Words similar to pro-apoptotic
Example sentences for: pro-apoptotic
How can you use “pro-apoptotic” in a sentence? Here are some example sentences to help you improve your vocabulary:
Naturally occurring triterpenoids, such as ursolic acid, have been found to have mild anti-inflammatory effects [ 18 27 ] . These have been improved with the development of synthetic triterpenoids such as CDDO, offering a potential therapeutic tool for the treatment of arthritis and other diseases [ 19 20 21 ] . Furthermore, it has been reported that CDDO at high doses (5-10 μM) can have pro-apoptotic effects, ideal for the treatment of leukemia but of concern with regard to chondrocyte cell death [ 25 26 ] . However, we found that CDDO, at concentrations that decrease MMP-1 and MMP-13 expression (namely 300 nM and 1 μM), did not cause cell death.
Dietary antioxidants confer significant protection to gut epithelial cells from pro-apoptotic oxidant stress.
Recently, we demonstrated that the targeting of the pro-apoptotic protein tBid to mitochondria depends upon the presence of the mitochondria-specific lipid cardiolipin in a possibly unique structure [ 9 ] . Cardiolipin has a defined distribution pattern within mitochondria [ 10 ] . It is found in high concentrations throughout the inner membrane, including at contact sites where the inner membrane and outer membrane interact.
The first, the ER overload response, triggers the activation of the transcription factor NFkB and the subsequent upregulation of inflammatory proteins [ 13 ] . The second, the unfolded protein response (UPR) induces three divergent cellular events: (i) the activation of transcription factor ATF6 leading to the upregulation of ER chaperones such as protein disulfide isomerase, (ii) upregulation of the pro-apoptotic transcription factor GADD153 and (iii) suppression of protein synthesis via phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) by pancreatic eIF2α kinase (PEK/PERK, [ 11 12 ] ). Upregulation of the ER chaperones, GADD153 and PERK in response to a toxic insult would constitute direct evidence of an ER stress response.
It is possible that NF-κB and CREB mediate the early phases of neutrophil activation, while C/EBP proteins function to maintain this response [ 50 ] . The observation that the temporal pattern of expression of activated C/EBP and PKB-α are similar suggests co-ordinated regulation of these proteins [ 51 ] . A decrease in activation of transcription factors like NF-κB and CREB and an increase in C/EBP may also contribute to reduced activity of pro-apoptotic genes, resulting in prolonged longevity of neutrophils in the lung vasculature.
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