Matches in Nanopublications for { ?s ?p "We demonstrate that co-expression of DIP1/2 and the N-terminal domain of DOC-2/DAB2 (i.e. Delta B) has an additive effect on suppressing either TPA-induced SRE or TRE reporter gene activity (Fig. 6B and Table I). Therefore, we believe that the in vivo interaction of DIP1/2 with the N-terminal domain of DOC-2/DAB2 acts as a feedback mechanism to modulate PKC-induced gene activation." ?g. }
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- _7 value "We demonstrate that co-expression of DIP1/2 and the N-terminal domain of DOC-2/DAB2 (i.e. Delta B) has an additive effect on suppressing either TPA-induced SRE or TRE reporter gene activity (Fig. 6B and Table I). Therefore, we believe that the in vivo interaction of DIP1/2 with the N-terminal domain of DOC-2/DAB2 acts as a feedback mechanism to modulate PKC-induced gene activation." provenance.
- _7 value "We demonstrate that co-expression of DIP1/2 and the N-terminal domain of DOC-2/DAB2 (i.e. Delta B) has an additive effect on suppressing either TPA-induced SRE or TRE reporter gene activity (Fig. 6B and Table I). Therefore, we believe that the in vivo interaction of DIP1/2 with the N-terminal domain of DOC-2/DAB2 acts as a feedback mechanism to modulate PKC-induced gene activation." provenance.
- _6 value "We demonstrate that co-expression of DIP1/2 and the N-terminal domain of DOC-2/DAB2 (i.e. Delta B) has an additive effect on suppressing either TPA-induced SRE or TRE reporter gene activity (Fig. 6B and Table I). Therefore, we believe that the in vivo interaction of DIP1/2 with the N-terminal domain of DOC-2/DAB2 acts as a feedback mechanism to modulate PKC-induced gene activation." provenance.
- _6 value "We demonstrate that co-expression of DIP1/2 and the N-terminal domain of DOC-2/DAB2 (i.e. Delta B) has an additive effect on suppressing either TPA-induced SRE or TRE reporter gene activity (Fig. 6B and Table I). Therefore, we believe that the in vivo interaction of DIP1/2 with the N-terminal domain of DOC-2/DAB2 acts as a feedback mechanism to modulate PKC-induced gene activation." provenance.