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The tumour microenvironment can include multiple cellular stresses, with hypoxia being an underlying theme.
Multiple cellular stresses can trigger an adaptive response by activating the Hippo signaling pathway, which may, in turn, maintain the cellular homeostasis.
OA is known to induce apoptotic cell death through protein phosphatase inhibition, which results in multiple cellular stresses; however, much less is known concerning the molecular mechanisms and the phenomenon involved in apoptotic responses (Fujita et al., 1999; Rossini et al., 2001).
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Previous work also suggested SBDS has a second role in multiple cellular stress response pathways, independent of its primary role in ribosome biogenesis (Ball et al., 2009).
In recent years, however, it has become clear that there are multiple cellular stress-response pathways and mechanisms activated in response to the polyphenols listed above.
The p53 tumour suppressor protein, encoded by TP53 gene (OMIM 191170), integrates endogenous and exogenous signals to modulate cell fate in response to multiple forms of environmental and cellular stresses [ 1].
The tumor suppressor p53 is one of the most studied and most important regulators of multiple signaling pathways, including normal cellular processes and those triggered by diverse cellular stresses.
ER stress-mediated autophagic pathways also integrate various cellular stresses.
191117), which encodes a tumor-suppressor protein that drives multiple cellular responses to stress, including cell-cycle arrest, DNA repair, apoptosis, metabolism and autophagy, is frequently mutated in cancer [1], [2], [3], [4], [5], [6].
As a molecular chaperone, HSp60 appears to have diverse effects on molecular surveillance functions in order to maintain the proper function and homeostasis of multiple cellular pathways under stress conditions.
Heat and other acute or chronic stresses provoke multiple cellular reactions, including activation of the heat shock or stress protein response.
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