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10.1016/j.tips.2015.01.001 http://scihub22266oqcxt.onion/10.1016/j.tips.2015.01.001 C4355084!4355084!25661257     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Trends+Pharmacol+Sci 2015 ; 36 (3): 137-44 Nephropedia Template TP {{tp|p=25661257|t=2015. The phospholipase D superfamily as therapeutic targets |pdf=|usr=}}{{25661257}} gab.com Text The phospholipase D superfamily as therapeutic targets JO: Trends Pharmacol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25661257 #FOAvip The Phospholipase D (PLD) lipid-signaling enzyme superfamily has long been studied for its roles in cell communication and a wide range of cell biological processes. With the advent of loss-of-function genetic mouse models that have revealed that PLD1 and PLD2 ablation is overtly tolerable, small molecule PLD1/2 inhibitors that do not cause unacceptable clinical toxicity, a PLD2 polymorphism that has been linked to altered physiology, and growing delineation of processes subtly altered in mice lacking PLD1/2 activity, the stage is being set for assessment of PLD1/2 inhibition for therapeutic purposes. Based on findings to date, PLD1/2 inhibition may be of more utility in acute rather than chronic settings, although this generalization will depend on the specific risks and benefits in each disease setting. Twit Text FOAVip The phospholipase D superfamily as therapeutic targets ????Trends Pharmacol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25661257 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25661257 #FOAvip English Wikipedia <ref>{{Cite pmid|25661257}}</ref> The phospholipase D superfamily as therapeutic targets #MMPMID25661257 Frohman MA Trends Pharmacol Sci 2015[Mar]; 36 (3): 137-44 PMID25661257show ga The Phospholipase D (PLD) lipid-signaling enzyme superfamily has long been studied for its roles in cell communication and a wide range of cell biological processes. With the advent of loss-of-function genetic mouse models that have revealed that PLD1 and PLD2 ablation is overtly tolerable, small molecule PLD1/2 inhibitors that do not cause unacceptable clinical toxicity, a PLD2 polymorphism that has been linked to altered physiology, and growing delineation of processes subtly altered in mice lacking PLD1/2 activity, the stage is being set for assessment of PLD1/2 inhibition for therapeutic purposes. Based on findings to date, PLD1/2 inhibition may be of more utility in acute rather than chronic settings, although this generalization will depend on the specific risks and benefits in each disease setting. äThe phospholipase D superfamily as therapeutic targets (epmc).pdf DeepDyve Pubget Overpricing