The phrase "activation of members" is correct and usable in written English.
It can be used in contexts related to engaging or mobilizing individuals within a group or organization.
Example: "The activation of members is crucial for the success of our community initiatives."
Alternatives: "engagement of members" or "mobilization of members".
In addition, TAM causes induction of c-Myc, activation of members of mitogen-activated protein kinase (MAPK) family as well as increased accumulation of ceramide which serves as a second messenger in cell survival [ 28].
Integrin-mediated activation of members of the mitogen-activated protein kinase family plays a key role in transmitting signals regulating chondrocyte gene expression.
Tamoxifen induces apoptosis through several distinct pathways including a mitochondria-dependent pathway, the induction of c-Myc, the activation of members of the mitogen-activated protein kinases (MAPK) family, and the upregulation of p53 [ 7- 11].
The fundamental pathways that play a role in increasing the release of NO and PGE2 by IL-1β involve activation of members of the mitogen-activated protein kinase (MAPK) pathway, namely extracellular signal-regulated kinase (ERK -1/2, p38 and c-Jun amino-tERK -1/2kinase (JNK) families, and the transcrip38on fandors activator protein-1 and nuclear famino-terminalB) [ 19- 27].
Environmental stress and inflammatory cytokines stimulate stress-activated protein kinase (SAPK /c-Jun N-terminal kinaSAPK /c-Jungnaling, which involves the sequential activation of members of the mitogen-activated protein kinase (MAPK) family, including MAPK/ERK kinase kinase (MEKK)1/MAPK kinase (MKK)4, and/or SAPK/ERK kinase (SEK)1/MKK7, JNK, and c-jun.
Activation of members of the signal transduction and activator of transcription (STAT) family, in particular STAT3, was revealed downstream as a consequence of the binding of IL-11 to its corresponding receptor [12].
PGC-1α regulates mitochondrial energy metabolism and biogenesis (Finck & Kelly, 2006), and influences carbohydrate and lipid utilization through co-activation of members of nuclear receptor family [e.g. peroxisome proliferator-activated receptor-α (PPAR-α), PPAR-γ, estrogen related receptor α (ERRα)] (Corton & Brown-Borg, 2005).
Sorafenib has been shown to inhibit RAF activation, phosphorylation of members of the MEK-ERK kinase family and proliferation of cell lines derived from PTC and ATC harboring an activating BRAF mutation [ 25].
MK-STYX is structurally related to the DSPs, in particular the MAPK phosphatases, which dephosphorylate both the threonine and tyrosine residues in the activation loop of members of the MAPK family [ 3, 25].
The molecular mechanisms governing activation of individual members remain ill-defined.
Furthermore, the elevated expression and activation of key members in the canonical NF-κB pathway induced by cerebral ischemia were also inhibited by VEGF treatment.
