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The clinical relevance of immune cell apoptosis in IBD is supported by evidence showing that induction of apoptosis is a mechanism common to most IBD therapies, including aminosalycilates (12), steroids (13), immunosupressants [40], and infliximab [41].
Studies showing that induction of autophagy by HDACi can occur along with cell death suggest that autophagy promotes cell death.
The ESAGs were also down regulated, showing that induction of a second VSG gene attenuates the entire active ES.
Flow cytometry on Akt1-GFP-HRS differentiating cells showing that induction of Akt1 with Tamoxifen (Tam) rescues HRS expression.
Using two different types of endothelial cells, we provided evidence showing that induction of Nox4 expression and subsequent increase in ROS production mediated TGF- β-induced endothelial apoptosis.
Current data have provided a mechanistic explanation, showing that induction of cAMP in brown adipocytes induces FGF21 release from BAT in response to noradrenergic stimulation (196).
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It was therefore pertinent to show that induction of eIF4E protects cells against apoptosis.
On the contrary, Firestein et al. showed that induction of SIRT1 suppresses intestinal tumorigenesis and colon cancer growth.
Mosieniak et al. showed that induction of cellular senescence was accompanied by autophagy in colon cancer cells with an increase in Beclin-1 and p62/SQSTM1 protein levels.
Furthermore, we show that induction of the inositol 1,4,5-trisphosphate receptor type 1 is controlled by the calcium/calcineurin/NF-ATc pathway.
In addition, experience in human trials has shown that induction of capsid-specific CD8+ T cell responses can lead to clearance of AAV vector-transduced cells3,5,6,17.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com