Reactome: A Curated Pathway Database
Results 1 to 10 of 34
Pathways (26) Reactions (7) Proteins (1) Others (0)
Protein: UniProt:P07477 PRSS1 (Homo sapiens)
Last changed: 2014-11-26 10:20:21

Pathway: Extracellular matrix organization (Homo sapiens)
The extracellular matrix is a component of all mammalian tissues, a network consisting largely of the fibrous proteins collagen, elastin and associated-microfibrils, fibronectin and laminins embedded in a viscoelastic gel of anionic proteoglycan polymers. It performs many functions in addition to its structural role; as a major component of the cellular microenvironment it influences cell behaviours su
Last changed: 2014-11-21 14:40:22

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 MTR causes methylmalonic aciduria and homocystinuria type cblG (Homo sapiens)
Defects in MTR cause methylcobalamin deficiency type G (cblG; MIM:250940), an autosomal recessive inherited disease that causes mental retardation, macrocytic anemia, and homocystinuria (Leclerc et al. 1996, Gulati et al. 1996, Watkins et al. 2002)
Last changed: 2014-11-21 19:49:01

Pathway: Defective GIF causes intrinsic factor deficiency (Homo sapiens)
Defects in GIF cause hereditary intrinsic factor deficiency (IFD, aka congenital pernicious anemia; MIM:261000). IFD is an autosomal recessive disorder characterized by megaloblastic anemia (Tanner et al. 2005)
Last changed: 2014-11-21 19:49:01

Pathway: Activation of Matrix Metalloproteinases (Homo sapiens)
The matrix metalloproteinases (MMPs), previously known as matrixins, are classically known to be involved in the turnover of extracellular matrix (ECM) components. However, recent high throughput proteomics analyses have revealed that ~80% of MMP substrates are non-ECM proteins including cytokines, growth factor binding protiens, and receptors. It is now clear that MMPs regulate ECM turnover not only b
Last changed: 2014-11-21 06:36:34

Pathway: Defective BTD causes biotidinase deficiency (Homo sapiens)
BTD deficiency is an autosomal recessive disorder in which the body is unable to recycle and reuse biotin (Btn). This results in a secondary Btn deficiency that leads to juvenile-onset multiple carboxylase deficiency (MIM:253260) (Wolf 2012, Wolf et al. 1983). Patients present with neurological and cutaneous symptoms, including seizures, hypotonia, skin rash, and alopecia, usually between the second an
Last changed: 2014-11-21 19:49:01

Pathway: Defective AMN causes hereditary megaloblastic anemia 1 (Homo sapiens)
Defects in AMN cause recessive hereditary megaloblastic anemia 1 (RH-MGA1 aka MGA1 Norwegian type or Imerslund-Grasbeck syndrome, I-GS; MIM:261100). The Norwegian cases described by Imerslund were due to defects in AMN (Imerslund 1960). The resultant malabsorption of Cbl (vitamin B12) leads to impaired B12-dependent folate metabolism and ultimately impaired thymine synthesis and DNA replication
Last changed: 2014-11-21 19:49:01

Pathway: Defects in cobalamin (B12) metabolism (Homo sapiens)
Cobalamin (Cbl, vitamin B12) is a nutrient essential for normal functioning of the brain and nervous system and for the formation of blood. Cbl-dependent methionine synthase (MTR) is required for conversion of 5-methyltetrahydrofolate (metTHF) to tetrahydrofolate (THF), in addition to its role in conversion of homocysteine to methionine. In Cbl deficiency, and in inborn errors of Cbl metabolism that af
Last changed: 2014-11-21 19:49:01

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