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results suggest that CBFbeta-SMMHC (zeige MYH11 Proteine) has complex actions on human ribosome biogenesis at both the genomic and posttranscriptional level
the presented study demonstrates that CBFB-MYH11-based MRD status during the first 3 months after allo-HCT, but not KIT mutations, can be used to identify patients with a high risk of relapse.
discussion of the role of CBFB in diseases caused by their mutations or deletions (review)
The co-existence of BCR (zeige BCR Proteine)-ABL1 (zeige ABL1 Proteine) and CBFB rearrangement is associated with poor outcome and a clinical course similar to that of CML (zeige BCR Proteine)-BP, and unlike de novo AML (zeige RUNX1 Proteine) with CBFB rearrangement, suggesting that high-intensity chemotherapy with TKI should be considered in these patients.
Moreover, using a CBF-beta loss-of-function mutant, the authors demonstrated that the interaction between CBF-beta and Vif (zeige BTG1 Proteine) was not sufficient for Vif (zeige BTG1 Proteine) assistance; a region including F68 in CBF-beta was also required for the stability and function of Vif (zeige BTG1 Proteine).
Vif (zeige BTG1 Proteine) stabilization by CBFbeta is mainly caused by impairing MDM2 (zeige MDM2 Proteine)-mediated degradation.
Mutational analysis of CBFbeta revealed that F68 and I55 (zeige FBXL14 Proteine) residues are important and participate in a tripartite hydrophobic interaction with W5 of Vif (zeige BTG1 Proteine) to maintain a stable and functional Vif (zeige BTG1 Proteine)-CBFbeta complex.
Thus, an NGF (zeige NGFB Proteine)/TrkA (zeige NTRK1 Proteine)-MAPK (zeige MAPK1 Proteine)-CBFbeta pathway converges with Islet1 (zeige ISL1 Proteine)-Runx1 (zeige RUNX1 Proteine) signaling to promote Runx1 (zeige RUNX1 Proteine)/CBFbeta holocomplex formation and nonpeptidergic nociceptor maturation.
Our findings demonstrate that HSPCs exposed to non-cytotoxic levels of environmental chemicals and chemotherapeutic agents are prone to topoisomerase II (zeige TOP2 Proteine)-mediated DNA damage at the leukemia-associated genes MLL (zeige MLL Proteine) and CBFB.
These results provide important information on the assembly of the Vif (zeige BTG1 Proteine)-CUL5 (zeige CUL5 Proteine)-E3 ubiquitin ligase (zeige MUL1 Proteine) and identify a new viV binding interface with CBF-beta at the C-terminus of HIV-1 Vif (zeige BTG1 Proteine).
Vif (zeige BTG1 Proteine) proteins of human and simian immunodeficiency viruses require cellular CBFbeta to degrade APOBEC3G (zeige APOBEC3G Proteine).
simian immunodeficiency virus (SIV) Vif (zeige BTG1 Proteine) binds to and requires CBF-beta to degrade rhesus macaque APOBEC3G (zeige APOBEC3G Proteine)
In neuronal fate determination, Runx co-factor Cbfbeta is essential for its function, but the high level of Runx3 (zeige RUNX3 Proteine) expression can overcome the loss of Cbfbeta, demonstrating that Cbfbeta in this context serves solely as a signal amplifier of Runx3 (zeige RUNX3 Proteine) activity.
characterization of cbfbeta gene
Our data suggest that runx1 and cbfb are required at 2 different steps during early hematopoietic stem cell development
Data demonstrate for the first time an essential role of JunB (zeige JUNB Proteine)-CBFbeta signaling for maintaining sarcomere architecture and function.
the expression of mouse Amtn gene in amelogenesis is mediated by Runx2/Cbfbeta complex. Runx2/Cbfbeta can bind to the two Runx2 binding motifs AACCACT (-1342/-1336) and AACCAAA (-98/-92) in the Amtn promoter and regulate Amtn gene expression.
Specific ablation of Runx1 (zeige RUNX1 Proteine), Runx3 (zeige RUNX3 Proteine), or their binding partner Cbfb in NK cells resulted in defective clonal expansion and memory formation during viral infection, with evidence for Runx1 (zeige RUNX1 Proteine)-mediated control of a cell cycle program.
results show that, besides its osteogenic role, Cbfbeta governs osteoblast-adipocyte lineage commitment both cell nonautonomously through enhancing beta-catenin (zeige CTNNB1 Proteine) signaling and cell autonomously through suppressing adipogenesis gene expression to maintain osteoblast lineage commitment, indicating Cbfbeta may be a therapeutic target for osteoporosis.
Cbfbeta knockdown mice also exhibited decreased expression of key genes within the corpora lutea and morphological changes in the ovarian structure, including the presence of large antral follicles well into the luteal phase. Overall, these data suggest a role for CBFs as significant regulators of gene expression, ovulatory processes, and luteal development in the ovary.
Chd7 (zeige CHD3 Proteine) deficiency delays leukemia initiation induced by Cbfb-MYH11 (zeige MYH11 Proteine).
results indicate that modulations in the relative levels of the isoforms may adjust transcriptional activation by Runx2 (zeige RUNX2 Proteine) to appropriate physiological levels. Cbfb2 was more abundant, but Cbfb1 was more potent for enhancing Runx2 (zeige RUNX2 Proteine) activity. Although only Cbfb2 loss generated overt skeletal phenotypes, both may play major roles in skeletal development with functional redundancy
High CBFB expression is associated with leukemia.
the mechanistic view that the proliferative function of Crlz-1 (zeige UTP3 Proteine) is caused by relaying Wnt (zeige WNT2 Proteine)/beta-catenin (zeige CTNNB1 Proteine) to pre-B cell receptor signaling pathways through the regulation of Runx/CBFbeta heterodimerization was verified
Core binding factor beta deficiency in chondrocytes caused a decrease of protein levels of Runx transcription factors by accelerating polyubiquitination-mediated proteosomal degradation in vitro
The protein encoded by this gene is the beta subunit of a heterodimeric core-binding transcription factor belonging to the PEBP2/CBF transcription factor family which master-regulates a host of genes specific to hematopoiesis (e.g., RUNX1) and osteogenesis (e.g., RUNX2). The beta subunit is a non-DNA binding regulatory subunit\; it allosterically enhances DNA binding by alpha subunit as the complex binds to the core site of various enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers and GM-CSF promoters. Alternative splicing generates two mRNA variants, each encoding a distinct carboxyl terminus. In some cases, a pericentric inversion of chromosome 16
, SL3-3 enhancer factor 1 beta subunit
, SL3-3 enhancer factor 1 subunit beta
, SL3/AKV core-binding factor beta subunit
, core-binding factor subunit beta
, polyomavirus enhancer binding protein 2, beta subunit
, polyomavirus enhancer-binding protein 2 beta subunit
, core binding factor beta subunit
, core-binding factor, beta subunit
, core binding factor beta
, core-binding factor beta
, CCAAT-binding transcription factor subunit B