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anti-Mouse (Murine) BCL9 Anticorps:
anti-Human BCL9 Anticorps:
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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 (Montrer BCL9L Anticorps) and Pygo1 (Montrer PYGO1 Anticorps)/2 act independently of beta-catenin (Montrer CTNNB1 Anticorps) to ensure proper enamel formation.
ARX positively regulates Wnt (Montrer WNT2 Anticorps)/ beta-catenin (Montrer CTNNB1 Anticorps) signaling and the C-terminal domain of ARX interacts with the armadillo (Montrer PKP1 Anticorps) repeats in beta-catenin (Montrer CTNNB1 Anticorps) to promote Wnt (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) signaling. In addition, we found BCL9 and P300 (Montrer NOTCH1 Anticorps) also interact with ARX to modulate Wnt (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) signaling.
Study demonstrates that the Golgi resident protein GM130 (Montrer GOLGA2 Anticorps) activates the spindle assembly factor TPX2 (Montrer DAZL Anticorps) to nucleate microtubules around the Golgi and further captures them to couple mitotic membranes to the spindle.
Pax6 (Montrer PAX6 Anticorps), the master regulator of eye development, directly activates Bcl9/9l transcription.
These results suggest a critical role of BCL9/9-2 in the Wnt (Montrer WNT2 Anticorps)-mediated regulation of adult, as opposed to embryonic, myogenic progenitors.
MEF2D (Montrer MEF2D Anticorps)-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 (Montrer HDAC9 Anticorps).
it was demonstrated that miR218 modulated a novel molecular target and the present study provided novel insights into potential mechanisms of RCC (Montrer XRCC1 Anticorps) 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 (Montrer CTNNB1 Anticorps) Signaling is Associated With Poor Outcome in Colorectal Cancer
BCL9 is a molecular driver of DCIS invasive progression.
PCDH10 (Montrer PCDH10 Anticorps) antagonized MM cell proliferation via the downregulation of Wnt (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps)/BCL-9 signaling, whereas PCDH10 (Montrer PCDH10 Anticorps) repressed the expression of AKT (Montrer AKT1 Anticorps) to promote the expression of GSK3beta (Montrer GSK3b Anticorps) and then to restrain the activation of beta-catenin (Montrer CTNNB1 Anticorps)
By beta-catenin's association with LEF1 (Montrer LEF1 Anticorps) and BCL9-2/B9L (Montrer BCL9L Anticorps).
MiR (Montrer MLXIP Anticorps)-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 (Montrer CTNNB1 Anticorps) interaction and selectively suppresses oncogenic Wnt (Montrer WNT2 Anticorps) transcription.
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