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Animal models have implicated PACAP38 in central nociceptive transmission [77] and in rats intrathecal capsaicin elevated PACAP levels in the cerebrospinal fluid [78].
Previous pharmacological, human genetical, and animal models have implicated the nicotinic acetylcholine receptor α4 subunit (CHRNA4) gene in the pathogenesis of ADHD.
Previous pharmacological, human genetics, and animal models have implicated the nicotinic acetylcholine receptor α4 subunit (CHRNA4) gene in the pathogenesis of attention deficit/hyperactivity disorder (ADHD).
To date these models have implicated RyRs in fundamental biological processes including excitation contraction coupling and long term plasticity as well as diseases including malignant hyperthermia, cardiac arrhythmias, heart failure, and seizures.
The existing GRN models have implicated approximately 80 TFs in the response to ROS [ 11, 31].
Animal models have implicated dysfunctional cilia of the ependyma and choroid plexus in the development of the disorder.
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Our results correspond well to studies in other mouse models that have implicated MMP-13 in development of arthritis.
These associations in human studies, in conjunction with functional studies in model systems, have implicated adiponectin in multiple metabolic processes.
Earlier studies using model organisms have implicated a role for p53 pathway in DBA pathogenesis.
Studies conducted in a sickle cell murine model system have implicated accelerated turn-over of cytotoxic free heme in protection (Ferreira et al., 2011).
Findings in ALS patients and model systems have implicated numerous genes in ALS pathogenesis, and have identified diverse processes, such as oxidative stress, excitotoxicity, mitochondrial dysfunction, protein aggregation, cytoskeletal abnormalities, impaired axonal transport, inflammation, and apoptosis, as contributing factors [ 1].
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