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Now a study in tomorrow's issue of the Proceedings of the National Academy of Sciences suggests that the drug protects nerve cells from being stimulated to death.
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For example, increased expression from a therapeutic drug may be part of tumor cells' attempt to try to survive the stress or the gene may be directly stimulated to induce cell death.
In response to death, neighboring cells are stimulated to proliferate and reconstitute tissue loss, a process defined as apoptosis-induced proliferation.
A general conservation in function between PrgI and the Bcl-2 protein family is readily apparent; both form membrane pores via a helix-turn-helix motif through oligomerization to release effectors to stimulate cell death.
This is consistent with a general conservation in function between PrgI and the Bcl-2 family of proteins that includes Bcl-xL; both form membrane pores through oligomerization using a conserved helix-turn-helix motif to release effectors to stimulate cell death.
WHO and UNFPA recognise the value of accurate and timely investigation of maternal deaths to stimulate actions to prevent maternal deaths in future.
Both proteins form membrane pores through this oligomerization to release effector proteins to stimulate cell death.
Further experiments will be required to address whether other ligands might be secreted to stimulate cell death receptors.
We used TNF and Fas antibody to stimulate cell death.
The complex role of mitochondria in mammalian cell death was highlighted when several studies elucidated resident mitochondrial proteins were able to stimulate cell death directly.
Because induction of apoptosis is one of the main mechanisms of anticancer drugs use to stimulate cell death, NEK2A-induced antiapoptosis may explain the high cancer cell drug resistance seen when NEK2A is increased.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com