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Our genome wide screening analysis has identified chromosomal regions, membrane receptor pathways and new candidate genes outside of the classical VDR signaling pathway that may be associated with 1,25D resistance.
Numerous studies have shown that nuclear steroid receptors can be activated by membrane receptor pathways to mediate genomic and physiologic responses in the absence of steroid ligand (reviewed in [ 35**]).
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It is well known that the increase in Bax expression can promote cell apoptosis [17], and the mechanism of apoptosis is divided into membrane receptor pathway and mitochondrial pathway.
Instead, five of the six identified pathways corresponded to membrane receptor signaling pathways involved in the cellular response to extracellular signals (Table 3): EGF, PDGF, FGF, Interleukins and Toll receptor pathways.
In a study of nerve growth cone migration, Rho GTPases mediated growth cone steering in electric fields, linking membrane receptor signaling pathways to spatial regulation of the cytoskeleton [15] [18].
The transcription rate is initiated by cell membrane receptor signaling pathways.
Instead, over-representation of multiple membrane receptor signaling pathways known to be involved in the control of proliferation and apoptosis were associated with the 1,25D resistant phenotype.
Expression arrays revealed that no single gene was differentially expressed between the sensitive and resistant cells, but multiple membrane receptor signaling pathways were altered in the 1,25D resistant cell lines.
Therefore not only can membrane receptor dependent-pathways be induced, but also cytoplasmic receptors such as NOD (nucleotide binding and oligomerization receptor) or others could help trigger an immune response.
Overexpression, activation, and dysregulation of various membrane receptors, signaling pathways, and other factors occur frequently in human breast cancer.
Hu, P., Han, Z., Couvillon, A. D., Kaufman, R. J. & Exton, J. H. Autocrine tumor necrosis factor α links endoplasmic reticulum stress to the membrane death receptor pathway through IRE1α-mediated NF-κB activation and down-regulation of TRAF2 expression.
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