This may be due to several factors, and one possibility would be the delay in the onset of therapeutic actions partly or fully influenced by the downstream effects, such as altered transcription [ 14, 33].
AKT stimulation triggers a series of downstream effects, such as activation of transcription factors p53 and NF-κB, which have major impact on cancer cell growth and survival4,5.
Overt downstream effects, such as cancer, birth defects, and infectious illnesses are typically discrete events.
A downstream effect, such as altered transcription, would explain the delay in the onset of therapeutic action.
The pathway linking probable antenatal depression and infant morbidity may be explained by downstream effects of reported consequences of antenatal depression such as: suboptimal care provided during the neonatal period, 39 poor maternal self-care, nutrition, lack of sleep 40 and peripartum/postpartum complications experienced by the mother.
As T cell activation requires receptor signalling, transcription factor activation, gene transcription, protein synthesis and protein trafficking, systemic abnormalities in these physiological processes in schizophrenia can potentially be traced in this model by using downstream effects of stimulation such as proliferation, cytokine production and gene transcription as readouts of cell function.
In nearly all cases, action potentials trigger downstream physiological effects, such as secretion or muscle contraction, by opening voltage-gated calcium-selective ion channels and elevating intracellular calcium concentration.
The authors propose that downstream effects of such a relationship would be measurable, e.g., by increased incidence of unplanned revisits to the ED.
At the molecular level the downstream effects of such a deficit are currently unknown.
In contrast, hypoxia can have extensive downstream transcriptional effects, such as activation of pro-apoptotic and pro-angiogenic pathways.
