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Several studies found that the splicing of several of the key genes in PD, α-synuclein, parkin, synphilin-1, FOSB and RGS9, are affected in diseased individuals and in mouse models of the disease [54], [55], [56].
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We found that the splicing of intron 13 in testicular ACE was species-dependent.
We investigated the geographical distribution of the splicing variant in 480 accessions of foxtail millet from various regions of Europe and Asia and part of Africa by dCAPS and found that the splicing variant is broadly distributed in Europe and Asia.
We found that the alternative splicing of the TOC1 and ELF3 genes is mediated by the retention of specific introns, supporting the notion that their alternative splicing is a regulated process rather than a simple splicing error.
We found that the expression of splicing factors as well as alternative splicing of analyzed genes were disturbed in majority of analyzed tissue samples.
Fortunately, we found that the in vitro splicing of E3-4 was dramatically accelerated by the addition of splicing-enhancer SR proteins (e.g. SC35), as evident by the amounts of splicing intermediates accumulated (Figure 1A, lanes 1 3).
Evidence was found that the activity of FOX2, the splicing factor shown to cause cancer-specific splicing patterns in breast and ovarian cancer, is not altered at the transcript level in several cancer types including lung cancer.
We found that the binding of same splicing factor onto different regions is often associated with regulated splicing in different tissues.
We found that the majority of known splices can be detected.
We also found that the number of alternative splice variants was positively correlated with CI.
They found that the mechanical performance of the splices improved with an increase in embedded length of bars and compressive strength of grout.
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