1 The transcription factor
c-ets-
1 (encoded by the Ets1 gene) has B cell-intrinsic
2 Although
c-Ets-
1 alone did not activate transcription from this e
3 We found that B cells lacking
c-ets-
1 are generally hyperresponsive in terms of Ab sec
4 However, peripheral B cells lacking
c-ets-
1 failed to become tolerant in response to stimuli
5 ent study, we investigated the regulation of
c-ets-
1 in cultured rat vascular smooth muscle cells as
6 a complex of c-Jun and c-Fos interacted with
c-Ets-
1 in vitro.
7 Therefore, maintenance of appropriate
c-ets-
1 levels is essential to prevent loss of self-tole
8 These findings suggest that
c-ets-
1 may be of importance in the mitogenic signaling
9 Arterial
c-ets-
1 mRNA content was induced with an identical time
10 erum for various time points express a major
c-ets-
1 mRNA transcript of 5.3 kb and minor bands of 4.0
11 These results suggest that AP-1 tethers
c-Ets-
1 to the TIMP-1 promoter via protein-protein inter
12 lve the mitogen-activated protein kinase and
c-Ets-
1 transcription factors.
13 ultiple cis-elements such as C/EBPbeta, YY1,
c-Ets-
1, AP1, AP2, and NFkappaB binding sites.
14 In Jurkat cells, overexpression of
c-Ets-
1, c-Ets-2, or PU.1 effectively represses dexameth
15 ing sites in the AKR1B10 promoter, including
c-Ets-
1, C/EBP, AP-1, and p53, but osmolytic response el
16 omain of SAP1a by aspartic acid (as found in
c-Ets-
1, Elk-1, and Net) enhanced ternary complex format
17 expression was increased by the induction of
c-ets-
1, suggesting that the Ets-1 transcription factor
18 the bone marrow was intact in the absence of
c-ets-
1.
19 ogen-activated protein kinases p42/p44; and (
c) ets-
2 phosphorylation at position threonine 72, a mit
20 s were found associated with chTERT only and
c-Ets-
2 and WT1 were associated with hTERT only.
21 In Jurkat cells, overexpression of c-Ets-1,
c-Ets-
2, or PU.1 effectively represses dexamethasone-med
22 anscriptional elements including TATA, CREB,
c-ets,
and AP1 sites.
23 Sequence analysis revealed two potential
c-Ets binding sites in the COX-2 promoter (COX-2p) which
24 GATA sequence and several putative c-myb and
c-ets binding sites.
25 We show here that c-Myb and
c-Ets family members (Ets-1/2, PU.1, and Spi-B) control
26 not an upstream NF-kappaB site or a putative
c-Ets located at the site of initiation.
27 te, three MZF1 sites, one p300 site, and one
c-Ets site.