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Pathways

PathWhiz ID Pathway Meta Data

PW000551

Pw000551 View Pathway
disease

11-beta-Hydroxylase Deficiency (CYP11B1)

Homo sapiens
11-beta-Hydroxylase Deficiency, also called congenital adrenal hyperplasia (CAH), is an autosomal recessive disorder and caused by a defective 11-beta-hydroxylase. 11-beta-hydroxylase catalyzes the conversion of cortexolone into cortisol which is useful for maintaining blood sugar levels and suppressing inflammation. This disorder is characterized by a large accumulation of cortexolone in the endoplasmic reticulum (ER). Symptoms of the disorder include abnormality of hair growth rate and menstrual cycle. It is estimated that 11-beta-hydroxylase deficiency affects 1 in 100,000 to 200,000 newborns.

PW122119

Pw122119 View Pathway
disease

11-beta-Hydroxylase Deficiency (CYP11B1)

Rattus norvegicus
11-beta-Hydroxylase Deficiency, also called congenital adrenal hyperplasia (CAH), is an autosomal recessive disorder and caused by a defective 11-beta-hydroxylase. 11-beta-hydroxylase catalyzes the conversion of cortexolone into cortisol which is useful for maintaining blood sugar levels and suppressing inflammation. This disorder is characterized by a large accumulation of cortexolone in the endoplasmic reticulum (ER). Symptoms of the disorder include abnormality of hair growth rate and menstrual cycle. It is estimated that 11-beta-hydroxylase deficiency affects 1 in 100,000 to 200,000 newborns.

PW121895

Pw121895 View Pathway
disease

11-beta-Hydroxylase Deficiency (CYP11B1)

Mus musculus
11-beta-Hydroxylase Deficiency, also called congenital adrenal hyperplasia (CAH), is an autosomal recessive disorder and caused by a defective 11-beta-hydroxylase. 11-beta-hydroxylase catalyzes the conversion of cortexolone into cortisol which is useful for maintaining blood sugar levels and suppressing inflammation. This disorder is characterized by a large accumulation of cortexolone in the endoplasmic reticulum (ER). Symptoms of the disorder include abnormality of hair growth rate and menstrual cycle. It is estimated that 11-beta-hydroxylase deficiency affects 1 in 100,000 to 200,000 newborns.

PW127367

Pw127367 View Pathway
disease

11-beta-Hydroxylase Deficiency (CYP11B1)

Homo sapiens
11-beta-Hydroxylase Deficiency, also called congenital adrenal hyperplasia (CAH), is an autosomal recessive disorder and caused by a defective 11-beta-hydroxylase. 11-beta-hydroxylase catalyzes the conversion of cortexolone into cortisol which is useful for maintaining blood sugar levels and suppressing inflammation. This disorder is characterized by a large accumulation of cortexolone in the endoplasmic reticulum (ER). Symptoms of the disorder include abnormality of hair growth rate and menstrual cycle. It is estimated that 11-beta-hydroxylase deficiency affects 1 in 100,000 to 200,000 newborns.

PW122551

Pw122551 View Pathway
signaling

1.      Barrier 1564688413

Homo sapiens

PW122539

Pw122539 View Pathway
signaling

1.      Barrier 1562761104

Homo sapiens

PW064700

Pw064700 View Pathway
signaling

1.      Barrier

Homo sapiens

PW146354

Pw146354 View Pathway
drug action

1-Palmitoyl-2-oleoyl-sn-glycero-3-(phospho-rac-(1-glycerol)) Drug Metabolism Action Pathway

Homo sapiens

PW126354

Pw126354 View Pathway
metabolic

1-Methylhistidine synthesis via METTL9-catalyzed methylation

Homo sapiens

PW126201

Pw126201 View Pathway
metabolic

1-Methylhistidine Metabolism

Homo sapiens
Methylhistidine is a modified amino acid that is produced in myocytes during the methylation of actin and myosin. It is also formed from the methylation of L-histidine, which takes the methyl group from S-adenosylmethionine and forms S-adenosylhomocysteine as a byproduct. After its formation in the myocytes, methylhistidine enters the blood stream and travels to the kidneys, where it is excreted in the urine. Methylhistidine is present in the blood and urine in higher concentrations after skeletal muscle protein breakdown, which can occur due to disease or injury. Because of this, it can be used to judge how much muscle breakdown is occurring. Methylhistidine levels are also affected by diet, and may differ between vegetarian diets and those containing meats.