-
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.
-
Vif stabilization by CBFbeta is mainly caused by impairing MDM2-mediated degradation.
-
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.
-
data provide, to our knowledge, the first evidence for the presence of B-1 progenitor cells in the fetal liver that arise independently of HSCs and implicate Cbfbeta as a critical molecule in the development of this lineage