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Dysregulation of Ca2+ homeostasis has long been implicated to play an important role in cell injury.
The one electron reduction has long been implicated to lead to the leakage of electrons, which in turn could react with cellular oxygen to form reactive oxygen species [ 12, 13].
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Serine/theonine protein kinases (STK) have long been implicated to play a role in signaling processes concerned with self verses non-self recognition and disease resistance [ 20].
Receptor downregulation has long been implicated in adaptive responses to continued pharmacological stimuli.
Beckett has long been implicated in the cover-up, to which further layers of concealment are being added.
The glial scar which composed primarily of reactive astrocytes has long been implicated as a major impediment to axon regeneration and functional outcome after SCI and other forms of CNS injury [2], [3].
The transmembrane span of HER2 has long been implicated as a key contributing factor to self-association and activation control.
Crosstalk between the ER and HER2 pathways has long been implicated in cancer onset and response to tamoxifen, but no direct connection at transcriptional level has been shown.
Jasmonic acid has long been implicated in the plant's systemic response to pathogen attack [ 67].
The hippocampus has long been implicated in spatial memory, from work in rodents to imaging and brain lesion studies in humans.
Chronic oxidative stress leading to oxidative damage has long been implicated in β-cell dysfunction in diabetes.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com