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Defects in these DNA damage responses (DDR) promote tumor initiation, drive tumor progression, and modulate tumor response to radiation, chemo, as well as immune therapies.
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Specifically, we saw that translation initiation driven solely by the cap structure or solely by the poly(A) tail was partially responsive to miCXCR4, while only an mRNA carrying both end modifications was subject to the full extent of translational repression [19].
Epigenomic DMR characteristics are identified that, in conjunction with miRNAs and transcription factors, regulate gene and protein expression and are a blueprint for spatio-temporal analyses of lesion initiation driven by endothelial dysfunction.
To explore the mechanism by which replication initiation drives chromatin decondensation, we first analyzed the CAPG-1 component of condensin I, which associates with condensed chromosomes during mitosis and is excluded from nuclei during interphase (Csankovszki et al., 2009; Hirano, 2005; Hudson et al., 2009).
Some manifestations of this damage, such as activation of the DNA damage response and generation of genomic instability, may promote tumor initiation and drive cell-autonomous tumor progression.
This suggests that the complete breakdown of replication repair, resulting in an explosion of SSMs, is an early mechanism associated with tumor initiation and drives tumor progression.
We hypothesized that cancer initiation is driven by disruption of the QS mechanism, either by genetic mutations, complying with the current notion of cancer evolution, or purely by the environment, genetic mutations being only a side-effect of excessive proliferation.
Additionally, to avoid confounding biased repair with initiation bias driven PRMD9 binding, we omit four events that overlap partial matches to the PRDM9 motif as described in 'Results'GC-biasedsed gene conversion').
Beclin-1 is one of several protein components required for autophagy initiation and drives the early steps of autophagosome formation through its interaction with Vps34, a phosphoinositide 3-kinase.
There is, therefore, perhaps the need for new and/or refined models to be developed and tested in order to conclusively demonstrate that exposure to magnetic fields at the relevant environmental levels neither induces molecular and genetic changes associated with leukaemia initiation, nor drives disease progression.
Research to date has not comprehensively addressed genome-editing specificity and off-target mismatches that may result in unintended changes within plant genomes or the potential for gene drive initiation.
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