Browsing Pathways

Zoledronate (also named zoledronic acid, Zometa or Reclast) is a type of medication that used to treat numbers of bone diseases because of its affinity for hydroxyapatite. Zoledronate targets farnesyl pyrophosphate (FPP) synthase by inhibiting the function of this enzyme in the mevalonate pathway, which prevent the biosynthesis of Geranyl-PP and farnesyl pyrophosphate. Geranyl-PP and farnesyl pyrophosphate are important for geranylgeranylation and farnesylation of GTPase signalling proteins. Lack of Geranyl-PP and farnesyl pyrophosphate will result in decreased rate of bond resorption and turnover as well as block the osteoclast activity, which lead to an increasing mass gain in bone (i.e. net gain in bone mass).

The discovery of AIDS prompted the search for agents that block the HIV replication process. Zidovudine (AZT) is a nucleoside analogue of thymidine, and was shown to reduce considerably the mortality of patients with AIDS. Zidovudine is toxic to the hemtopoietic system, causing anemia and neutropenia. It is clear, however, that disease progression can occur during continued administration of zidovudine. Moreover, zidovudine is not effective in treating Kaposi sarcoma, a common complication of HIV infection. Zidovudine therapy is also associated with a high incidence of toxicity, primarily bone marrow suppression, that requires dosage reduction or discontinuation of the therapy.

Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.

Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.

Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.

Zeaxanthin biosynthesis is a pathway that occurs in the chloroplast by which lycopene becomes zeaxanthin, one of the most common carotenoid alcohols found in nature . The first two reactions are catalyzed by lycopene beta cyclase which uses NAD(P)H as a cofactor to convert lycopene into gamma-carotene and gamma-carotene into beta-carotene. The last two reactions are catalyzed by beta-carotene 3-hydroxylase which uses ferredoxin and Fe2+ as cofactors to convert beta-carotene into beta-cryptoxanthin and beta-cryptoxanthin into zeaxanthin.

Zalcitabine (ddc) is a dideoxynucleoside antiretroviral drug that when used in combination with zidovudine improves the viral load and CD4+ cell count of patients infected with Human Immunodeficiency Virus Type 1 (HIV-1). Zalcitabine is phosphorylated to it’s active form metabolite 2′,3′-dideoxycytidine 5′-triphosphate (ddCTP) in both healthy and infected cells. ddCTP competes with deoxycytidine triphosphate inhibiting the enzyme reverse transcriptase from using the substrates to elongate the viral DNA strand ultimately halting HIV replication.

Escherichia coli can utilize D-xylose as the sole source of carbon and energy for the cell. A low-affinity proton motive force or a high-affinity ATP-driven (ABC) transport system brings unphosphorylated D-xylose into the cell. Following entry, D-xylose is converted to D-xylulose by an isomerase and then converted to the pentose phosphate pathway intermediate, D-xylulose 5-phosphate via a kinase. D-xylulose 5-phosphate can then enter pathways of metabolism to meet the cells needs.

Escherichia coli can utilize D-xylose as the sole source of carbon and energy for the cell. A low-affinity proton motive force or a high-affinity ATP-driven (ABC) transport system brings unphosphorylated D-xylose into the cell. Following entry, D-xylose is converted to D-xylulose by an isomerase and then converted to the pentose phosphate pathway intermediate, D-xylulose 5-phosphate via a kinase. D-xylulose 5-phosphate can then enter pathways of metabolism to meet the cells needs.

The degradation of xylose begins with NADP dependent trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase resulting in the release of a NADPH, hydrogen ion and Xylitol. Xylitol reacts with a NAD D-xylulose reductase resulting in the release of NADH, a hydrogen ion and D-xylulose. Xylulose reacts with ATP through a xylulose kinase resulting in a release of ADP, hydrogen ion and xylulose 5-phosphate. The latter compound, xylulose 5-phosphate through a Ribulose-phosphate 3-epimerase resulting in the release of D-ribulose 5-phosphate. D-ribulose 5-phosphate and xylulose 5-phosphate react with a transketolase resulting in the release of D-glyceraldehyde 3-phosphate and D-sedoheptulose 7-phosphate. These two compounds react through a transaldolase resulting in the release of a D-erythrose 4-phosphate and Beta-D-fructofuranose 6-phosphate. D-erythrose 4-phosphate reacts with a xylulose 5-phosphate through a transketolase resulting in the release of Beta-D-fructofuranose 6-phosphate and D-glyceraldehyde 3-phosphate