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A better understanding of the complex mechanisms of immune escape operated by neoplastic cells and the ability to unleash an efficient anti-tumor immune response by targeting regulatory immune checkpoint(s) with immunomodulatory monoclonal antibodies (mAbs), is leading to very promising clinical results in different tumor types.
These volumes changes might influence the cytosolic protein concentration with the potential to influence enzymatic rates involved in regulating signaling checkpoint(s) during cell division.
As Chk1 is involved in maintaining tumor cell viability following activation of the replication checkpoint, the Chk1-regulated checkpoint(s) may protect cells from ionizing radiation-induced killing.
In human somatic cells, the low levels of telomerase cannot maintain the length of the telomere tracts and hence precipitates senescence checkpoint(s).
The full spectrum of checkpoint(s) that are responsible for restraining cells mutated for BRCA1 or BRCA2 from continued proliferation remains to be defined.
We proposed a redox signalling system that gates H2B expression, coordinates the expression of other histone genes and affects other redox-sensitive machineries to dictate S-phase progression; indeed, perturbing the redox eventually led to an activation of intra-S-phase checkpoint(s) to hamper S-phase progression [ 19].
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Next we analysed the effect of KEN box mutations on spindle checkpoint function(s) of Mad3p.
This suggests that E-cadherin participates in the checkpoint through factor(s) other than Apc2 (Figure 4D).
Given a checkpointing transition (v s,λ,v d ), the state v s refers the location of fault detection and v d refers the location of a checkpoint.
The intra-S checkpoint is regulated by two parallel pathways mediated by ATM-NBS1-SMC-1 and ATM/ATR-Chk1/Chk2-Cdc25A ATM/ATR-Chk1/Chk2-Cdc25A ATM/ATR-Chk1/Chk2-Cdc25A [42]
The "cell size" node represents the checkpoint entering S phase in the cell cycle if the yeast cell grows to a critical size [ 16, 17].
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