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Synthesis of Sphingosine and the Ceramides
The sphingolipids, like the phospholipids, are composed of a polar head group and two nonpolar tails. The core of sphingolipids is the long-chain amino alcohol, sphingosine. The sphingolipids include the sphingomyelins and glycosphingolipids (the cerebrosides, sulfatides, globosides and gangliosides). Sphingomyelins are the only sphingolipid class that are also phospholipids. Sphingolipids are components of all membranes but are particularly abundant in the myelin sheath.
"n" indicates any fatty acid may be N-acetylated at this position.
Top: Sphingosine
Bottom: Basic composition of a ceramide
The initiation of the synthesis of the sphingoid bases (sphingosine, dihydrosphingosine, and ceramides) takes place via the condensation of palmitoyl-CoA and serine as shown in the Figure below. This reaction occurs on the cytoplasmic face of the endoplasmic reticulum (ER) and is catalyzed by serine palmitoyltransferase (SPT). The acylation of dihydrosphingosine (also called sphinganine) occurs through the activities of six different ceramide synthases (CerS) in humans. These CerS enzymes introduce fatty acids of varying lengths [designated by the –(CH2)n– in the structure] and degrees of unsaturation. In other organisms the ceramide synthases are referred to as sphinganine N-acyl transferases. The actions of CerS and the role of ceramide in biological responses is covered below.
Following conversion to ceramide, sphingosine is released via the action of ceramidase. Sphingosine can be re-converted to a ceramide by condensation with a fatty-acylCoA catalyzed by the various CerS. There are at least two ceramidase genes in humans both of which are defined by their pH range of activity: acid and neutral. Acid ceramidase is encoded by the ASAH1 gene. When studied in mice it has been shown that the ASAH1 gene is critical for early embryo survival and for removing ceramide from the embryo to prevent the default apoptosis pathway. Defects in the human ASAH1 gene result in the lysosomal storage disease Farber lipogranulomatosis. Neutral ceramidase is encoded by the ASAH2 gene and the enzyme is expressed in the apical membranes of the proximal and distal tubules of the kidney, endosome-like organelles in heptocytes, and in the epithelial cells of the gut. By studying the effects of ASAH2 knock-out mice it has been determined that neutral ceramidase is involved in the catabolism of dietary sphingolipids and the regulation of bioactive sphingolipid metabolites in the intestinal tract.
Pathway for sphingosine synthesis
back to the topSphingomyelin Synthesis and Metabolism
Sphingomyelins are sphingolipids that are also phospholipids. Sphingomyelins are important structural lipid components of nerve cell membranes. The predominant sphingomyelins contain palmitic or stearic acid N-acylated at carbon 2 of sphingosine.
A sphingomyelin
The sphingomyelins are synthesized by the transfer of phosphorylcholine from phosphatidylcholine to a ceramide in a reaction catalyzed by sphingomyelin synthases (SMS). There are two SMS genes in humans identified as SMS1 and SMS2. SMS1 is found in the trans-Golgi apparatus while SMS2 is predominantly associated with the plasma membrane.
Metabolism of the sphingomyelins
As shown in the Figure above, sphingomyelins are degraded via the action of sphingomyelinases resulting in release of ceramides and phosphocholine. The sphingomyelinase in humans functions at acidic pH and is, therefore, referred to as acid sphingomyelinase (ASMase). The human ASMase is encoded for by the sphingomyelin phosphodiesterase-1 gene (gene symbol = SMPD1) located on chromosome 11p15.1–11p15.4. Defects in the SMPD1 gene result in the lysosomal storage disease known as Niemann-Pick disease. There are in fact two major forms of Niemann-Pick (NP) disease. NP disease caused by acid sphingomyelinase deficiencies comprises types A and B, referred to as NPA and NPB. The other form of NP disease comprises types C1 and C2, the former due to defects in the NPC1 gene and the latter due to defects in a gene identified as NPC2.
back to the topMetabolism of the Ceramides
The overall level of ceramides in a cell is a balance between the need for sphingosine and sphingosine derivatives, such as sphingosine-1-phosphate (discussed in detail below), and the sphingomyelins. With respect to the sphingomyelins they serve a dual purpose of being important membrane phospholipids and as a reservoir for ceramides. The conversion of both dihydrosphingosine (sphinganine) and sphingosine to ceramide is catalyzed by the ceramide synthases (CerS). As indicated above there are six CerS in humans identified as CerS1 through CerS6 encoded for by six genes. CerS were originally referred to as Lass genes (for Longevity Assurance) based on their homology to the yeast gene, longevity assurance gene-1 (LAG1). LAG1 was so-called because deletion of the gene in yeast prolonged their life-span. An additional related gene in yeast is referred to as LAC1 and when both genes are deleted yeast exhibit poor growth or die. A human gene, originally identified as UOG-1 (upstream of growth and differentiation factor-1), was shown to complement a LAG1 deletion in yeast and when overexpressed in mammalian cells resulted in increased ceramide synthesis. The ceramides synthesized by the enzyme contained exclusively stearic acid (a C18 fatty acid). Subsequent studies demonstrated that other human LAG homologs, originally identified as translocating chain-associating membrane proteins (TRH) synthesized ceramides with varying fatty acyl chain length. Each of these genes are now identified as CerS.
Each CerS exhibits fatty acyl chain length specificity as well as differential tissue distribution. CerS1 is specific for stearic acid (C18) and is expressed in brain, skeletal muscle, and testis. CerS2 is specific for C20–C26 fatty acids and is expressed in the liver and kidney. CerS3 is specific for C22–C26 fatty acids and is expressed in the skin and testis. CerS4 is specific for C18–C20 fatty acids and is ubiquitously expressed but with highest levels in liver, heart, skin, and leukocytes. CerS5 is specific for palmitic acid (C16) and is ubiquitously expressed at low levels. CerS6 is specific for myristic (C14) and palmitic acid and is expressed at low levels in all tissues. CerS1 is structurally and functionally distinct from the other five CerS all of which contain a homeobox-like domain.
The biological significance of ceramide synthesis and the activity of the CerS is demonstrated by studies in several different types of human cancers. In this regard CerS1 appears to most significant. Head and neck squamous cell carcinomas (HNSCC) exhibit a downregulation of C18-ceramide levels when compared to adjacent normal tissue. In addition, a balance between the levels of C16- and C18-ceramides is associated with the state of clinical progression of HNSCC. In the chemotherapy of certain cancers CerS1 activity may also play a role. Enhanced expression of CerS1 has been shown to sensitize cells to a variety of chemotherapeutic drugs such as cisplatin, vincristine, and doxorubicin. In HNSCC CerS1 is involved in regulating apoptotic cell death via doxorubicin-induced caspase activation. When myeloid leukemia cells are treated with Gleevec® (imatinib) there is an increased production of C18-ceramide which is involved in the induction of apoptosis. The proposed mechanism for ceramide involvement in apoptotic processes involves the activation of the aspartate protease cathepsin D. Cathepsin D is associated with membranes and when activated by ceramides is released to the cytosol where it triggers the mitochondrial apoptosis pathway. Further evidence for the role of ceramides in negative growth responses is seen in cell cultures to which ceramide analogues are added. These types of assays demonstrate that ceramides induce oxidative stress, growth arrest, and apoptosis and/or necrosis.
When derived from the sphingomyelins, ceramides are the products of the action of acid sphingomyelinase (ASMase). The importance of sphingomyelin as a source of ceramide can be evidenced by the fact that the activation of the ASAase pathway is a shared response to the effects of cytokines, stress, radiation, chemotherapeutic drugs, and pathogenic and cytotoxic agents. Several receptor- and non-receptor-mediated pathways, activated in response to stress such as those involving death ligands like TNF-α and TNF-related apoptosis inducing ligands (TRAIL) are coupled to the activation of ASMase activity. The induction of ASMase in response to apoptotic triggers results in increased production of ceramides which then can initiate aspects of the apoptosis pathway as described above.
back to the topThe Glycosphingolipids
Glycosphingolipids, or glycolipids, are composed of a ceramide backbone with a wide variety of carbohydrate groups (mono- or oligosaccharides) attached to carbon 1 of sphingosine. The four principal classes of glycosphingolipids are the cerebrosides, sulfatides, globosides and gangliosides.
Cerebrosides have a single sugar group linked to ceramide. The most common of these is galactose (galactocerebrosides), with a minor level of glucose (glucocerebrosides). Galactocerebrosides are found predominantly in neuronal cell membranes. By contrast glucocerebrosides are not normally found in membranes, especially neuronal membranes; instead, they represent intermediates in the synthesis or degradation of more complex glycosphingolipids.
Galactocerebrosides are synthesized from ceramide and UDP-galactose. Excess lysosomal accumulation of glucocerebrosides is observed in Gaucher disease. Glucocerebrosides are only intermediates in the synthesis of complex gangliosides or are found at elevated levels only in disease states such as Gaucher disease, where there is a defect in the catabolism of the complex gangliosides. Thus, the presence of high concentrations of glucocerebrosides in cells such as monocytes and macrophages is indicative of a metabolic defect.
A glucocerebroside
Sulfatides: The sulfuric acid esters of galactocerebrosides are the sulfatides. Sulfatides are synthesized from galactocerebrosides and activated sulfate, 3'-phosphoadenosine 5'-phosphosulfate (PAPS). Excess accumulation of sulfatides is observed in metachromatic leukodystrophy (sulfatide lipodosis).
Globosides: Globosides represent cerebrosides that contain additional carbohydrates, predominantly galactose, glucose or GalNAc. Lactosyl ceramide is a globoside found in erythrocyte plasma membranes. Globotriaosylceramide (also called ceramide trihexoside) contains glucose and two moles of galactose and accumulates, primarily in the kidneys, of patients suffering from Fabry disease.
Gangliosides: Gangliosides are very similar to globosides except that they also contain NANA in varying amounts. The specific names for gangliosides are a key to their structure. The letter G refers to ganglioside, and the subscripts M, D, T and Q indicate that the molecule contains mono-, di-, tri and quatra(tetra)-sialic acid. The numerical subscripts 1, 2 and 3 refer to the carbohydrate sequence that is attached to ceramide; 1 stands for GalGalNAcGalGlc-ceramide, 2 for GalNAcGalGlc-ceramide and 3 for GalGlc-ceramide.
Structure of a GM2 ganglioside
Deficiencies in lysosomal enzymes, which normally are responsible for the degradation of the carbohydrate portions of various gangliosides, underlie the symptoms observed in rare autosomally inherited diseases termed lysosomal storage diseases, (also called the sphingolipidoses or lipid storage diseases) many of which are listed below.
back to the topSphingosine-1-phosphate (S1P) Signal Transduction
Lysophospholipids (LPs) are minor lipid components compared to the major membrane phospholipids such as phosphatidylcholline (PC), phosphatidylethanolamine (PE), and sphingomyelin. The LPs were originally presumed to be simple metabolic intermediates in the de novo biosynthesis of phospholipids. However, subsequent studies demonstrated that the LPs exhibited biological properties resembling those of extracellular growth factors or signaling molecules. The most biologically significant LPs are sphingosine 1-phosphate (S1P), lysophosphatidic acid (LPA), lysophosphatidylcholine (LPC), and sphingosylphosphorylcholine (SPC). More information on the biological activities of the lysophospholipids can be found in the Signal Transduction page.
Synthesis of S1P occurs exclusively from sphingosine via the action of sphingosine kinases. Degradation of S1P occurs through the action of S1P lyase or S1P phosphatases. Sphingosine is phosphorylated in humans through the action of two related sphingosine kinases encode by the SPHK1 and SPHK2 genes. The importance of the action of the sphingosine kinases can be shown by the fact that when both are knocked out in transgenic mice embryos are not viable due to the incomplete development of the brain and the vascular system. The intermediate in sphinosine synthesis, dihydrosphingosine, is also a substrate for sphinogosine kinases. When used as a substrate for phospholipid synthesis, S1P is degraded by S1P lyase to yield hexadecanal and phosphoethanolamine. Phosphoethanolamine is the direct precursor for the synthesis of the phospholipid phosphatidylethanolamine (PE).
Metabolism of sphingosine-1-phosphate
Each of the LPs functions via interaction with specific G-protein coupled receptors (GPCRs) leading to autocrine or paracrine effects. The first GPCR shown to bind S1P was called S1P1. Currently there are five characterized S1P receptors. Because several of the LP receptors were independently identified in unrelated assays, there are several different names for some members of this receptor family. In particular, there is a group of genes that were originally identified as GPCRs and called endothelial differentiation genes (EDGs) that were later found to be the same as several of the LP receptors. Thus S1P1 is also known as EDG-1, S1P2 as EDG-5, S1P3 as EDG-3, S1P4 as EDG-6, and S1P5 as EDG-8.
The biological activities attributed to S1P interaction with any of the five identified receptors are broad. These activities include involvement in vascular system and central nervous system development, viability and reproduction, immune cell trafficking, cell adhesion, cell survival and mitogenesis, stress responses, tissue homeostasis, as well as angiogenesis.
S1P1 is expressed in brain, heart, spleen, liver, kidney, skeletal muscle, thymus, and numerous white blood cells. Within the immune system activation of S1P1 has been shown to block B cell and T cell chemotaxis and infiltration into tissues. In addition S1P1 activation results in inhibition of late-stage maturation processes associated with T cells. Within the central nervous system S1P1 is involved in astrocyte migration and increased migration of neural stem cells. Within the vasculature S1P1 is involved in early vascular system development and endothelial cell functions such as adherens junction assembly and vascular smooth muscle cell development.
S1P2 is expressed in the brain, heart, spleen, liver, lung, kidney, skeletal muscle, and thymus. S1P2 is involved in the development of epithelial cells, enhancing the survival of cardiac myocytes to ischemic-reperfusion injury, and hepatocyte proliferation and matrix remodeling. Within the vasculature S1P2 promotes mast cell degranulation and decreases vascular smooth muscle cell responses to PDGF-induced migration. In the eye S1P2 activation can result in pathologic angiogenesis and disruption in adherens junction formation.
S1P3 is expressed in the brain, heart, spleen, liver, lung, kidney, skeletal muscle, testis, and thymus. S1P3 activation is associated with a worsening of sepsis, increased inflammation and coagulation. However, with respect to cardiac tissues S1P3 promotes survival in response to ischemic-reperfusion injury.
S1P4 is expressed in lymphoid tissues (leukocytes) and within a restricted subset of cells in the lung that includes airway smooth muscle cells. The primary responses to S1P4 activation are increased T cell migration and secretion of cytokines.
S1P5 is expressed in the brain, spleen, and the skin. Within the brain S1P5 activation is associated with inhibition of migration of oligodendrocyte progenitors while increasing the survival of oligodendrocytes. S1P5 also stimulates natural killer (NK) cell trafficking.
Recent studies have shown that SPHK2 (which contains a nuclear localization signal) and its product S1P are found in the nucleus associated with transcriptional co-repressor complexes that contain histone deacetylase 1 (HDAC1) and HDAC2. The S1P-containing HDAC complexes are prevented from deacetylating lysine residues in the histone tails, thereby altering gene expression patterns. One gene whose expression is upregulated in cells with S1P-HDAC complexes is the cell cycle regulating protein p21 which is an inhibitor of cyclin-dependent kinases (CDK) and is involved in p53-mediated apoptosis. This observation suggests that enhancing SPHK2-S1P-associated complexes in the nucleus could be of clinical benefit in p53-deficient types of cancer. Given that mutations in p53 are some of the most commonly occurring genetic abnormalities in cancer, this could prove highly significant.
back to the topSphingolipids and Insulin Resistance
Numerous studies have demonstrated that inhibition of several enzymes of sphingosine and ceramide synthesis, including serine palmitoyltransferase (SPT), ceramide synthases (CerS), and dihydroceramide desaturase (DES1, also identified as the DESG-1 homolog), all result in increased sensitivity to insulin. Given that several different enzymes of sphingolipid metabolism can affect sensitivity to insulin, and thus be involved in the pathogenesis of diabetes, it is important to determine which of the sphingolipids imparts the greater effect. As indicated above, numerous studies have implicated ceramides in the processes of cell growth inhibition and apoptosis. However, whether ceramides or the products of ceramide metabolism are involved in insulin responsiveness is only now being clearly investigated. Ceramides can be deacetylated by ceramidases to form sphingosine. As discussed above, sphingosine can be phosphorylated to S1P which is an important biologically active lipid. Ceramides can be glucosylated (catalyzed by glucosylceramide synthase, GCS) forming glucosylceramides which are the building blocks of complex glycosphingolipids, act as substrates for the sphingomyelin synthases yielding sphingomyelins, or phosphorylated (by ceramide kinase) to yield ceramide-1-phosphate. Thus, it is clear that multiple products of the actions of SPT, CerS, and DESG-1 could potentially contribute to the development of insulin resistance and diabetes.
As discussed in the Insulin Functions page, a required intermediate in the insulin receptor-mediated signal transduction cascade is the PKB/Akt kinase (hereafter identified as PKB), which itself is phosphorylated and activated by insulin receptor activation. Mice in which this kinase gene has been knocked-out become resistant to the actions of insulin. Related to this is the fact that when sphingolipid synthesis is increased in mice the ability of PKB to become phosphorylated and activated by the insulin receptor is impaired. However, all events initiated by insulin receptor activation upstream of PKB phosphorylation are unaffected. Chemical inhibition of acid ceramidase results in increased levels of ceramides and inhibited PKB activity. Conversely, overexpression of acid ceramidase results in enhanced signaling activation of PKB. The use of chemical inhibitors of GCS have the same effect as inhibition of acid ceramidase. Results of these studies indicate that it is ceramide, not sphingosine or glucosylceramides, that is the principle sphingolipid antagonist of PKB activity.
Although GCS inhibitors antagonize insulin signaling in cells in culture suggesting that glucosylceramides are not involved, the results of their use in vivo strongly indicate that glucosylceramides are indeed involved in the development of insulin resistance and diabetes. In mouse models of obesity the administration of GCS inhibitors improves insulin sensitivity, prevents pancreatic β-cell failure, resolves hepatic steatosis, and improves adipocyte morphology (fewer infiltrating macrophages and smaller size). In humans with Gaucher disease, which is associated with impaired catabolism of glucosylated ceramides, there is an associated insulin resistance. These results suggest that both ceramides and glycosylated ceramides function independently to inhibit insulin function.
Evidence gathered from studies in animal models suggest that the primary target tissues for the pathophysiological actions of the sphingolipids are skeletal muscle and adipose tissue. In mice the insulin-sensitizing effects of sphingolipid depletion can be seen in isolated muscle tissue and muscle cells in culture. Cardiac muscle is also sensitive to manipulations in sphingolipid metabolism as evidenced in transgenic mice with disrupted SPT activity. In human muscle biopsy assays it has been shown that accumulation of ceramides is higher in patients with insulin resistance. These observations are independent of whether the patient is obese or what level of free fatty acids or diacylglycerols there is. In adipose tissue ceramides inhibit insulin signaling and inhibition of SPT and GCS alters adipocyte morphology to a more favorable status. Treatment of obese mice with GCS inhibitors not only improves insulin responsiveness but also adipocyte morphology. In addition, inhibition of GCS negates the impairment of insulin signaling in adipocytes exerted by TNF-α.
Given the increased interest in the role of sphingolipids in the pathogenesis of insulin resistance, diabetes, and obesity it should not be surprising that modulation of their metabolism is a high priority for pharmaceutical intervention in these disorders.
back to the topClinical Significances of Sphingolipids
Some of the most devastating inborn errors in metabolism are those associated with defects in the enzymes responsible for the lysosomal degradation of membrane glycosphingolipids which are particularly abundant in the membranes of neural cells. Many of these disorders lead to severe psycho-motor retardation and early lethality. Because the disorders are caused by defective lysosomal enzymes, with the result being lysosomal accumulation of pathway intermediates, these are often referred to as lysosomal storage diseases. The mucopolysaccharidoses are another class of disorders that are members of the lysosomal storage diseases.
The following figure shows several of the pathways and intermediates in glycosphingolipid metabolism. Enzymes are indicated in green and the disease(s) associated with defects in the indicated enzyme are shown in blue. SAP-A, SAP-B, SAP-C, and SAP-D are the saposins which are a family of small glycoproteins. The saposins (A, B, C, and D) are all derived from a single precursor, prosaposin. The mature saposins, as well as prosaposin, activate several lysosomal hydrolases involved in the metabolism of various sphingolipids. Prosaposin is proteolytically processed to saposins A, B, C and D, within lysosomes but also exists as an integral membrane protein not destined for lysosomal entry. Uncleaved prosaposin can be found in many biological fluids such as seminal plasma, human milk, and cerebrospinal fluid, where it appears to have a different function. Each of the disease names in the image can be clicked to go to a descriptive page of that disease. The Table below the Figure lists some additional lysosomal storage diseases caused by defective sphingolipid metabolism. Click here for a large scale version of this image.
Disorders Associated with Abnormal Sphingolipid Metabolism
| Disorder | Enzyme Deficiency | Accumulating Substance | Symptoms |
| Tay-Sachs disease | HexA | GM2 ganglioside | infantile form: rapidly progressing mental retardation, blindness, early mortality |
| Sandhoff disease | HexA and HexB | globoside; GM2 ganglioside | infantile form: same symptoms as Tay-Sachs, progresses more rapidly |
| Tay-Sachs AB variant
GM2 activator deficiency |
GM2 activator (GM2A) | GM2 ganglioside | infantile form: same symptoms as Tay-Sachs |
| Gaucher disease | acid β-glucosidase (glucocerebrosidase) |
glucocerebrosides | hepatosplenomegaly, mental retardation in infantile form, long bone degeneration |
| Fabry disease | α-galactosidase A | globotriaosylceramide; also called ceramide trihexoside (CTH) | kidney failure, skin rashes |
| Niemann-Pick diseases Types A and B Type C |
sphingomyelinase NPC1 protein |
sphingomyelins LDL-derived cholesterol |
type A is severe disorder with heptosplenomegaly, severe neurological involvement leading to early death, type B only visceral involvement |
| Krabbe disease; globoid cell leukodystrophy (GLD) | galactocerebrosidase | galactocerebrosides | mental retardation, myelin deficiency |
| GM1 gangliosidosis | β-galactosidase-1 | GM1 gangliosides | mental retardation, skeletal abnormalities, hepatomegaly |
| Metachromatic leukodystrophy; sulfatide lipodosis |
arylsulfatase A | sulfatides | mental retardation, metachromasia of nerves |
| Fucosidosis | α-fucosidase | pentahexosylfucoglycolipid | cerebral degeneration, thickened skin, muscle spasticity |
| Farber lipogranulomatosis | acid ceramidase | ceramides | hepatosplenomegaly, painful swollen joints |
One of the most clinically important classes of sphingolipids are those that confer antigenic determinants on the surfaces of cells, particularly the erythrocytes. The ABO blood group antigens are the carbohydrate moieties of glycolipids on the surface of cells as well as the carbohydrate portion of serum glycoproteins. When present on the surface of cells the ABO carbohydrates are linked to sphingolipid and are therefore of the glycosphingolipid class. When the ABO carbohydrates are associated with protein in the form of glycoproteins they are found in the serum and are referred to as the secreted forms. Some individuals produce the glycoprotein forms of the ABO antigens while others do not. This property distinguishes secretors from non-secretors, a property that has forensic importance such as in cases of rape.
R represents the linkage to protein in the secreted forms, sphingolipid (ceramide) in the cell-surface bound form, open square = GlcNAc, open diamond = galactose, filled square = fucose, filled diamond = GalNAc. The linkage in the glycolipid form may include a glucose in a β-1,3 or β-1,4 to the initial galactose residue.
Structure of the ABO blood group carbohydrates
A significant cause of death in premature infants and, on occasion, in full term infants is respiratory distress syndrome (RDS) or hyaline membrane disease. This condition is caused by an insufficient amount of pulmonary surfactant. Under normal conditions the surfactant is synthesized by type II endothelial cells and is secreted into the alveolar spaces to prevent atelectasis following expiration during breathing. Surfactant is comprised primarily of dipalmitoyllecithin; additional lipid components include phosphatidylglycerol and phosphatidylinositol along with proteins of 18 and 36 kDa (termed surfactant proteins). During the third trimester the fetal lung synthesizes primarily sphingomyelin, and type II endothelial cells convert the majority of their stored glycogen to fatty acids and then to dipalmitoyllecithin. Fetal lung maturity can be determined by measuring the ratio of lecithin to sphingomyelin (L/S ratio) in the amniotic fluid. An L/S ratio less than 2.0 indicates a potential risk of RDS. The risk is nearly 75-80% when the L/S ratio is 1.5.
The carbohydrate portion of the ganglioside, GM1, present on the surface of intestinal epithelial cells, is the site of attachment of cholera toxin, the protein secreted by Vibrio cholerae.
These are just a few examples of how sphingolipids and glycosphingolipids are involved in various recognition functions at the surface of cells. As with the complex glycoproteins, an understanding of all of the functions of the glycolipids is far from complete.
back to the topReturn to The Medical Biochemistry Page
Michael W King, PhD | © 1996–2012 themedicalbiochemistrypage.org, LLC | info @ themedicalbiochemistrypage.org
Last modified: March 23, 2012
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