The phrase "activation of a sustained" is grammatically correct and can be used in written English.
It can be used in contexts related to processes, systems, or mechanisms that require a continuous or prolonged activation.
Example: "The activation of a sustained response is crucial for the success of the project."
Alternatives: "initiation of a prolonged" or "triggering of a continuous".
Striking responses have been seen in preclinical cancer models using MEDIC, where an immunogenic cancer chemotherapeutic agent is administered intermittently and at an intermediate dose, designed to impart strong and repeated cytotoxic damage to tumors, and on a schedule compatible with activation of a sustained anti-tumor immune response, thereby maximizing anti-cancer activity.
The efficacy of immune surveillance and antigen-specific cancer immunotherapy equally depends on the activation of a sustained immune response targeting cancer antigens and the susceptibility of cancer cells to immune effector mechanisms.
Lange C, Caprara C, Tanimoto N, Beck S, Huber G, Samardzija M, et al. Retina-specific activation of a sustained hypoxia-like response leads to severe retinal degeneration and loss of vision.
Activation of a sustained protein hypercatabolic response mainly accounts for muscle depletion [7].
Whereas activation of cholangiocyte CD40 by sCD154 produced transient upregulation of NFkB (Rel A), sustained activation of AP-1 (cJun/cFos) and pSTAT 3 resulting in cholangiocyte apoptosis [5], the sCD154/C4BP complex failed to activate these pathways and resulted in inhibition of apoptosis and enhanced cell survival.
We have previously shown [3], [5] and confirmed here, that activation of CD40 on cholangiocytes results in a transient rise in NFkB activation and a sustained activation of ERK/JNK and cFos/cJun (AP-1 subunits) and STAT 3 phosphorylation associated with death by apoptosis [5].
Several preclinical models have further shown that PTEN-deficient tumours present an enhanced sensitivity to mTOR inhibitors because of a sustained activation of PI3K/Akt signaling (Neshat et al, 2001; Podsypanina et al, 2001; Shi et al, 2002; Steelman et al, 2008).
Further activation of εPKC (by a sustained treatment with the PKC-selective activator, ψεRACK) increased cardiac fibrosis and HF, whereas εPKC inhibition (by sustained treatment with the εPKC-selective inhibitor, εV1-2) prolonged survival, reduced hypertrophy, excessive fibrosis, vascular remodelling, and inflammation and corrected cardiac dysfunction.
Ultimately, GF-induced activation of CPCs elicited a sustained regenerative response that resulted in a 20% rescue of the infarct by replacing fibrotic tissue with viable myocardium.
Our observation of a sustained p38 activation after anisomycin- or sorbitol-treatment is in accordance with other reports showing persistent activation of p38 after cellular stress, e.g. in C3H10T1/2 cells in response to anisomycin or UV [ 41] or in several cell lines in response to γ-irradiation, genotoxic compounds or during premature senescence [[ 42, 43], reviewed in [ 6]].
Few reports have described different mechanisms of a sustained Cn activation due to the gain-of-function mutation in the CnA in T or B lymphoma-derived cell lines [ 111, 112].
