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MLL normally maintains activation of target genes through multiple epigenetic mechanisms including the trimethylation of histone 3 on lysine 4 (H3K4Me3) via the activity of its C-terminal SET domain, and through the recruitment of transcriptional coactivators such as RBBP5, WDR5, ASH2L, and the H4 acetyltransferase MOF (Dou et al., 2005; Milne et al., 2002; Nakamura et al., 2002).
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It is possible that while erlotinib has direct inhibitory effects on phospho-EGFR and phospho-ERK, other upstream signalling activators maintain activation of the downstream cascade.
We assessed the ability of EPO to maintain activation of Akt1 during gene reduction of Wnt1.
Is the continued presence of the instigator tumor necessary to maintain activation of the bone marrow cells?
This is probably due to maintained activation of the SAC, which delays mitosis until all chromosome kinetochores are captured [19].
120 Hypoxia can maintain activation of signaling pathways downstream from ERBB2, including extracellular signal-regulated kinase (ERK), in the presence of lapatinib, a dual ERBB2 EGFR inhibitor.
Accordingly, the RH's role in semantic processing appears to be to maintain activation of multiple interpretations that can be called upon by the LH when complex meaning integration is required [ 17].
In their studies they found that abolished CD25 binding of IgG-IL2v led to a lack of preferential regulatory T cell (Treg) activation while maintaining activation of NK, CD4+ and CD8+ T cells when compared with IL-2 alone or IgG-IL2wt.
Neither BPA nor BPS could maintain activation of JNK by themselves during the 60-min time course; however, their combination with E2 (3-compound mixture) did activate JNK with a significant 60-min response, by which time the response to E2 had declined to control values.
Diploid tissues such as the brain and wing disc appear to be able to grow and proliferate thanks to maintained activation of TOR signaling by sustained receptor Tyrosine kinase signaling, originating from Alk in neurons and Stit in future wing cells, respectively [ 97, 98].
It is possible that every chondrogenic differentiation protocol would induce an epigenetic state that maintains activation potential of genes required both for the desired and also for related differentiation pathways [ 15].
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