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抗Rat (Rattus) 抗体:
抗Mouse (Murine) 抗体:
Vif (显示 BTG1 抗体) proteins of human and simian immunodeficiency viruses require cellular CBFbeta to degrade APOBEC3G (显示 APOBEC3G 抗体).
simian immunodeficiency virus (SIV) Vif (显示 BTG1 抗体) binds to and requires CBF-beta to degrade rhesus macaque APOBEC3G (显示 APOBEC3G 抗体)
High CBFB expression is associated with leukemia.
Vif (显示 BTG1 抗体) stabilization by CBFbeta is mainly caused by impairing MDM2 (显示 MDM2 抗体)-mediated degradation.
the mechanistic view that the proliferative function of Crlz-1 (显示 UTP3 抗体) is caused by relaying Wnt (显示 WNT2 抗体)/beta-catenin (显示 CTNNB1 抗体) 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 (显示 RUNX2 抗体) protein stability is less dependent on Cbfb in calvariae than in cartilaginous limb skeletons
findings indicate that Cbfbeta stabilizes Runx2 (显示 RUNX2 抗体) in osteoblasts by forming a complex and thus facilitates the proper maintenance of bone mass, particularly cortical bone
Runx/Cbfb signaling regulate androgen receptor (显示 AR 抗体) 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 (显示 IHH 抗体) expression to promoter chondrocyte proliferation and osteoblast differentiation, and inhibiting PPR (显示 PTH1R 抗体) expression to enhance chondrocyte differentiation.
results demonstrate that Cbfbeta mediates cartilage and bone development by interacting with Runx1 (显示 RUNX1 抗体) and Runx2 (显示 RUNX2 抗体) to regulate the expressions of Col (显示 HDAC1 抗体) X and Osx (显示 SP7 抗体) for chondrocyte and osteoblast development
In neuronal fate determination, Runx co-factor Cbfbeta is essential for its function, but the high level of Runx3 (显示 RUNX3 抗体) expression can overcome the loss of Cbfbeta, demonstrating that Cbfbeta in this context serves solely as a signal amplifier of Runx3 (显示 RUNX3 抗体) 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 (显示 JUNB 抗体)-CBFbeta signaling for maintaining sarcomere architecture and function.
discussion of the role of CBFB in diseases caused by their mutations or deletions (review)
The co-existence of BCR (显示 BCR 抗体)-ABL1 (显示 ABL1 抗体) and CBFB rearrangement is associated with poor outcome and a clinical course similar to that of CML (显示 BCR 抗体)-BP, and unlike de novo AML (显示 RUNX1 抗体) 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 (显示 BTG1 抗体) was not sufficient for Vif (显示 BTG1 抗体) assistance; a region including F68 in CBF-beta was also required for the stability and function of Vif (显示 BTG1 抗体).
Mutational analysis of CBFbeta revealed that F68 and I55 (显示 FBXL14 抗体) residues are important and participate in a tripartite hydrophobic interaction with W5 of Vif (显示 BTG1 抗体) to maintain a stable and functional Vif (显示 BTG1 抗体)-CBFbeta complex.
Thus, an NGF (显示 NGFB 抗体)/TrkA (显示 NTRK1 抗体)-MAPK (显示 MAPK1 抗体)-CBFbeta pathway converges with Islet1 (显示 ISL1 抗体)-Runx1 (显示 RUNX1 抗体) signaling to promote Runx1 (显示 RUNX1 抗体)/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 (显示 TOP2 抗体)-mediated DNA damage at the leukemia-associated genes MLL (显示 MLL 抗体) and CBFB.
These results provide important information on the assembly of the Vif (显示 BTG1 抗体)-CUL5 (显示 CUL5 抗体)-E3 ubiquitin ligase (显示 MUL1 抗体) and identify a new viV binding interface with CBF-beta at the C-terminus of HIV-1 Vif (显示 BTG1 抗体).
CBF-beta promoted steady-state levels of HIV-1 Vif (显示 BTG1 抗体) by inhibiting the degradation of HIV-1 Vif (显示 BTG1 抗体) 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 (显示 MYH11 抗体) in proliferation and maintenance of the leukemic phenotype.
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
core binding factor beta
, core-binding factor subunit beta
, core-binding factor, beta subunit
, core binding factor beta subunit
, SL3-3 enhancer factor 1 subunit beta
, SL3/AKV core-binding factor beta subunit
, polyomavirus enhancer-binding protein 2 beta subunit
, CCAAT-binding transcription factor subunit B
, core-binding factor beta
, SL3-3 enhancer factor 1 beta subunit
, polyomavirus enhancer binding protein 2, beta subunit
, CAAT box DNA-binding protein subunit A
, CAAT-box DNA-binding protein subunit A
, nuclear transcription factor Y subunit A
, nuclear transcription factor Y subunit alpha
, CAAT box DNA-binding protein subunit B
, CAAT-box DNA-binding protein subunit B
, CCAAT binding transcription factor of CBF-B/NFY-B
, CCAAT-binding transcription factor subunit A
, nuclear transcription factor - Y beta
, nuclear transcription factor Y subunit B
, nuclear transcription factor Y subunit beta