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Co-expression of mCherry-actin and EGFP-MBD-VVCA allowed confirmation of actin assembly on microtubules by observation in the light microscope (Figure 3A, B), and subsequent processing of the same cells by negative staining and electron microscopy.
Among these, Cdk1 is the main kinase player during G2/M transition [39] which controls execution of a transcriptional program required for mitosis through phosphorylation of Plk1 and Aurora B and subsequent activation of FoxM1, a key transcription factor during G2/M transition [35], [40].
Western blot analysis (B) and subsequent quantification (C) demonstrated an increase in CD44 and EMT markers and a decease in E-Cadherin in respect to the parental cell line (total population).
This suggests that mutations outside the MHR can also lead to the development of escaped mutant strains of hepatitis B and subsequent serological diagnostic failure, which concur with previous studies [ 29].
For glucose quantification the following multi-step procedure was used: isocratic separation (5 min, 95% A + 5% B), column wash (2 min, 99% B) and subsequent column equilibration (2.5 min, 95% A + 5% B).
The allene attack on PdII complex A through allylic C H bond cleavage 12, 13a– d would give B and subsequent alkyne insertion would generate intermediate C. Transmetalation of C with B2pin2 and reductive elimination would form product 4.
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One such addition to the Th1 Signaling network was the regulatory influence of early growth response 2 (EGR2) on T-cell activation; the submitted evidence demonstrated that overexpression of EGR2 promoted increased activity of the E3 ubiquitin ligase CBL-B and subsequent inhibition of T-cell activation.
These nucleosomes lead to breaking of immune tolerance and development of autoimmunity through the activation of T cells and B cells and subsequent production of large amounts of anti-nucleosome, anti-histone, and anti-DNA autoantibodies.
In these mice glucose-6-phosphate isomerase (GPI) is the target autoantigen, and T-cell reactivity to this ubiquitous antigen results in recruitment of anti-GPI B cells and subsequent immune complex-mediated arthritis [ 32, 33].
Indeed, many bacteria contain repetitive epitopes in their surface and/or lipid antigens that can favour internalization by specific MZ B cells and subsequent interaction with splenic NKT cells to allow early antibody responses.
Uptake of autoantigens by CD5+ B cells and subsequent presentation to T cells by cells that coexpress FasL would lead to selective elimination of the autoreactive T cells and protection from autoimmunity.
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