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Song, et al's"Deep RNA Sequencing Reveals Novel Cardiac Transcriptomic Signatures for Physiological and Pathological Hypertrophy"

Table 1

    This table highlights some specific features of 33 genes alternatively spliced in PAH and PHH models, using information derived from past literature on alternative splicing between these models. 

   In the Smox gene – listed as one example of how to read this table – the exon listed in the "Exon Position" column is present as normal in PAH models but excluded in PHH models, as noted in the "Inclusion/Exclusion" column. Biological function of the normal splice variants noted in noted in the "Function" column. The PAO3 isoform of this gene (which should lack the exon noted) is the dominant isoform in PHH, the hypertrophy condition in which a change in expression of the Smox gene occurs. The exclusion of this exon of the Smox gene in PHH does not bring about a noted change in protein functional domain presence (D), protein activity (A) or protein localization (L).

Overall this table describes a number of functional differences in genes between PAH and PHH conditions that result specifically from changes in AS as opposed to differential gene expression, highlighting a new level by which gene expression can be altered in two conditions. A follow up to some of these previous studies' data in Song, et al.'s study, showing how RNA-seq can account for AS, is provided in figure 3.


Introduction

Figure 1

Figure 2

Proceed to Figure 3

Figure 4


References 

Song, H. K., Hong, S. E., Kim, T., Kim D. H., et al. (2012). Deep RNA sequencing reveals novel cardiac transcriptomic signatures for physiological and pathological hypertrophy. PLoS One, 7, e35552.

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