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results suggest that CBFbeta-SMMHC (show MYH11 Antibodies) 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 (show BCR Antibodies)-ABL1 (show ABL1 Antibodies) and CBFB rearrangement is associated with poor outcome and a clinical course similar to that of CML (show BCR Antibodies)-BP, and unlike de novo AML (show RUNX1 Antibodies) 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 (show BTG1 Antibodies) was not sufficient for Vif (show BTG1 Antibodies) assistance; a region including F68 in CBF-beta was also required for the stability and function of Vif (show BTG1 Antibodies).
Vif (show BTG1 Antibodies) stabilization by CBFbeta is mainly caused by impairing MDM2 (show MDM2 Antibodies)-mediated degradation.
Mutational analysis of CBFbeta revealed that F68 and I55 (show FBXL14 Antibodies) residues are important and participate in a tripartite hydrophobic interaction with W5 of Vif (show BTG1 Antibodies) to maintain a stable and functional Vif (show BTG1 Antibodies)-CBFbeta complex.
Thus, an NGF (show NGFB Antibodies)/TrkA (show NTRK1 Antibodies)-MAPK (show MAPK1 Antibodies)-CBFbeta pathway converges with Islet1 (show ISL1 Antibodies)-Runx1 (show RUNX1 Antibodies) signaling to promote Runx1 (show RUNX1 Antibodies)/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 (show TOP2 Antibodies)-mediated DNA damage at the leukemia-associated genes MLL (show MLL Antibodies) and CBFB.
These results provide important information on the assembly of the Vif (show BTG1 Antibodies)-CUL5 (show CUL5 Antibodies)-E3 ubiquitin ligase (show MUL1 Antibodies) and identify a new viV binding interface with CBF-beta at the C-terminus of HIV-1 Vif (show BTG1 Antibodies).
Vif (show BTG1 Antibodies) proteins of human and simian immunodeficiency viruses require cellular CBFbeta to degrade APOBEC3G (show APOBEC3G Antibodies).
simian immunodeficiency virus (SIV) Vif (show BTG1 Antibodies) binds to and requires CBF-beta to degrade rhesus macaque APOBEC3G (show APOBEC3G Antibodies)
In neuronal fate determination, Runx co-factor Cbfbeta is essential for its function, but the high level of Runx3 (show RUNX3 Antibodies) expression can overcome the loss of Cbfbeta, demonstrating that Cbfbeta in this context serves solely as a signal amplifier of Runx3 (show RUNX3 Antibodies) 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 (show JUNB Antibodies)-CBFbeta signaling for maintaining sarcomere architecture and function.
results show that, besides its osteogenic role, Cbfbeta governs osteoblast-adipocyte lineage commitment both cell nonautonomously through enhancing beta-catenin (show CTNNB1 Antibodies) 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 (show CHD3 Antibodies) deficiency delays leukemia initiation induced by Cbfb-MYH11 (show MYH11 Antibodies).
results indicate that modulations in the relative levels of the isoforms may adjust transcriptional activation by Runx2 (show RUNX2 Antibodies) to appropriate physiological levels. Cbfb2 was more abundant, but Cbfb1 was more potent for enhancing Runx2 (show RUNX2 Antibodies) 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 (show UTP3 Antibodies) is caused by relaying Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) 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
Cbfb plays an important role in the stabilization of Runx family proteins; and that Runx2 (show RUNX2 Antibodies) protein stability is less dependent on Cbfb in calvariae than in cartilaginous limb skeletons
findings indicate that Cbfbeta stabilizes Runx2 (show RUNX2 Antibodies) in osteoblasts by forming a complex and thus facilitates the proper maintenance of bone mass, particularly cortical bone
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