Synonyms for cerebroside or Related words with cerebroside
Examples of "cerebroside"
-sulfatase (, "arylsulfatase A", "
sulfate sulfatase") is an enzyme with systematic name "
-3-sulfate 3-sulfohydrolase". This enzyme catalyses the following chemical reaction
Arylsulfatase A (or
-sulfatase) is an enzyme that breaks down sulfatides, namely
and sulfate. In humans, arylsulfatase A is encoded by the "ARSA" gene.
A galactocerebroside (or galactosylceramide) is a type of
consisting of a ceramide with a galactose residue at the 1-hydroxyl moiety.
The fundamental structure of a
is ceramide. Monoglycosyl and oligoglycosylceramides having a mono or polysaccharide bonded glycosidically to the terminal OH group of ceramide are defined as cerebrosides. Sphingosine is the main long-chain base present in ceramide.
However, experimentation using renal cancer cell lines has given some insight into the mechanism for the elevated levels of sulfatide expression in cancer cells. Specifically,
sulfotransferase (CST) is elevated as it passes along a signaling pathway which involves:
A globoside is a type of glycosphingolipid with more than one sugar as the side chain (or R group) of ceramide. The sugars are usually a combination of "N"-acetylgalactosamine, -glucose or -galactose. A glycosphingolipid that has only one sugar as the side chain is called a
In glycolipids, the sugar component is attached to this group. The simplest glycolipid is
, in which there is only one sugar residue, either Glc or Gal. More complex glycolipids, such as gangliosides, contain a branched chain of as many as seven sugar residues.
This enzyme belongs to the family of transferases, specifically the sulfotransferases, which transfer sulfur-containing groups. The systematic name of this enzyme class is 3'-phosphoadenylyl-sulfate:galactosylceramide 3'-sulfotransferase. Other names in common use include GSase, 3'-phosphoadenosine-5'-phosphosulfate-
sulfotransferase, galactocerebroside sulfotransferase, galactolipid sulfotransferase, glycolipid sulfotransferase, and glycosphingolipid sulfotransferase. This enzyme participates in sphingolipid metabolism.
In conclusion, the early phase of myelination was correlated with the increases synthesis of lipids, cholesterol,
, and sulfatide. It is likely that these compounds are synthesized and packaged in the Golgi Apparatus of oligodendroglia. Even though the transport of these lipids is unknown, it appears that myelination is delayed without their synthesis.
Monogalactosylceramide is the largest single component of the myelin sheath of nerves.
synthesis can therefore give a measurement of myelin formation or remyelination. The sugar moiety is linked glycosidically to the C-1 hydroxyl group of ceramide, such as in lactosylceramide. Cerebrosides containing a sulfuric ester (sulfate) group, known as sulfatides, also occur in the myelin sheath of nerves. These compounds are preferably named as sulfates of the parent glycosphingolipid.
The studies on a rat optic nerve revealed that 15 days post-natal is when an increase in myelination is observed. Before this time period, most of the axons, roughly about 70%, are not myelinated. At this time, [35S] Sulfate was incorporated into sulfatide and the activity of
, sulfotransferase reached a peak in enzyme activity. This time frame also showed a period of maximal myelination based on the biochemical data.
Metachromatic leukodystrophy (MLD, also called Arylsulfatase A deficiency) is a lysosomal storage disease which is commonly listed in the family of leukodystrophies as well as among the sphingolipidoses as it affects the metabolism of sphingolipids. Leukodystrophies affect the growth and/or development of myelin, the fatty covering which acts as an insulator around nerve fibers throughout the central and peripheral nervous systems. MLD involves
sulfate accumulation. Metachromatic leukodystrophy, like most enzyme deficiencies, has an autosomal recessive inheritance pattern.
Aqueous extracts of the fruit bodies contain polysaccharides that have been shown in laboratory tests to be highly efficient at inhibiting infection by tobacco mosaic virus. Several bioactive compounds have been isolated and identified from the mushroom, including allitol, stearic acid, furan-3-carboxylic acid, (22"E",24"R")-3β-hydroxyergosta-5,22-diene, 3β-hydroxy-5α,8α-epidioxy-24ξ-methylcholesta-6-ene, dihydrofuran-2,5-dione,3β-hydroxy-5α,8α-epidioxyergosta-6,22-diene, palmitic acid, uracil, "cis"-butenedioic acid, thioacetic anhydride, succinic acid, 1-ethylic-βD-glycoside, 2-acetamino-2-deoxy-β-D-glucose, and
One early study showed that in the developing rat optic nerves, formation of oligodendrocytes and subsequent myelination occurs postnatal. In the optic nerve, the oligodendrocyte cells divided for the final time at five days, with the onset of myelin formation occurring on or around day 6 or 7. However, the exact process by which the oligodendrocytes were stimulated to produce myelin was not yet fully understood, but early myelination in the optic nerve has been linked to a rise in the production of various lipids – cholesterol,
, and sulfatide.
The melting point of cerebrosides is considerably greater than physiological body temperature, >37.0 °C, giving glycolipids a paracrystalline, similar to liquid crystal structure.
molecules are able form up to eight intermolecular hydrogen bonds between the polar hydrogens of the sugar and the hydroxy and amide groups of the sphingosine base of the ceramide. These hydrogen bonds within the cerebrosides result in the molecules having a high transition temperature and compact alignment. Monoglycosylceramides in conjunction with cholesterol are prevalent in the lipid-raft micro domain, which are important sites in the binding of proteins, and enzyme-receptor interactions.
Influenza A virus (IAV) binds strongly to sulfatide. However, sulfatide receptors have no sialic acid, which has been shown to play a necessary role as a virus receptor that facilitates the binding of the influenza A virus. Sulfatide has also been shown to inhibit influenza A virus sialidase activity. However, this is only under acidic conditions not neutral conditions. To fully understand the role of sulfatide in the cycle of IAV infection, research have expressed sulfatide in Madin-Darby canine kidney cells, which can express sulfatide and support IAV replication and in COS-7 cells, which do not have the ability to express sulfatide and do not support IAV replication sufficiently. Consequently,the COS-7 cells were transfected with galactosyltransferase and
sulfotransferase genes from the Madin-Darby canine kidney cells and used to make two cell clones with the ability to express sulfatide .
Sulfatide synthesis begins with a reaction between UDP-galactose and 2-hydroxylated or non-hydroxylated ceramide. This reaction is catalyzed by galactosyltransferase (CGT), where galactose is transferred to 2-hydroxylated, or non-hydroxylated ceramide, from UDP-galactose. This reaction occurs in the luminal leaflet of the endoplasmic reticulum, and its final product is GalCer, or galactocerebroside, which is then transported to the Golgi apparatus. Here, GalCer reacts with 3’-phosphoadenosine-5’-phosphosulfate (PAPS) to make sulfatide. This reaction is catalyzed by
sulfotransferase (CST). CST is a homodimeric protein that is found in the Golgi apparatus. It has been demonstrated that mice models lacking CST, CGT, or both are incapable of producing sulfatide indicating that CST and CGT are necessary components of sulfatide synthesis.
Sulfatide has also been shown to play a role in myelin maintenance and glial-axon signaling, which was indicated by research in older
sulfotransferase (CST)-deficient mice. These mice had vacuolar degeneration, uncompacted myelin, and moderate demyelination of the spinal cord. This occurs because improper glial-axon signaling and contact and disruption of paranodal glial-axon junctions causes improper placement and maintenance of sodium and potassium channel clusters in the axons at the nodes of Ranvier. As a result, the maintenance of Nav1.6 sodium clusters is impaired as there is a decrease in the number of clusters of sodium channels at the nodes of Ranvier. Additionally, Kv1.2 channels are moved from the paranodal position to the juxtaparanodal position causing impairment of these channels; this is also associated with the loss of neurofascin 155 and Caspr clusters, which are important components of the glial-axon junction.
Sulfatide is also important for glial-axon junctions in the peripheral nervous system. In peripheral nerves that are
sulfotransferase (CST) deficient, the nodes of Ranvier form enlarged axonal protrusions filled with enlarged vesicles, and neurofascin 155 and Caspr clusters are diminished or absent. In order to form a paranodal junction, Caspr and contactin form a complex with neurofascin 155. It has been shown that sulfatide may be involved in the recruitment and formation of neurofascin 155 in lipid rafts; neurofascin 155 protein clusters then bring Caspr and contactin into the membrane to form the complex, which allows the formation of stable glial-axon junctions. Consequently, sulfatide plays an important role in maintaining the paranodal glial-axon junctions, which allows for proper glial-axon interaction and signaling. Sulfatide has also been shown to be an inhibitor of myelin-associated axon outgrowth, and small amounts of sulfatide have been found in astrocytes and neurons, which is also indicative of its importance in glial-axon junctions.
The first of Bachhawat's major research findings came when he was working with Minor J. Coon at the University of Michigan. Both the scientists together discovered HMG-CoA lyase, an intermediate in the mevalonate and ketogenesis pathway, thus broadening the understanding of the "formation of ketone bodies in mammals", which was later elucidated further in his article "Enzymic cleavage of p-Hydroxy-f3-Methyl-Glutaryl coenzyme A 10 acetoacctate and acetyl coenzyme A.", published in 1995. On his return to India, he focused his studies on amino acids and inorganic sulphate metabolism, as well as glycosaminoglycan. His researches revealed, for the first time, that Metachromatic leukodystrophy, an autosomal recessive disease, was caused by the absence of Arylsulfatase A, an enzyme responsible for the breaking down on sulfatides. This discovery assisted other scientists in the elucidation of similar glycolipid storage diseases such as Gaucher's disease and Tay–Sachs disease and in their prenatal diagnosis. His proposals on the biosynthesis and degradation of
-3-sulfate, a lipid found in high concentrations in patients afflicted with Metachromatic leukodystrophy were known to have helped in the later-day therapeutic protocols.
Copyright © 2017