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1 inding sites for ETS-domain proteins and the core binding factor.
2 not affect the expression of osteocalcin and core binding factor.
3 s a DNA-binding subunit of the heterodimeric core-binding factor.
4 teins that either can or cannot activate the core binding factor 1 (CBF1) in 32D (clone 3) myeloblast
5 ptor gamma (PPARgamma), leptin, osteonectin, core binding factor 1 (CBFA1), and FBJ murine osteosarco
6 s studied include transcription factors like core binding factor 1 (Cbfa1), bone morphogenetic protei
8 on of the osteogenic markers osteocalcin and core-binding factor-1 genes, the latter of which is cons
10 on of both c-Fos and c-Jun in osteoblasts or core-binding factor a1 increased collagenase-3 promoter
11 hermore, overexpression of c-Fos, c-Jun, and core-binding factor a1 synergistically increased collage
12 ulted in the inability of c-Fos and c-Jun or core-binding factor a1 to increase collagenase-3 promote
13 Overexpression of Fra-2 and JunD repressed core-binding factor a1-induced collagenase-3 promoter ac
14 ed from patient platelet RNA exons 3 to 6 of core-binding factor A2 (CBFA2) cDNA, which encompasses t
17 Timed-Sequential Induction in Patients With Core Binding Factor Acute Myeloid Leukemia and Treating
23 ion of the osteoblast differentiation factor core binding factor alpha-1 (Cbfa1) and several bone-ass
24 including Id1, Id2, and Id3, associate with core binding factor alpha-1 (Cbfa1) to cause diminished
26 lysis for gene expression (up to 10 days for core binding factor alpha-1 [Cbfa1], bone sialoprotein [
27 ne expression using Northern blot for Cbfal (core binding factor alpha-1); OCN (osteocalcin), OPN (os
29 olyoma enhancer-binding protein (PEBP2alpha)/core-binding factor alpha (CBFA) class are key transacti
31 tein (MEPE); bone markers: osteocalcin (OC), core-binding factor alpha 1 (CBFalpha1), and alkaline ph
33 Our results of the expression pattern of core binding factor alpha1 (Cbfa1), which binds to the r
38 imulated cells expressed increased levels of core-binding factor alpha1, osteocalcin, alkaline phosph
40 We report that the Ets-1 partner protein core-binding factor alpha2 (CBFalpha2; also known as AML
43 16 to 60 years of age, excluding those with core binding factor AML and acute promyelocytic leukemia
50 nx family members can interact with Cbfbeta (core-binding factor b, encoded by Cbfb), a role for Cbfb
51 f complex is composed of the unique cofactor core binding factor beta (CBF-beta) and canonical ligase
53 ene encodes a chimeric protein involving the core binding factor beta (CBFbeta) and the smooth-muscle
55 sion between the transcription factor called core binding factor beta (CBFbeta) on 16q and a smooth m
60 e transcription factor fusion CBFbeta-SMMHC (core binding factor beta and the smooth-muscle myosin he
61 ng of most of the runt-related X1 co-factor, core binding factor beta fused to the smooth muscle myos
62 duct that fuses the first 165 amino acids of core binding factor beta to the coiled-coil region of a
63 in acts by dominantly interfering with AML-1/core binding factor beta-dependent transcriptional regul
64 K4b expression was caused by inv(16)-encoded core binding factor beta-smooth muscle myosin heavy chai
70 strong expression of RUNX1 and its cofactor, core-binding factor beta (CBFbeta), in megakaryocytes an
71 he presence of AML-1 and its partner protein core-binding factor beta in this osteoblast-restricted c
73 ts interaction with the transcription factor core-binding factor beta subunit (CBFbeta), and induces
74 eins and correlated with the binding of Runx/core-binding factor beta to regulatory elements within t
76 ription factor 1 (RUNX1) and its associating core binding factor-beta (CBFB) play pivotal roles in le
78 os, c-Jun, osteoblast-specific factor-2, and core binding factor-beta increased the response to parat
79 tes transcription in part by helping recruit core binding factors, but nothing is known about the mec
80 minimal residual disease (MRD) monitoring in core binding factor (CBF) acute myeloid leukemia (AML) b
81 icated as a prognostic factor in adults with core binding factor (CBF) acute myeloid leukemia (AML).
82 ding the AML1 (RUNX1) or CBFbeta subunits of core binding factor (CBF) are commonly altered by transl
84 eins, we found that the human enhancer bound core binding factor (CBF) between the muA and mu element
85 were, in 5'-to-3' order, a binding site for core binding factor (CBF) called core II, a binding site
87 ing subunit of a transcription factor of the core binding factor (CBF) family, is required for the es
88 Because both t(8;21) and inv(16) disrupt core binding factor (CBF) in acute myeloid leukemia (AML
93 a luciferase gene, focusing initially on the core binding factor (CBF) site, which is footprinted in
97 a binding site for the transcription factor core binding factor (CBF; also called AML1, PEBP2, and S
98 val, complex > or = 5, rare aberrations, and core-binding factor (CBF) abnormalities were prognostic
101 served for t(15;17), MLL rearrangements, and core-binding factor (CBF) AMLs including both t(8;21) an
103 s with leukemogenic fusion proteins, such as core-binding factor (CBF) leukemia and MLL fusion leukem
104 t report of recurring FLT3 N676 mutations in core-binding factor (CBF) leukemias and suggests a defin
105 the DNA-binding subunit of the heterodimeric core-binding factor (CBF) that binds to the transcriptio
110 betaRE and contains the transcription factor core-binding factor (CBF; also known as acute myeloid le
112 protein that binds the core site, one of the core-binding factors (CBF) is highly expressed in thymus
120 B) is a DNA-binding subunit in the family of core-binding factors (CBFs), heterodimeric transcription
124 velopment, and situate an essential role for core-binding factors during the earliest stages of T-cel
125 that members of the activator protein-1 and core-binding factor families, binding to the activator p
126 es of hematopoiesis for which members of the core binding factor family are required, as well as the
127 bind members of the activator protein-1 and core-binding factor family of transcription factors, res
128 %): 30 patients had complex karyotype, 2 had core-binding factor gene lesions, and 18 had abnormaliti
132 Runx1 (AML1), the DNA binding subunit of a core binding factor, is required for the emergence and/o
136 of KIT occur in almost half of patients with core-binding factor leukemias, in which they have been a
137 acute myeloid leukemia 1, also called RUNX1, core binding factor protein (CBF alpha), and PEBP2 alpha
138 utations, KIT mutations, FLT3 mutations, and core binding factor rearrangements in AML, and JAK2 muta
139 on of nuclear factor, erythroid 2 (Nfe2) and core-binding factor, runt domain, alpha subunit 2, trans
140 aemogenic endothelium population whereas the core binding factor Runx1 (also known as AML1) is critic
141 nv(16)/t(16;16) rearrangements affecting the core-binding factors RUNX1 and CBFB, respectively, are f
142 ndependence in EMPs is not mediated by other core binding factors (Runx2 and/or Runx3); however, dele
143 significantly higher in AML-associated with core binding factor translocations or mutations in CEBPA
144 ized to one of three cytogenetic groups: (a) core binding factor type [(CBF); ie., t(8;21) inv(16), t
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