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Type 1 diabetes (T1D) is characterized by insulin dependence for survival due to the destruction of the insulin-producing beta cells.
However compared to the induction profile of protein expression as in case of β-galactosidase where we have an excellent window of expression, the dose dependence for survival kinetics with antisense expression has a much smaller window (data not shown).
This dependence for survival and proliferation on critical cellular constituents that are not mutated and that alone do not serve to transform cells (sometimes called 'non-oncogene addiction') represents an under-explored opportunity for development of targeted cancer therapies directed at these components and pathways.
The fact that both netrin-1 and its receptors are upregulated upon conventional drug treatments suggests that the dependence for survival on netrin-1 is amplified in chemotherapy-treated cancer cells.
T-bet expression alone also accounted for down-regulation of CD127 and SOCS-1 and up-regulation of CD122 and IL-15Rα, thereby switching the dependence for survival signals from IL-7 to IL-15.
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While helper T cells clearly supported the size of the effector CD8+ T cell pool, the CD4-dependence for survival was not absolute, as helpless T cells were readily detected at ten and thirty days post-immunization (Figure 2A, 3A).
To investigate whether Foxp3 is important in Treg cells for the extreme cytokine dependence for their survival, we isolated CD25+ cells from the Scurfy mice and tested their survival in the presence or in the absence of IL-2.
Thus, this is not an appropriate way to test "whether Foxp3 is important in Treg cells for the extreme cytokine dependence for their survival" as these mice don't have Treg cells.
A key aspect of enabling an affordable and sustainable program of human exploration beyond low Earth orbit is the ability to locate, extract, and harness the resources found in space to reduce what needs to be launched from Earth's deep gravity well and to minimize the risk of dependence on Earth for survival.
Glycolysis inhibition attenuates the growth of BNip3-null tumor cells, revealing an increased dependence on autophagy for survival.
In resistant cells, RAS effector pathways maintained BAD phosphorylation in the presence of JAK inhibitors, yielding a specific dependence on BCL-XL for survival.
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