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Both XBcl9 and XPygo2 are required to induce supernumerary axis and dorsal gene activation in Xenopus embryos.
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.
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).
MiR (show MLXIP Proteins)-30-5p downregulation occurs as a result of interaction between multiple myeloma cells and bone marrow stromal cells, which in turn enhances expression of BCL9.
we detected five SNPs in the first two genes/loci - BCL9 and C9orf5 - strongly associated with negative symptoms of schizophrenia
Inhibition of the BCL9-beta-catenin (show CTNNB1 Proteins) interaction and selectively suppresses oncogenic Wnt (show WNT2 Proteins) transcription.
growth factor induced proliferation mediates a neutralizing response by significantly increasing miR (show MLXIP Proteins)-30c-2* which reduces BCL9 expression and cell proliferation in SKOV-3 and OVCAR-3 cells
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