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The precise mechanism by which TGF-β regulates angiogenesis remains the subject of much debate, however, it is generally accepted that TGF-β can have both pro- and anti-angiogenic activities and that these activities are mediated by differential activation of the ALK5-SMAD2/3 ALK1-SMAD1/5/8 ALK1-SMAD1/5/8nsignalon patransduction
The precise promoter activity level in each combination can be quantitatively explained by differential activation of each promoter by the master carbon regulator CRP-cAMP.
This experiment demonstrates unambiguously that mitochondrial movement can be reversibly modulated by differential activation of the two dopamine receptor subtypes.
The protein p53 responds to a variety of cellular stresses and may induce cell cycle arrest or apoptosis In fact, by differential activation of a large number of target genes and by mitochondrial functions, p53 is able to sense the intensity of the damage and modulate biological responses that can range from transient growth arrest to permanent replicative senescence or apoptosis [1].
While many Hox genes are functionally redundant between paralog group members, the Adb-B related HoxC and HoxD genes regulate endometrial proliferation and HoxA genes regulate endometrial differentiation and are required for successful blastocyst implantation [23], [24], suggesting the distinct roles of these transcription factors is mediated by differential activation of downstream target genes.
We show that type II cells are more DCA-sensitive than macrophages and respond by differential activation of pathways that detoxify superoxide anion and H2O2.
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It also could be extended by spatial aspects, for example by the differential activation of the Rac- and Rho-pathways in different parts of the cell.
Type 2 diabetes is preceded by a differential activation of components of the innate immune system (1, 2).
In vitro cultivation was accompanied by a differential activation of RESMAC and INFMAC, which was evident from the change in the proportion of CD14+ cells.
This is exemplified by the differential activation of EGFR-driven feedback control in BRAF-mutant colorectal cancer and melanomas in response to BRAF inhibition [ 62].
In contrast to apoptosis, Wood and Van Der Kraak [ 22, 80] proposed that proteolytic degradation of yolk proteins, mediated by the differential activation of Catl in the oocyte, may be the initial event leading to follicular atresia in fish.
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