| protein
| interacting with ERBB2 (ERBB2-induced signaling is also directly liked to the cadherin-mediated cell adhesion and "invasion-suppressor" system through CTNNB1 and plakoglobin in cancers)  |
|
RUVBL2 interaction partner (binds beta-catenin in the region of Armadillo repeats 2-5 and, more importantly, also binds the TATA box binding protein, and involved in the nuclear function of beta-catenin) |
|
beta-catenin forms a 1:1 heterodimer with alpha-catenin |
|
in normal retina tissues and in retinoblstoma, beta-catenin is associated with N-cadherin |
|
14-3-3-zeta protein |
|
beta-catenin interacts with FOXO transcription factors |
|
beta-catenin is required for osteoblast lineage differentiation |
|
interacting with DKK3 (is a negative regulator of beta-catenin and its downregulation contribute to an activation of the beta-catenin signaling pathway) |
|
ZEB1 is an effector of CTNNB1/TCF4 signaling in epithelial-to-mesenchymal transition and tumor progression |
|
stimulates KCNA5 and thus participates in the shaping of the cardiac action potential and further KCNA5 sensitive cellular functions |
|
CTNNB1 activates the HOXA10 and CDX4 genes in myeloid progenitor cells |
|
ARRB1 is a nuclear transcriptional regulator of EDN1-induced CTNNB1 signaling |
|
expression of BRMS1L depends on CTNNB1 activity and contributes to FSHB induction by GNRH1 |
|
CDH5 interacts with CTNND1and CTNNB1 through its cytoplasmic tail |
|
WNT/RSPO1/CTNNB1 signals control axonal sorting and lineage progression in Schwann cell development |
|
SKP2 may regulate CTNNB1 and its target gene expression to orchestrate hematopoietic stem cell (HSC) homing |
|
MMP7 catalytic activity regulates CTNNB1 localization and signaling activation in lung epithelial cells |
|
SIRT2, inhibits the Wnt signaling pathway in nonmalignant cells by binding to CTNNB1 |
|
a COPS5/CTNNB1/SIAH1 interaction network that might control CTNNB1 degradation in colorectal cancer cells |
|
complex role for HSF1 in the regulation of ELAVL1 and CTNNB1 expression that may be significant in mammary carcinogenesis |
|
TRAF4 mediated the translocation of CTNNB1 from the cytoplasm to the nucleus, thereby facilitating activation of the Wnt signaling pathway in breast cancer |
|
PROM1 associates with membrane CTNNB1 in early placodes, and its continued expression correlates with loss of CTNNB1 and CDH1 from the cell membrane at a time when CDH1 transcriptional repressors SNAI1 and SNAI2 are not implicated |
|
CTNNB1 links VHL to AURKA and loss of primary cilia in renal cell carcinoma |
|
HDAC7 suppresses RUNX2 activity and osteoblast differentiation, and suppresses proliferation and CTNNB1 activity in chondrocytes |
|
HSPH1 is required for WNT signaling, since depletion of HSPH1 compromises CTNNB1 accumulation and target gene transcription upon WNT stimulation |
|
molecular mechanism by which glucose deprivation can induce the GSK3B-independent protein degradation of CTNNB1, leading to autophagy |
| Other morbid association(s)
|
| Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
|---|
| tumoral
| germinal mutation
|
|
|
| |
missense mutations in exon-3 associated to histologically, a more aggressive hepatocellular carcinoma (also, mutations might lead to HCC in the absence of cirrhosis) | | tumoral
| germinal mutation
|
|
|
| |
highly common in desmoid tumors (patients harboring CTNNB1 (45F) mutations are at particular risk for recurrence) | | tumoral
| somatic mutation
|
|
|
| |
in ovarian malignant transformation with a characteristic phenotype: endometrioid ovarian carcinoma | | tumoral
| somatic mutation
|
|
|
| |
in HNPCC tumors existed within the regulatory domain of beta-catenin | | tumoral
|
|
| --over
|
| |
beta-catenin accumulation may play a role in the development of hepatoblastoma and activating mutations may substitute biallelic APC inactivation in this tumor type | | tumoral
| germinal mutation
|
|
|
| |
in pilomatricomas | | constitutional
|
|
|
| loss of function
| |
of YAP1- and CTNNB1-mediated transcription blocked cell cycle reentry and progression through G1 into S phase, respectively | |
|
| deletion of exon 3 in beta -catenine mice leads to adenomatous intestinal polyps resembling those in Apc knockout mice | |
Transgenic mice that overproduced an oncogenic form of beta-catenin in the epithelial cells of the kidney developed severe polycystic lesions |
|
inactivation of mouse beta-catenin leads to ectopic formation of chondrocytes at the expense of osteoblast differentiation during both intramembranous and endochondral ossification |
|
conditional inactivation of mouse beta-catenin blocks the differentiation and the development of osteoblast precursors into chondrocytes |
|
conditional deletion of beta-catenin in mouse proepicardium led to impaired formation of coronary arteries. Mutant mice exhibited impaired epicardial development, including failed expansion of the subepicardial space, blunted invasion of the myocardium, and impaired differentiation of epicardium-derived mesenchymal cells into coronary smooth muscle cells |
|
mice carrying CTNNB1 loss-of-function mutations show a delay in axonal sorting |
