall survival rates, and can serve as novel prognostic markers.
5. Yang, Feng, et al. "Circ-CTNNB1 drives aerobic glycolysis and osteosarcoma progression via m6A modification through interacting with RBM15." Cell proliferation 56.1 (2023): e13344. https://doi.org/10.1111/cpr.13344
Studies have found that the circular RNA circ-CTNNB1 is highly expressed in osteosarcoma. It promotes the m6A modification of key glycolytic genes such as HK2 and GPI through interaction with RBM15, thereby driving the proliferation and metastasis of osteosarcoma cells.
Creative Biolabs: CTNNB1 Antibodies for Research
Creative Biolabs specializes in the production of high-quality CTNNB1 antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.
- Custom CTNNB1 Antibody Development: Tailor-made solutions to meet specific research requirements.
- Bulk Production: Large-scale antibody manufacturing for industry partners.
- Technical Support: Expert consultation for protocol optimization and troubleshooting.
- Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.
For more details on our CTNNB1 antibodies, custom preparations, or technical support, contact us at email.
References
- Ledinek, Živa, Monika Sobočan, and Jure Knez. "The role of CTNNB1 in endometrial cancer." Disease markers 2022.1 (2022): 1442441.https://doi.org/10.1155/2022/1442441
- He, Juan, et al. "Characterization of novel CTNNB1 mutation in Craniopharyngioma by whole-genome sequencing." Molecular cancer 20.1 (2021): 168.https://doi.org/10.1186/s12943-021-01468-7
Anti-CTNNB1 antibodies

Hot products 
- AActivation
- AGAgonist
- APApoptosis
- BBlocking
- BABioassay
- BIBioimaging
- CImmunohistochemistry-Frozen Sections
- CIChromatin Immunoprecipitation
- CTCytotoxicity
- CSCostimulation
- DDepletion
- DBDot Blot
- EELISA
- ECELISA(Cap)
- EDELISA(Det)
- ESELISpot
- EMElectron Microscopy
- FFlow Cytometry
- FNFunction Assay
- GSGel Supershift
- IInhibition
- IAEnzyme Immunoassay
- ICImmunocytochemistry
- IDImmunodiffusion
- IEImmunoelectrophoresis
- IFImmunofluorescence
- IHImmunohistochemistry
- IMImmunomicroscopy
- IOImmunoassay
- IPImmunoprecipitation
- ISIntracellular Staining for Flow Cytometry
- LALuminex Assay
- LFLateral Flow Immunoassay
- MMicroarray
- MCMass Cytometry/CyTOF
- MDMeDIP
- MSElectrophoretic Mobility Shift Assay
- NNeutralization
- PImmunohistologyp-Paraffin Sections
- PAPeptide Array
- PEPeptide ELISA
- PLProximity Ligation Assay
- RRadioimmunoassay
- SStimulation
- SESandwich ELISA
- SHIn situ hybridization
- TCTissue Culture
- WBWestern Blot
