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tscript(p(MGI:Tbx2)) =| r(MGI:Cdkn2a)
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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TBX2 and TBX3 bind to a variant T-site present in the p14ARF promoter. A, EMSA with probe -14/+35 and extracts of COS-7 cells overexpressing TBX2, TBX2RD, TBX2TB(R122E, R123E), TBX2TB(A272E), TBX3, TBX3 L143P, or TBX3 Y149S. Competitor oligos and antibodies as indicated. Note that TBX2, TBX2RD, and TBX3 can bind probe in both the absence and presence of anti-TBX2 antibody as opposed to the DNA binding inability of T-box mutants of TBX2 and TBX3.The Variant T-site of p14ARF Is Required for p14ARF Promoter Repression. To prove that the variant T-site is the relevant site via which TBX2 and TBX3 mediate repression we mutated the site in p14ARF promoter-reporter constructs at exactly the same positions as those used in EMSAs. Because these mutations reside in the core promoter region, it was not surprising that substantial and progressive activity loss was observed. However, in agreement with the binding data obtained in EMSA, T-half-site mutants could still be repressed by TBX2, whereas mutants in which both T-half-sites were disrupted were insensitive to TBX2 even at a very high dose in MEFs (Fig. 3A).
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Selventa
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2014-07-03T14:31:49.095+02:00
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