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This study investigated the role of circ-CBFB in chronic lymphocytic leukemia. The ID of circ-CBFB in circBase is hsa_circ_0000707, which locates at chromosome 16q22.1 and derived from the back-splicing of CBFB transcript.
results suggest that CBFbeta-SMMHC 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)
Both c-kit receptor (KIT) D816V and KIT N822K mutations underwent autophosphorylation in the absence of growth factor in leukemia TF-1 cell line.
The co-existence of BCR-ABL1 and CBFB rearrangement is associated with poor outcome and a clinical course similar to that of CML-BP, and unlike de novo AML 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 was not sufficient for Vif assistance; a region including F68 in CBF-beta was also required for the stability and function of Vif.
Vif stabilization by CBFbeta is mainly caused by impairing MDM2-mediated degradation.
Mutational analysis of CBFbeta revealed that F68 and I55 residues are important and participate in a tripartite hydrophobic interaction with W5 of Vif to maintain a stable and functional Vif-CBFbeta complex.
Thus, an NGF/TrkA-MAPK-CBFbeta pathway converges with Islet1-Runx1 signaling to promote Runx1/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-mediated DNA damage at the leukemia-associated genes MLL and CBFB.
These results provide important information on the assembly of the Vif-CUL5-E3 ubiquitin ligase and identify a new viV binding interface with CBF-beta at the C-terminus of HIV-1 Vif.
CBF-beta promoted steady-state levels of HIV-1 Vif by inhibiting the degradation of HIV-1 Vif through the proteasome pathway.
CBFB contributes to the transcriptional regulation of ribosomal gene expression and provide further understanding of the epigenetic role of CBFB-SMMHC in proliferation and maintenance of the leukemic phenotype.
we report a novel hypomethylation pattern, specific to CBFB-MYH11 fusion resulting from inv(16) rearrangement in acute myeloid leukemia the expression of which correlated with PBX3 differential methylation
suggest that a different mechanism exists for the Vif-APOBEC interaction and that non-primates are not suitable animal models for exploring pharmacological interventions that disrupt Vif-CBF-beta interaction
Our findings indicate that RUNX1 and CBF-beta cooperate in cells to modulate HIV-1 replication
Suggest that CBFbeta retention in the midbody during cytokinesis reflects a novel function that contributes to epigenetic control.
Transcriptional analysis revealed that upon fusion protein knockdown, a small subset of the CBFbeta-MYH11 target genes show increased expression, confirming a role in transcriptional repression
Authors propose that CBFbeta acts as a chaperone to stabilize HIV-1 Vif during and after synthesis and to facilitate interaction of Vif with cellular cofactors required for the efficient degradation of APOBEC3G.
Vif proteins of human and simian immunodeficiency viruses require cellular CBFbeta to degrade APOBEC3G.
simian immunodeficiency virus (SIV) Vif binds to and requires CBF-beta to degrade rhesus macaque APOBEC3G
In neuronal fate determination, Runx co-factor Cbfbeta is essential for its function, but the high level of Runx3 expression can overcome the loss of Cbfbeta, demonstrating that Cbfbeta in this context serves solely as a signal amplifier of Runx3 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-CBFbeta signaling for maintaining sarcomere architecture and function.
Runx/Cbfb complexes protect group 2 innate lymphoid cells from exhausted-like hyporesponsiveness during allergic airway inflammation.
CBFbeta plays an essential role in female fertility by acting as a critical cofactor of CBF transcription factor complexes, which regulate the expression of specific key ovulatory and luteal genes, thus coordinating the ovulatory process and luteal development/function in mice.
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, Runx3, or their binding partner Cbfb in NK cells resulted in defective clonal expansion and memory formation during viral infection, with evidence for Runx1-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 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 deficiency delays leukemia initiation induced by Cbfb-MYH11.
results indicate that modulations in the relative levels of the isoforms may adjust transcriptional activation by Runx2 to appropriate physiological levels. Cbfb2 was more abundant, but Cbfb1 was more potent for enhancing Runx2 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 is caused by relaying Wnt/beta-catenin to pre-B cell receptor signaling pathways through the regulation of Runx/CBFbeta heterodimerization was verified
These findings demonstrate that Cbfbeta2 is a central regulator of the MALT developmental program, but the dependency of Runx proteins on the lymphoid tissue development would differ among types of mucosa.
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 protein stability is less dependent on Cbfb in calvariae than in cartilaginous limb skeletons
findings indicate that Cbfbeta stabilizes Runx2 in osteoblasts by forming a complex and thus facilitates the proper maintenance of bone mass, particularly cortical bone
Runx/Cbfb signaling regulate androgen receptor pathway, but does not affect the circulating testosterone levels or the enzymatic conversion to DHT.
Cbfb deficiency results in differentiation blocks and stem cell expansion in hematopoiesis.
Cbfbeta functions in upregulating Ihh expression to promoter chondrocyte proliferation and osteoblast differentiation, and inhibiting PPR expression to enhance chondrocyte differentiation.
results demonstrate that Cbfbeta mediates cartilage and bone development by interacting with Runx1 and Runx2 to regulate the expressions of Col X and Osx for chondrocyte and osteoblast development
It is concluded from the result that miR-125b is a key regulatory factor of osteoblastic differentiation by directly targeting Cbfbeta and indirectly acting on Runx2 at an early stage osteoblastic differentiation.
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