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This could be because this gene has evolved in response to P. falciparum infection in this species.
We examined Arf1-depleted cells at higher resolution because this gene has been shown to be directly involved in the early steps of endocytosis via GEECs in mammalian cells [10].
For example, I did not detect pclob because this gene has not been properly annotated, likely due to the duplications I describe herein.
Nonetheless, our identification of Hsp83 is significant because this gene has previously been singled-out in relation to honey bee caste differentiation [ 51, 52], oogenesis [ 53], and is a marker for changes in queen reproductive status [ 10, 54].
For the suppressed mark (DiMethH3K9) a region of the alpha-fetoprotein (Afp) start site (−82 to +94 bp) was chosen as a positive control because this gene has been shown to be silenced in adult mouse tissues [ 26].
Among the nearly 100 predicted targets, FKBP51 was chosen for further investigation because this gene has an active role in cancer aetiology and responds to antineoplastic therapy (Baughman et al, 1995; Febbo et al, 2005; Pei et al, 2009).
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The rpoB gene is likely functional in chlorophycean algae because gene disruption of this gene has revealed an essential function in C. reinhardtii (Fischer et al. 1996) and also because no chloroplast-targeted RNA polymerase gene was identified in the nuclear genome of C. reinhardtii (Merchant et al. 2007).
We suggest using ACTB as reference gene, when comparing gene expression in normal thyroid and goiter, because this gene had the lowest intra- and intergroup variations.
In the present study we focused on GRIA2 because this gene had low P-values and displayed a large fold change.
Specifically, we chose to explore the role PfM18.1 played in RAP3 (PFE0075c) expression because this gene had a simple structure with no introns making the identification of the true start codon relatively straightforward.
Because this gene had been previously shown to integrate signals from reproductive tissues (germ cells) to elicit longevity effects in nonreproductive (somatic) tissues [16] and interacts with cep-1, an important mediator of germ cell death [7, 8], we asked whether kri-1 is involved in a novel, cell-nonautonomous mechanism to regulate germ cell death.
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