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The ATP generated is then bound by the ABC transporter, hydrolyzed and the energy from this process activates the ABC transporter to extrude the noxious agent.
This process activates neutrophils.
This process activates kinase protein signaling, which culminates in the stabilization of type II ACSs.
Neurotransmitter binding to the receptors causes the entire Golf-AC5complex to rearrange and this process activates AC5.
This process activates the expression of detoxifying enzymes and antioxidant proteins such as Hmox-1, Nqo1, glutathione transferase (Gst), and glutathione (GSH) [ 16– 16].
This process activates these cells, leading to the release of granules that contain preformed inflammatory mediators (eg, histamine), as well as de novo synthesis and/or release of inflammatory mediators (eg, leukotrienes), proteases (eg, tryptase), inflammatory cytokines (eg, IL4), and chemotactic molecules.
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During this process, activated Akt directly modulated the promoter activity of HCCR-1 located in the 5'upstream region of HCCR-1 gene.
This process activated the surface of the In2O3 NPs by leaving extra In- and O-free bonds.
During this process, activated DCs undergo distinct changes in phenotype and function, termed DC maturation [ 62, 64].
We observed an increase in total protein acetylation in the wound area, as determined by acetylation of α-tubulin and histone H3 Lysine 9. We reasoned that this process activated cell function as well as regulated gene expression to foster tissue repair.
In this process, Notch activates Snail expression that in turn down-regulates VE-cadherin [ 48].
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