This week, we use IPA to "model, analyze and understand complex biological and chemical systems." (IPA)
In IPA, there are no drugs associated with the product of the GLA gene.
Growing a Pathway
The following is the direct pathway grown using limited to humans as species and deselecting chemicals and biological drugs. Two relationships with GLA are identified. The HNF1A molecule is located in the nucleus and is a transcription regulator. It has an reaction relationship with the GLA product as Protein-DNA binding (PD). The TFEB molecule is also located in the nucleus and is also a transcription regulator. It also has a reaction relationship with the GLA product involving expression (E).
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As depicted below, the GLA gene product is located in the cytoplasm.
Canonical Pathway
IPA does not have a canonical pathway for GLA. As such, a pathway involving HNF1A was identified. HNF1A is involved with the Maturity Onset Diabetes of Young (MODY) Signaling canonical pathway. This is a disease-specific pathway involving the endocrine system. "MODY, the monogenic form of diabetes, results from defects that affect the functioning of islet beta-cells where the pancreas does not produce enough insulin. This in turn leads to hyperglycemia...The impaired secretion of insulin seen in MODY is similar to the deficiency found in Type-1 diabetes. Yet, unlike Type 1 diabetes, MODY develops slowly and does not completely destroy the ability of the pancreas to produce insulin. Rather, it impairs insulin secretion so that the body cannot adequately control blood glucose levels from one moment to the next." Molecular defects in 6 different genes including the HNF1A gene have been identified in MODY patients. "A mutation in one of the alleles encoding HNF1A leads to a reduction in beta-cell glucokinase activity resulting in decreased glucose phosphorilation in the beta-cell and glucose stimulated insulin release at any blood glucose concentration."
