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anti-Mouse (Murine) BCL9 Antibodies:
anti-Human BCL9 Antibodies:
anti-Rat (Rattus) BCL9 Antibodies:
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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 Antibodies) and Pygo1 (show PYGO1 Antibodies)/2 act independently of beta-catenin (show CTNNB1 Antibodies) to ensure proper enamel formation.
ARX positively regulates Wnt (show WNT2 Antibodies)/ beta-catenin (show CTNNB1 Antibodies) signaling and the C-terminal domain of ARX interacts with the armadillo (show PKP1 Antibodies) repeats in beta-catenin (show CTNNB1 Antibodies) to promote Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling. In addition, we found BCL9 and P300 (show NOTCH1 Antibodies) also interact with ARX to modulate Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling.
Study demonstrates that the Golgi resident protein GM130 (show GOLGA2 Antibodies) activates the spindle assembly factor TPX2 (show DAZL Antibodies) to nucleate microtubules around the Golgi and further captures them to couple mitotic membranes to the spindle.
Pax6 (show PAX6 Antibodies), 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 Antibodies)-mediated regulation of adult, as opposed to embryonic, myogenic progenitors.
High BCL9 expression is associated with cisplatin-resistance in non-small cell lung cancer.
miR (show MLXIP Antibodies)-1301 inhibits hepatocellular carcinoma cell migration, invasion, and angiogenesis by decreasing Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling through targeting BCL9.
results from this study demonstrated that hypoxia induced BCL-9 expression in human CRC (show CALR Antibodies) cells mainly through HIF-1alpha (show HIF1A Antibodies), which could be an important underlying mechanism for increased BCL-9 expression in CRC (show CALR Antibodies).
SOX7 (show SOX7 Antibodies) inhibits oncogenic beta-catenin (show CTNNB1 Antibodies)-mediated transcription by disrupting the beta-catenin (show CTNNB1 Antibodies)/BCL9 interaction.
The authors used CRISPR/Cas9 genome engineering of Drosophila legless (lgs) and human BCL9 and B9L (show BCL9L Antibodies) to show that the C-terminus downstream of their adaptor elements is crucial for Wnt (show WNT2 Antibodies) responses.
MEF2D (show MEF2D Antibodies)-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 Antibodies).
it was demonstrated that miR218 modulated a novel molecular target and the present study provided novel insights into potential mechanisms of RCC (show XRCC1 Antibodies) 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 Antibodies) Signaling is Associated With Poor Outcome in Colorectal Cancer
BCL9 is a molecular driver of DCIS invasive progression.
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