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A cell or organism may activate numerous compensatory pathways to maintain steady, homeostatic levels of critical metabolites when challenged with disruptive conditions.
These initiating factors may activate numerous systems involving complement, cytokines, immune cellular response with dysfunction of endothelium, and alteration of coagulation-fibrinolytic cascades [ 1].
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The numerous mechanisms by which OX40L may activate inflammation or abrogate immunosuppression, particularly in the complex ocular immune environment in which immune privilege is critical to immunoregulation, remain incompletely understood.
Although numerous studies have revealed that Bcr-Abl may activate multiple signaling pathways that are involved in cytoskeletal functions (4– 14), precise mechanisms by which Bcr-Abl induces abnormal cytoskeletal functions in leukemic cells are not completely understood.
Numerous studies suggested that the interaction between S100/calgranulin or HMGB1 and RAGE may activate inflammatory and stress signaling pathways of inflammatory cells, vascular cells, epithelial cells, terminally differentiated cells such as neurons and cardiomyocytes, and transformed cells [ 11, 12, 14].
Numerous studies have shown that both free fatty acids and high glucose levels in diabetes may activate PKC in various vascular cells via de novo synthesis of diacylglycerol (DAG) [ 41].
Numerous members of the NAC gene family have been shown to respond to biotic and abiotic stresses which may activate the plant defense response [ 48– 52].
An arrest may activate the clause, or only a conviction.
Oncogenic KRAS can activate numerous effector pathways to drive malignant progression.
Endogenous uterine agonists can activate numerous signaling pathways to effect increased force.
RONS may activate AMPK by direct an indirect mechanisms.
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