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While Ig+ B cells appear to be the principal cell type expressing immunogenic minor lymphocyte stimulatory (Mls) determinants, both T cells and B cells are capable of mediating deletion of developing Mls-reactive thymocytes.
ISs have been implicated in large changes to genome structure, by expanding in copy number in microbial genomes, with subsequent loss of ISs resulting in inactivation of genes, pseudogene formation, mediating deletion of intervening sequences between two copies of the IS, or rearrangements of the genome [ 3].
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We tested the ability of FLP and Cre recombinases, expressed conditionally in P. falciparum, to mediate deletion of the human dihydrofolate reductase (hdhfr) drug resistance gene.
The DNA was used in a semi-quantitative PCR assay in order to determine the efficiency of cre recombinase mediated deletion of Nbn exon 6 and thus the proportion of homozygous or heterozygous null mutant cells.
Based on our study with human cell lines, combination of CAPE and ruxolitinib will help in protecting gene transduced air way epithelial cells to prolong transgene expression by curtailing NK cell mediated deletion of gene transduced cells.
The most noteworthy difference was the loss of all the animal T3SS associated genes[15] in an apparent IS mediated deletion containing contiguous genes (two sets of T3SS: one consists of 23 genes from BMA_A1530-A1552 (the Bsa genes) and a second set from BMA_A1625-A1637 cofsists of 13 genes, Genbank accession numbers, ATCC 23344 small chromosome- CP000011 and SAVP1- CP000525).
These results demonstrate that both xid mice and SCID animals express Mls determinants that mediate deletion of developing, Mls-responsive thymocytes and stimulate proliferation of mature, Mls-reactive T cells.
In our model, Cre recombinase expression is driven by the DAT promoter and mediates deletion of exon 5 of the pten gene approximately at embryonic day 15 [15].
We hypothesized that the amelioration of in vivo and in vitro defects in keratinocytes from aging hpm and K5-β1 mice, respectively, could be due to the expansion of keratinocytes that escaped NMD or Cre-mediated deletion of the floxed allele and had elevated β1 integrin levels.
This induces overexpression of exogenous FoxN1 after Cre-mediated deletion of the roadblock STOPflox.
Thus, Cre-mediated deletion of exon 2 generates a truncated form of REST unable to bind to DNA.
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