PathWhiz ID | Pathway | Meta Data |
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PW123548View Pathway |
1,6-Anhydro-N-acetylmuramic Acid RecyclingPseudomonas aeruginosa
Most bacteria, including Escherichia coli, are composed of murein which protects and stabilizes the cell wall. Over half of the murein is broken down by Escherichia coli and recycled for the next generation. The main muropeptide is GlcNAc-anhydro-N-acetylmuramic acid (anhMurNAc)-l-Ala-γ-d-Glu-meso-Dap-d-Ala which enters the cytoplasm by AmpG protein. The peptide is then released from the muropeptide. 1,6-Anhydro-N-acetylmuramic acid (anhMurNAc) is recycled by its conversion to N-acetylglucosamine-phosphate (GlcNAc-P). The sugar is phosphorylated by anhydro-N-acetylmuramic acid kinase (AnmK) to produce MurNAc-P. Etherase cleaves MurNAc-P to produce N-acetyl-D-glucosamine 6-phosphate. The product can undergo further degradation or be recycled into peptidoglycan monomers. The pathway's final product is a peptidoglycan biosynthesis precursor, UDP-N-acetyl-α-D-muramate. The enzyme muropeptide ligase (mpl), attaches the recovered Ala-Glu-DAP tripeptide to the precursor UDP-N-acetyl-α-D-muramate to return to the peptide to the peptidoglycan biosynthetic pathway to synthesize the cell wall.
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Creator: Ana Marcu Created On: August 12, 2019 at 22:30 Last Updated: August 12, 2019 at 22:30 |
PW126201View Pathway |
1-Methylhistidine MetabolismHomo 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.
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Creator: Selena Created On: August 23, 2021 at 15:10 Last Updated: August 23, 2021 at 15:10 |
PW126354View Pathway |
1-Methylhistidine synthesis via METTL9-catalyzed methylationHomo sapiens
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Creator: Selena Created On: October 13, 2021 at 21:24 Last Updated: October 13, 2021 at 21:24 |
PW146354View Pathway |
drug action
1-Palmitoyl-2-oleoyl-sn-glycero-3-(phospho-rac-(1-glycerol)) Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 18:00 Last Updated: October 07, 2023 at 18:00 |
PW064700View Pathway |
signaling
1. BarrierHomo sapiens
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Creator: Guest: Anonymous Created On: March 16, 2018 at 21:18 Last Updated: March 16, 2018 at 21:18 |
PW000551View 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.
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Creator: WishartLab Created On: August 29, 2013 at 10:39 Last Updated: August 29, 2013 at 10:39 |
PW122119View 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.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:52 Last Updated: September 10, 2018 at 15:52 |
PW121895View 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.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:50 Last Updated: September 10, 2018 at 15:50 |
PW127367View 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.
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Creator: Ray Kruger Created On: December 19, 2022 at 12:15 Last Updated: December 19, 2022 at 12:15 |
PW122336View Pathway |
11-cis-3-Hydroxyretinal BiosynthesisDrosophila melanogaster
(3S)-11-cis-3-hydroxyretinal is one of three chromophores, which then associate with rhodopsins. Specifically, this chromophore associates with the Rh1 rhodopsin, a blue/green sensitive visual pigment found in 6 of the 8 photoreceptor cells in Drosophila melanogaster.
The production of this chromophore begins with zeaxanthin obtained from Drosophila’s dietary sources. This lipid is broken down into (3R)-11-cis-3-hydroxyretinal and (3R)-all-trans-3-hydroxyretinal by a carotenoid isomerooxygenase. The (3R)-cis-3-hydroxyretinal is then attached to a retinoid binding protein, and this complex goes on to be used in the visual cycle of the organism. However, (3R)-all-trans-3-hydroxyretinal must be further processed. It too binds to a retinoid binding protein that will remain unchanged through the rest of the reactions. First, this complex will have a hydrogen added by a photoreceptor dehydrogenase in order to form (3R)-all-trans-3-hydroxyretinol, and then a photoreceptor epimerase will invert its stereochemistry to form (3S)-all-trans-3-hydroxyretinol. From here, an unknown protein, an oxidoreductase that transposes C=C bonds, will form (3S)-11-cis-3-hydroxyretinol. Finally, another photoreceptor dehydrogenase removes a hydrogen from that complex, forming the final product, (3S)-11-cis-3-hydroxyretinal. This complex then joins (3R)-11-cis-3-hydroxyretinal in the visual cycle.
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Creator: Eponine Oler Created On: February 04, 2019 at 11:14 Last Updated: February 04, 2019 at 11:14 |