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Pathways

PathWhiz ID Pathway Meta Data

PW126210

Pw126210 View Pathway
drug action

Sitagliptin Action Pathway

Homo sapiens
Sitagliptin is an oral dipeptidyl peptidase-4 (DPP-4) inhibitor used for the management of type 2 diabetes mellitus. Sitagliptin is an oral dipeptidyl peptidase-4 (DPP-4) inhibitor used in conjunction with diet and exercise to improve glycemic control in patients. Inhibition of DPP-4 by sitagliptin slows DPP-4 mediated inactivation of incretins like GLP-1. GLP-1 is then able to go on to stimulate insulin secretion in beta cells. GLP-1 activates GLP-1 receptors on beta cells, triggering the Gs signaling cascade by activating adenylate cyclase to produce cAMP. cAMP activates protein kinase A (PKA) and Rap guanine nucleotide exchange factor 4 (EPAC2). PKA inhibits the ATP-sensitive potassium channel, preventing K+ efflux, leading to an accumulation of K+ ions in the cell causing depolarization of the cell. This depolarization activates the voltage gated L-type calcium channel, causing calcium influx. PKA may also directly activate the voltage gated L-type calcium channel. EPAC2 activates the ryanodine receptor on the endoplasmic reticulum, causing calcium to move from the endoplasmic reticulum and into the cytosol. The high concentration of calcium ions in the cytosol triggers insulin release via exocytosis, lowering blood glucose levels. Sitagliptin may also increase insulin biosynthesis, increase beta cell proliferation, decrease beta cell apoptosis and decrease glucagon secretion since these are also effects mediated by GLP-1.

PW145344

Pw145344 View Pathway
drug action

Sitagliptin Drug Metabolism Action Pathway

Homo sapiens

PW145697

Pw145697 View Pathway
drug action

Sitaxentan Drug Metabolism Action Pathway

Homo sapiens

PW176176

Pw176176 View Pathway
metabolic

Sitaxentan Predicted Metabolism Pathway new

Homo sapiens
Metabolites of Sitaxentan are predicted with biotransformer.

PW124281

Pw124281 View Pathway
signaling

Sjogren Pathway

Homo sapiens

PW121769

Pw121769 View Pathway
disease

Smith-Lemli-Opitz Syndrome (SLOS)

Mus musculus
The autosomal recessive disorder Smith-Lemli-Opitz Syndrome (SLOS; SLO Syndrome; RSH; Rutledge Lethal Multiple Congenital Anomaly, Syndrome; Polydactyly, Sex Reversal, Renal Hypoplasia, and Unilobar Lung; Lethal Acrodysgenital Syndrome) is characterized by disordered steroid biosynthesis. It results from a mutation in the DHCR7 gene coding for the enzyme sterol delta-7-reducatase. This enzyme catalyzes the production of cholesterol by reducing the C7-C8 double bond of 7-dehydrocholesterol (7-DHC). SLOS causes the accumulation of 7-dehydrocholesterol and 8-dehydrocholesterol, and a decrease of cholesterol in plasma; and 3-methylglutaconic acid in urine. All patients with SLOS have mental retardation, and symptoms include ambiguous genitalia, hypotonia, microcephaly, syndactyly, limb abnormalities and deformities and polydactyly.

PW121994

Pw121994 View Pathway
disease

Smith-Lemli-Opitz Syndrome (SLOS)

Rattus norvegicus
The autosomal recessive disorder Smith-Lemli-Opitz Syndrome (SLOS; SLO Syndrome; RSH; Rutledge Lethal Multiple Congenital Anomaly, Syndrome; Polydactyly, Sex Reversal, Renal Hypoplasia, and Unilobar Lung; Lethal Acrodysgenital Syndrome) is characterized by disordered steroid biosynthesis. It results from a mutation in the DHCR7 gene coding for the enzyme sterol delta-7-reducatase. This enzyme catalyzes the production of cholesterol by reducing the C7-C8 double bond of 7-dehydrocholesterol (7-DHC). SLOS causes the accumulation of 7-dehydrocholesterol and 8-dehydrocholesterol, and a decrease of cholesterol in plasma; and 3-methylglutaconic acid in urine. All patients with SLOS have mental retardation, and symptoms include ambiguous genitalia, hypotonia, microcephaly, syndactyly, limb abnormalities and deformities and polydactyly.

PW127199

Pw127199 View Pathway
disease

Smith-Lemli-Opitz Syndrome (SLOS)

Homo sapiens
The autosomal recessive disorder Smith-Lemli-Opitz Syndrome (SLOS; SLO Syndrome; RSH; Rutledge Lethal Multiple Congenital Anomaly, Syndrome; Polydactyly, Sex Reversal, Renal Hypoplasia, and Unilobar Lung; Lethal Acrodysgenital Syndrome) is characterized by disordered steroid biosynthesis. It results from a mutation in the DHCR7 gene coding for the enzyme sterol delta-7-reducatase. This enzyme catalyzes the production of cholesterol by reducing the C7-C8 double bond of 7-dehydrocholesterol (7-DHC). SLOS causes the accumulation of 7-dehydrocholesterol and 8-dehydrocholesterol, and a decrease of cholesterol in plasma; and 3-methylglutaconic acid in urine. All patients with SLOS have mental retardation, and symptoms include ambiguous genitalia, hypotonia, microcephaly, syndactyly, limb abnormalities and deformities and polydactyly.

PW000095

Pw000095 View Pathway
disease

Smith-Lemli-Opitz Syndrome (SLOS)

Homo sapiens
The autosomal recessive disorder Smith-Lemli-Opitz Syndrome (SLOS; SLO Syndrome; RSH; Rutledge Lethal Multiple Congenital Anomaly, Syndrome; Polydactyly, Sex Reversal, Renal Hypoplasia, and Unilobar Lung; Lethal Acrodysgenital Syndrome) is characterized by disordered steroid biosynthesis. It results from a mutation in the DHCR7 gene coding for the enzyme sterol delta-7-reducatase. This enzyme catalyzes the production of cholesterol by reducing the C7-C8 double bond of 7-dehydrocholesterol (7-DHC). SLOS causes the accumulation of 7-dehydrocholesterol and 8-dehydrocholesterol, and a decrease of cholesterol in plasma; and 3-methylglutaconic acid in urine. All patients with SLOS have mental retardation, and symptoms include ambiguous genitalia, hypotonia, microcephaly, syndactyly, limb abnormalities and deformities and polydactyly.

PW126929

Pw126929 View Pathway
physiological

Smooth muscle contraction - relaxation

Homo sapiens