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The RAS/RAF/MEK/ERK pathway is a critical proliferation pathway in many human cancers.
Critical proliferation pathways including PI3K/Akt pathway in cancer cells were inhibited by AChE overexpression [ 5].
Our data show that SSeCKS suppresses several critical proliferation- and angiogenesis-associated genes while it induces differentiation and cell cycle control functions, strongly suggesting that SSeCKS is capable of reprogramming normal gene expression controls downstream of activated Src.
To examine the role of Su z 2 in regulating dE2F1 activity, we depleted Su z 2 in cultured Drosophila SL2 cells and analyzed the expression of dE2f1 and a subset of critical proliferation target genes by qRT-PCR.
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Above the critical temperature, proliferation of unbound vortices is expected.
However, which of the common tumour-associated metabolic activities are critical for proliferation remains unclear.
The inhibition of Hsp90 depletes these kinases from cancer cells and disrupts signaling pathways that are critical for proliferation and survival, and thus are an exciting therapeutic target [47].
At the cellular level, ATF4 is critical for proliferation and differentiation as well as survival in osteoblasts [32], [33].
We have shown that CSDA expression and RSK activity are both critical for proliferation in CML.
Interestingly, EphA2 was identified as a novel, downstream ubiquitylated target of the epidermal growth factor receptor that is critical for proliferation and cell migration in response to EGF.
When bound to GTP, the RAS family of small guanosine triphosphatases activates several signalling pathways that transduce critical cell proliferation and survival signals.
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