Regarding the comment concerning cryptic sites, we always mean non-canonical splice sites activated by sequence-level variation, which are distinctly different from tissue-related alternatively spliced isoforms lacking one or more constitutive exons.
Serve sequences produced additional regions of activation in the parietal lobe (bilateral IPL, right SPL) and in the right frontal cortex (IFGd, IFGv), and these areas were not activated by non-serve sequences.
Transcription can be activated by these enhancer sequences independent of their location, distance or orientation with respect to the genes promoters.
After integration into the plant genome, this reporter gene is activated by flanking promoter sequences thus enabling study of native expression patterns within original genomic contexts.
Apparently, such TNF-independent mechanisms are also responsible for the expression of the δ-isoform of p38MAPK in the synovial fibroblast, which is activated by retrotransposable viral sequences termed L1 elements [ 33].
Importantly, the fluorescence of Sp-I recovered to about 90% of that of Sp in the presence of 3-fold molar excess of a DNA strand complementary to the internal blocking sequence and its neighboring bases (Anti-I-DNA), demonstrating that Sp-I can be activated by sequestering the blocking sequence by hybridization.
Specifically, Binder et al. (1996) demonstrated in their fMRI study that the left supramarginal gyrus was more strongly activated by nonlinguistic stimuli (tone sequences) than by words when subjects performed active listening tasks involving tone sequence analysis in comparison to analysis of words.
Specifically, muscle-specific miR-206, which is directly activated by MyoD, can target sequences in the Fstl1 and Utrn gene and these sequences are sufficient to suppress gene expression in the presence of miR-206 [ 8]. miR-1 promotes myogenesis by targeting HDAC4, a transcriptional repressor of muscle gene expression.
In this case, ανβ3, αIIbβ3, and α5β1 can be activated by collagen-derived RGD sequences [ 20].
An element (-40 to -25) that overlaps one of the E2F binding sites can be bound and activated by 53BP1 in a sequence-specific manner and functions as a positive regulatory element [ 21].
Somewhat contrary to these results, Kim et al. recently produced a different MYC-based mouse model in which MYC was activated by removing a floxed "STOP" sequence (present in the Z-MYC mice) using Cre recombinase driven by the Probasin promoter (present in the Pb-Cre4 mice) [83].
