Reactome: A Curated Pathway Database
Results 1 to 10 of 23
Pathways (18) Reactions (3) Proteins (1) Others (1)
Protein: UniProt:P22309 UGT1A1 (Homo sapiens)
Last changed: 2014-11-26 10:20:21

Pathway: Disease (Homo sapiens)
Biological processes are captured in Reactome by identifying the molecules (DNA, RNA, protein, small molecules) involved in them and describing the details of their interactions. From this molecular viewpoint, human disease pathways have three mechanistic causes: the inclusion of microbially-expressed proteins, altered functions of human proteins, or changed expression levels of otherwise functionally
Last changed: 2014-11-21 19:49:01

Pathway: Metabolism (Homo sapiens)
Metabolic processes in human cells generate energy through the oxidation of molecules consumed in the diet and mediate the synthesis of diverse essential molecules not taken in the diet as well as the inactivation and elimination of toxic ones generated endogenously or present in the extracellular environment. The processes of energy metabolism can be classified into two groups according to whether the
Last changed: 2014-11-21 19:49:01

Pathway: Defective GSS causes Glutathione synthetase deficiency (GSS deficiency) (Homo sapiens)
In mammalian cells, many antioxidant defence systems exist which protect cells from subsequent exposure to oxidant stresses. One antioxidant is glutathione (GSH), a tripeptide present in virtually all cells that regulates the intracellular redox state and protects cells from oxidative injury. It is metabolised via the gamma-glutamyl cycle, which is catalysed by six enzymes. In man, hereditary deficienc
Last changed: 2014-11-21 19:49:01

Pathway: Defective GGT1 causes Glutathionuria (GLUTH) (Homo sapiens)
To be excreted in urine, glutathione conjugates undergo several hydrolysis steps to form mercapturic acids which are readily excreted. The first step is the hydrolysis of a gamma-glutamyl residue from the conjugate catalysed by gamma-glutamyltransferases (GGTs). These are membrane-bound, heterodimeric enzymes composed of light and heavy peptide chains. Extracellular glutathione (GSH) or its conjugates
Last changed: 2014-11-21 19:49:01

Pathway: Defective UGT1A1 causes hyperbilirubinemia (Homo sapiens)
UDP-glucuronosyltransferases (UGTs) play a major role in the conjugation and therefore elimination of potentially toxic xenobiotics and endogenous compounds. The 1-1 isoform UGT1A1 is able to act upon lipophilic bilirubin, the end product of heme breakdown. Defects in UGT1A1 can cause hyperbilirubinemia syndromes ranging from mild forms such as Gilbert syndrome (GILBS; MIM:143500) and transient familia
Last changed: 2014-11-21 19:49:01

Pathway: Metabolism of porphyrins (Homo sapiens)
Porphyrins are heterocyclic macrocycles, consisting of four pyrrole subunits (tetrapyrrole) linked by four methine (=CH-) bridges. The extensive conjugated porphyrin macrocycle is chromatic and the name itself, porphyrin , is derived from the Greek word for purple . The aromatic character of porphyrins can be seen by NMR spectroscopy. Porphyrins readily combine with metals by coordinatin
Last changed: 2014-11-21 19:49:01

Pathway: Defective UGT1A4 causes hyperbilirubinemia (Homo sapiens)
UDP-glucuronosyltransferases (UGTs) play a major role in the conjugation and therefore elimination of potentially toxic xenobiotics and endogenous compounds. The 1-4 isoform UGT1A4 is able to act upon lipophilic bilirubin, the end product of heme breakdown. Defects in UGT1A4 can cause hyperbilirubinemia syndromes ranging from mild forms such as Gilbert syndrome (GILBS; MIM:143500) to the more severe Cr
Last changed: 2014-11-21 19:49:01

Pathway: Biological oxidations (Homo sapiens)
All organisms are constantly exposed to foreign chemicals every day. These can be man-made (drugs, industrial chemicals) or natural (alkaloids, toxins from plants and animals). Uptake is usually via ingestion but inhalation and transdermal routes are also common. The very nature of many chemicals that make them suitable for uptake by these routes, in other words their lipophilicty (favours fat so
Last changed: 2014-11-21 19:49:01

Pathway: Defective TPMT causes Thiopurine S-methyltransferase deficiency (TPMT deficiency) (Homo sapiens)
Methylation is a major biotransformation route of thiopurine drugs such as 6-mercaptopurine (6MP), used in the treatment of inflammatory diseases such as rheumatoid arthritis and childhood acute lymphoblastic leukemia. 6MP and its thioguanine nucleotide metabolites are principally inactivated by thiopurine methyltransferase (TPMT)-catalysed S-methylation. Defects in TPMT can cause thiopurine S-m
Last changed: 2014-11-21 19:49:01

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