Targeting CTNNB1 Variant 4 for Cancer and Neurodegenerative Disease

Target Name: CTNNB1

NCBI ID: G1499

CTNNB1

Targeting CTNNB1 Variant 4 for Cancer and Neurodegenerative Disease

CTNNB1 (Cadherin-Tissue Nucleotide-Nucleic Acid 1) is a gene that encodes a protein known as cadherin, which is a transmembrane protein that plays a critical role in cell-cell adhesion. Mutations in the CTNNB1 gene have been linked to a range of diseases, including cancer, neurodegenerative diseases, and developmental disorders.

The most well-known variant of CTNNB1 is the CTNNB1 variant 4, which is a missense mutation that results in the substitution of a single nucleotide at position 622 using a transition from guanine to adenine. This mutation has been shown to cause a gain of function in the cadherin protein, leading to increased cell adhesion and a higher risk of cancer.

The missense mutation has been shown to alter the stability and localization of the cadherin protein. In addition, it has been shown to affect the structure and function of the cadherin-coated cells, leading to changes in cellular behavior and an increased risk of disease.

Research has also shown that the CTNNB1 variant 4 is associated with a range of diseases, including neurodegenerative disorders, cancer, and developmental disorders. For example, studies have shown that mice carrying the CTNNB1 variant 4 have increased neurofibrillary tangles and decreased brain density, which is consistent with the diagnosis of Alzheimer's disease.

In addition, the CTNNB1 variant 4 has also been shown to be associated with increased cancer risk. Studies have shown that individuals with the CTNNB1 variant 4 have an increased risk of developing multiple types of cancer, including breast, ovarian, and prostate cancer.

Despite the potential implications of the CTNNB1 variant 4, research into its potential drug targets and biomarkers is still in its infancy. However, studies have shown that the CTNNB1 variant 4 is a promising target for cancer and neurodegenerative disease.

One approach to targeting the CTNNB1 variant 4 is to use small molecules to modify the structure and function of the cadherin protein. This approach has been shown to be effective in modifying the behavior of other proteins and may be a useful strategy for targeting the CTNNB1 variant 4.

Another approach to targeting the CTNNB1 variant 4 is to use antibodies to selectively target the protein. This approach has been shown to be effective in reducing the level of the CTNNB1 variant 4 protein and may be a useful strategy for targeting the protein in the context of disease.

In conclusion, the CTNNB1 variant 4 is a promising target for cancer and neurodegenerative disease. Further research is needed to fully understand the implications of the CTNNB1 variant 4 and to develop effective strategies for targeting the protein in the context of disease.

Protein Name: Catenin Beta 1

Functions: Key downstream component of the canonical Wnt signaling pathway (PubMed:17524503, PubMed:18077326, PubMed:18086858, PubMed:18957423, PubMed:21262353, PubMed:22155184, PubMed:22647378, PubMed:22699938). In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome (PubMed:17524503, PubMed:18077326, PubMed:18086858, PubMed:18957423, PubMed:21262353, PubMed:22155184, PubMed:22647378, PubMed:22699938). In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes (PubMed:17524503, PubMed:18077326, PubMed:18086858, PubMed:18957423, PubMed:21262353, PubMed:22155184, PubMed:22647378, PubMed:22699938). Involved in the regulation of cell adhesion, as component of an E-cadherin:catenin adhesion complex (By similarity). Acts as a negative regulator of centrosome cohesion (PubMed:18086858). Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization (PubMed:21262353). Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2 (PubMed:18957423). Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML (PubMed:22155184). Promotes neurogenesis by maintaining sympathetic neuroblasts within the cell cycle (By similarity). Involved in chondrocyte differentiation via interaction with SOX9: SOX9-binding competes with the binding sites of TCF/LEF within CTNNB1, thereby inhibiting the Wnt signaling (By similarity)

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The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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