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Both XBcl9 and XPygo2 are required to induce supernumerary axis and dorsal gene activation in Xenopus embryos.
Transcriptional cofactors Bcl9, Bcl9l (show BCL9L Proteins) and Pygo1 (show PYGO1 Proteins)/2 act independently of beta-catenin (show CTNNB1 Proteins) to ensure proper enamel formation.
ARX positively regulates Wnt (show WNT2 Proteins)/ beta-catenin (show CTNNB1 Proteins) signaling and the C-terminal domain of ARX interacts with the armadillo (show PKP1 Proteins) repeats in beta-catenin (show CTNNB1 Proteins) to promote Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling. In addition, we found BCL9 and P300 (show NOTCH1 Proteins) also interact with ARX to modulate Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling.
Study demonstrates that the Golgi resident protein GM130 (show GOLGA2 Proteins) activates the spindle assembly factor TPX2 (show DAZL Proteins) to nucleate microtubules around the Golgi and further captures them to couple mitotic membranes to the spindle.
Pax6 (show PAX6 Proteins), the master regulator of eye development, directly activates Bcl9/9l transcription.
These results suggest a critical role of BCL9/9-2 in the Wnt (show WNT2 Proteins)-mediated regulation of adult, as opposed to embryonic, myogenic progenitors.
results from this study demonstrated that hypoxia induced BCL-9 expression in human CRC (show CALR Proteins) cells mainly through HIF-1alpha (show HIF1A Proteins), which could be an important underlying mechanism for increased BCL-9 expression in CRC (show CALR Proteins).
SOX7 (show SOX7 Proteins) inhibits oncogenic beta-catenin (show CTNNB1 Proteins)-mediated transcription by disrupting the beta-catenin (show CTNNB1 Proteins)/BCL9 interaction.
The authors used CRISPR/Cas9 genome engineering of Drosophila legless (lgs) and human BCL9 and B9L (show BCL9L Proteins) to show that the C-terminus downstream of their adaptor elements is crucial for Wnt (show WNT2 Proteins) responses.
MEF2D (show MEF2D Proteins)-BCL9-positive patients had B-cell precursor immunophenotype and were characterized as being older in age, being resistant to chemotherapy, having very early relapse, and having leukemic blasts that mimic morphologically mature B-cell leukemia with markedly high expression of HDAC9 (show HDAC9 Proteins).
it was demonstrated that miR218 modulated a novel molecular target and the present study provided novel insights into potential mechanisms of RCC (show XRCC1 Proteins) oncogenesis.
findings indicate that BCL9 most likely does not harbor a common genetic variant that can increase the risk for schizophrenia in the Japanese population
BCL9/9L-beta-catenin (show CTNNB1 Proteins) Signaling is Associated With Poor Outcome in Colorectal Cancer
BCL9 is a molecular driver of DCIS invasive progression.
PCDH10 (show PCDH10 Proteins) antagonized MM cell proliferation via the downregulation of Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins)/BCL-9 signaling, whereas PCDH10 (show PCDH10 Proteins) repressed the expression of AKT (show AKT1 Proteins) to promote the expression of GSK3beta and then to restrain the activation of beta-catenin (show CTNNB1 Proteins)
By beta-catenin's association with LEF1 (show LEF1 Proteins) and BCL9-2/B9L (show BCL9L Proteins).
BCL9 is associated with B-cell acute lymphoblastic leukemia. It may be a target of translocation in B-cell malignancies with abnormalities of 1q21. Its function is unknown. The overexpression of BCL9 may be of pathogenic significance in B-cell malignancies.
B-cell CLL/lymphoma 9
, B-cell lymphoma 9
, B-cell CLL/lymphoma 9 protein-like
, b-cell CLL/lymphoma 9 protein-like
, B-cell CLL/lymphoma 9 protein
, B-cell lymphoma 9 protein
, nuclear co-factor of beta-catenin signalling
, protein legless homolog