Pathways

PathWhiz ID Pathway Meta Data

PW123807

Pw123807 View Pathway
signaling

chebulagic acid Metabolism 1581839290

Homo sapiens
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Creator: Guest: Anonymous

Created On: February 16, 2020 at 00:48

Last Updated: February 16, 2020 at 00:48

PW064753

Pw064753 View Pathway
metabolic

Mapa metabólico

Homo sapiens
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Creator: Guest: Anonymous

Created On: June 10, 2018 at 16:58

Last Updated: June 10, 2018 at 16:58

PW013304

Pw013304 View Pathway
metabolic

Metabolic pathways

Mus musculus
bdnf symthesis
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Creator: Guest: Anonymous

Created On: May 02, 2017 at 07:48

Last Updated: May 02, 2017 at 07:48

PW002064

Pw002064 View Pathway
metabolic

1,6-Anhydro-N-acetylmuramic Acid Recycling

Escherichia coli
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: October 09, 2015 at 12:00

Last Updated: October 09, 2015 at 12:00

PW123548

Pw123548 View Pathway
metabolic

1,6-Anhydro-N-acetylmuramic Acid Recycling

Pseudomonas 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

PW064700

Pw064700 View Pathway
signaling

1.      Barrier

Homo sapiens
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Creator: Guest: Anonymous

Created On: March 16, 2018 at 21:18

Last Updated: March 16, 2018 at 21:18

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.
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Creator: WishartLab

Created On: August 29, 2013 at 10:39

Last Updated: August 29, 2013 at 10:39

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.
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Creator: Ana Marcu

Created On: September 10, 2018 at 15:52

Last Updated: September 10, 2018 at 15:52

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.
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Creator: Ana Marcu

Created On: September 10, 2018 at 15:50

Last Updated: September 10, 2018 at 15:50

PW122336

Pw122336 View Pathway
metabolic

11-cis-3-Hydroxyretinal Biosynthesis

Drosophila 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