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In chromaffin cell-transfected CHGA 3′-UTR and promoter/luciferase reporter plasmids, the functional consequences of the regulatory/non-coding allelic variants were documented.
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For porphobilinogen synthase, the existence of zinc binding and non-zinc binding variants is documented in the literature [ 85].
All in silico splicing analysis tools were run at default threshold values and the outputs for wildtype versus variant were documented.
In contrast, no new terms were proposed for cell types, embryonic structures, or the immune system, because no evolutionary variants of these anatomical structures were documented in the literature we curated.
When these lengths were applied to NBCI and GeneLoc databases, found that these bands are Bax α (NCBI Reference Sequence: NM_138761.3), Bax d (GenBank: AW008643.1), Bax Δ (NCBI Reference Sequence: NM_138763.3), and Bax ζ (GenBank: AF250190.1), Figure 3. Bax α, Δ, and ζ were documented in cancer cells but variant d is documented in thymus and pooled tissues (NCBI, ACEView).
were documented.
These variants have been documented to be of importance in phase I and phase II drug metabolism and disease manifestation.
RASGRP1 splice variants have been documented for patients with SLE (Yasuda et al., 2007) and abnormal microRNA-driven downregulation of Rasgrp1 expression may play a role in aberrant DNA methylation in Lupus CD4+ T cells (Pan et al., 2010).
Again, we note that histone 1.0 belongs to replication-independent histone mRNAs [ 36, 37] and thus could in principle be spliced even though no such splice variant has been documented so far.
This variant has not been documented previously using techniques such as SELEX or protein-binding microarrays.
Interestingly, two splice variants of IR have been documented.
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