By blocking surface nucleolin, HB-19 could perturb signaling events during induction of cell proliferation in response to various stimuli, thus illustrating that surface nucleolin could be implicated in mechanisms that link extracellular signals with intracellular signaling [30].
However, differently from ERK1/2 cascade, linked to the regulation of anti-inflammatory and proliferative programs following cytokine exposure, PI3K/AKT pathway seems to be implicated in mechanisms aimed at rescuing keratinocytes from apoptosis.
A number of amyloid diseases involve deposition of extracellular protein aggregates, which are implicated in mechanisms of cell damage and death.
Urokinase that also binds the RGG domain of nucleolin is implicated in mechanisms regulating pericellular proteolysis, cell-surface adhesion, and mitogenesis [21], [24].
We have focused on the canonical Wnt pathway, which has an established role in developmental processes, but has recently been implicated in mechanisms of neurodegeneration/neuroprotection in the adult brain [25] [27].
Laminin-1 that induces differentiation of cells binds surface nucleolin, while urokinase that is implicated in mechanisms regulating pericellular proteolysis, cell-surface adhesion, and mitogenesis binds and is co-internalized with surface nucleolin [14], [18], [19].
Oxidative stress has been implicated in mechanisms leading to neuronal cell injury in various pathological states of the brain (Calabrese et al 2003).
Urokinase that is implicated in mechanisms regulating pericellular proteolysis, cell-surface adhesion, and mitogenesis binds and is co-internalized with surface nucleolin [ 17, 18].
In addition, exogenous PED/PEA-15 overexpression inhibits myotubes generation and differentiation leading us to hypothesize that PED/PEA-15 is implicated in mechanisms controlling myogenesis.
Periostin has been implicated in mechanisms of wound repair and collagen fibrillogenesis 10, 12, 14; thus, periostin deficiency with a concomitant decrease in TGF-β1 might have been expected to inhibit allergen-induced airway fibrosis.
Receptors for advanced glycation end-products (RAGE) are cell-surface receptors expressed by alveolar type I (ATI) epithelial cells and are implicated in mechanisms of alveolar development and sustained pulmonary inflammation.
