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