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They found they could do this by inhibiting two genes: JunB and c-Jun, both known to regulate cell proliferation and mutations.
Of particular interest are the microtubule severing enzymes such as Katanin or the microtubule-destabilizing Kinesins which are both known to regulate the flagellum length [24], [25].
Since EHD3 [26] and EHD4 [43] are both known to regulate trafficking out of sorting endosomes, and in view of the appearance of abnormal vesicular structures in endothelial cells as seen by TEM, it is possible that altered recycling of VEGFR2 out of sorting endosomes in Ehd3 /–; Ehd4–/– glomerular endothelial cells might impair VEGF signaling resulting in the phenotypes we observe.
In contrast, lentiviral down-regulation of GARP in human alloantigen-specific Treg cells by specific small interfering RNA (siRNA) substantially impairs suppressor function and FOXP3 expression that is associated with impaired induction of CD83 and CD27, both known to regulate FOXP3 [ 21, 32, 33].
Two MYB transcription factors, one of which is production of anthocyanin pigment 2 (Pand) and a closely related R2R3 class MYB transcription factor MYB114, both known to regulate the conversion of flavonol precursors (dihydrokaempferol and dihydroquercetin) to anthocyanin precursors (anthocyanidins) in the flavonoid biosynthetic pathway, were also located in this region.
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Both proteins are known to regulate Rab5-mediated neuronal endocytic pathways.
Both genes are known to regulate cell wall polysaccharide synthesis [ 34, 35].
As arrestin3 expression is enhanced in mesenteric vessels and MSMCs from 12-wk-old SHR, and both proteins are known to regulate ETA receptor function (22), we have also examined whether developing hypertension has effects on ET1-induced PLC signaling.
SORT1 is known to regulate both neuronal viability and function through its regulation of both protein transport and signal transduction (Willnow et al., 2008) and is known to bind proNTs to control neuronal survival and cessation (Nykjaer and Willnow, 2012).
Both kinases are well known to regulate cell growth and proliferation, largely through enhancing ribosome biogenesis [ 4, 5].
Although the mechanism by which activated AMPK represses the translation of ribosomal proteins is unclear, it would be independent of ribosomal protein S6 kinase or ribosomal protein S6 (rphosphorylationation, both of which are known to regulate translation [ 25].
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both known to produce
both known to increase
both known to consume
both known to fire
both known to have
both known to influence
both known to decrease
both known to inhibit
both known to cause
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both known to disperse
both known to adsorb
both required to regulate
both known to mediate
both known to devour
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