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This suggests a lack of transcripts or an unstable Slc10a1 product in KO mice.
In contrast, the presence of a MAR within a gene correlates with a lack of transcripts, consistent with nuclear matrix attachment-induced silencing.
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It remains to be tested whether this is due to a lack of transcript polyadenylation in this organelle.
Semi-quantitative RT PCR analysis showed that the levels of recombinant transcript were similar in cells transfected with either the wild-type GFP-Fbn or C1564Y mutant (Supplementary Material, Fig. S1), indicating that the lack of recombinant protein observed in the medium in the C1564Y samples was not due to a lack of transcript.
A lack of omp6 transcripts suggests that this gene may not be expressed in tick cells or only at very low levels.
This was confirmed by TaqMan qRT PCR: amplification failed in MatDp(dist2) newborn brain due to a lack of Blcap_v2a transcripts, while an approximately 2-fold increase of Blcap_v2a was observed in PatDp(dist2) newborn brain relative to the non-UpDp control (Fig. 3A).
Previously, Sun et al (1998) reported a lack of STAT1 transcript in IFN resistant lymphoma cells.
The Northern blot wherein the Mup1 sequence was used as a probe reveals a lack of Mup transcript signal in SC, EP, RP and BAT of WAT of ob/ob mice.
Semi-quantitative RT PCR was carried out on RNA samples from cultures of HEK293T cells transfected with either the wild-type or MFS-associated GFP-Fbn constructs to ensure that the lack of secretion was not due to a lack of recombinant transcript (Supplementary Material, Fig. S1).
No paired miRNA-mRNA data from human PBMCs after IR have been published thus far [ 16– 19], and a precise analysis of negatively correlated miRNA-mRNA pairs has been hindered by a lack of paired mRNA transcripts.
This difference may be the result of abnormalities in post-transcriptional regulation of cytokine expression, leading to a lack of correlation between transcript levels and protein levels.
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