Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spin-labeled cardiolipin 1-(3-sn-phosphatidyl)-3-[1-acyl-2-(16-doxylstearoyl)glycero(3)phosphol]-sn-glycerol has been prepared. The stereoselective synthesis makes use of the monolysocardiolipin 1-(3-sn-phosphatidyl)-3-[1-acyl-2-lyso-sn-glycero(3)phospho]-sn-glycerol, available from the stereospecific hydrolysis of cardiolipin by phospholipase A2 (phosphatide 2-acylhydrolase, EC 3.1.1.4) of Trimeresurus flavoviridis. The results of treatment of the spin-labeled cardiolipin with the cardiolipin-specific phospholipase D (phosphatidylcholine phosphatidohydrolase, EC 3.1.4.4) (Hemophilus parainfluenzae) of known specificity and with phospholipase C (phosphatidylcholine cholinephosphohydrolase, EC 3.1.4.3) of Bacillus cereus are consistent with the assigned structure. The spin-labeled cardiolipin is further characterized and the unique features of this diastereomer are discussed in the context of the unusual stereochemistry of the natural phospholipid.
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PMID:Cardiolipin: a stereospecifically spin-labeled analogue and its specific enzymic hydrolysis. 27 15

A highly active phospholipase D that is specific for cardiolipin was detected in the gram-negative bacterium Haemophilus parainfluenzae. Previously reported phospholipase D preparations have come exclusively from higher plants. The bacterial enzyme hydrolyzed cardiolipin to phosphatidyl glycerol and phosphatidic acid. During the incubation, phosphatidic acid disappeared. Phosphatidyl ethanolamine, methylated phosphatidyl ethanolamines, phosphatidyl choline, and phosphatidyl glycerol were not hydrolyzed when cardiolipin was rapidly hydrolyzed.
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PMID:Cardiolipin-specific phospholipase D activity in Haemophilus parainfluenzae. 431 62

A phospholipase specific for cardiolipin (CL) was found in the membrane of Haemophilus parainfluenzae. The enzyme hydrolyzed CL to phosphatidic acid (PA) and phosphatidylglycerol (PG), indicating that it was a phospholipase D (an enzyme activity believed to be confined to higher plants). In addition to its substrate specificity, this enzyme was unusual in its requirement for Mg(2+) (K(m) of 1.3 mm) for maximal activity and its inhibition by chelating agents, heavy metals, some detergents, and organic solvents. When inhibitors of phospholipase activity were added to the growth medium, CL accumulated and PG disappeared in the membrane, suggesting that the phospholipase D was active in vivo. The activity of phospholipase D in cell-free homogenates was greater than expected from earlier studies of CL metabolism and greater than the other phospholipase activities detected in the homogenate. The high activity of the CL-specific phospholipase D suggests there might be a very active degradation of CL to PG and PA and an active resynthesis of CL from the hydrolysis products.
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PMID:Cardiolipin-specific phospholipase D of Haemophilus parainfluenzae. II. Characteristics and possible significance. 432 31

Heterogeneity in the metabolism of cardiolipin (CL) has been detected in Haemophilus parainfluenzae. Pulse-chase experiments showed that a portion of the total CL incorporated and then lost (32)P much more rapidly than the rest of the CL in the cells. The metabolism of each phosphate of the CL differed. The phosphate of the phosphatidyl glycerol (PG) portion of the CL had a more active metabolism than the phosphate of the phosphatidic acid portion of the molecule. Only a portion of the PG pool contributed to the formation of CL. Ethylenediaminetetraacetic acid inhibited the CL-specific phospholipase D in vitro and, when added to growing cells, resulted in more rapid PG metabolism, suggesting that CL hydrolysis contributed to the PG pool.
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PMID:Detection of a rapidly metabolizing portion of the membrane cardiolipin in Haemophilus parainfluenzae. 500 72

Staphylococcus aureus accumulated cardiolipin (CL) and lost phosphatidylglycerol (PG) during the stationary phase of growth. The minor lipids, phosphatidylethanolamine and phosphatidylglucose, also accumulated, whereas the lysylphosphatidylglycerol (LPG) content of the membrane remained constant as stationary phase continued. During exponential growth, the proportions and total content of phospholipids per cell remained constant. The metabolism of the phospholipids was examined under these conditions. In pulse-chase experiments, the phospholipids lost (14)C from the glycerols slower than (32)P. When the phospholipids were labeled with (14)C glycerol, the unacylated glycerols of PG and LPG lost (14)C, whereas the diacylated glycerols either accumulated or did not lose (14)C. In all experiments, the PG showed a more rapid metabolism than the LPG. When staphylococcal CL was hydrolyzed by Haemophilus parainfluenzae CL-specific phospholipase D into phosphatidic acid (PA) and PG, the incorporation of (32)P into both of the phosphates of CL was found to be parallel at both the PG and PA ends of the molecule. However, the specific activity of the (32)P at the PA end was twice that at the PG end of the molecule. The PG end of the CL apparently came from a portion of the cellular PG pool with about 20% the specific activity of the total cellular PG. The turnover of two of the glycerols of the PG portion of CL was like that of the cellular PG. The diacylated glycerol of the PG and of CL and of the membrane PG showed neither turnover nor incorporation of (14)C. Half of the radioactivity was lost from the middle glycerol of CL and the free glycerol of the cellular PG in one bacterial doubling. The diacylated glycerol from the other end of the CL molecule (the PA end) lost radioactivity almost as rapidly as the middle glycerol for 10 min. After the initial rapid loss, the turnover slowed to a rate 10 times slower than the middle glycerol, indicating that the (14)C was actually accumulating at this end of the molecule. The phosphates and glycerols involved in the hydrolysis and resynthesis of the CL molecule during exponential growth in S. aureus apparently come from different pools of PG.
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PMID:Metabolism of phosphatidylglycerol, lysylphosphatidylglycerol, and cardiolipin of Staphylococcus aureus. 512 4

Examination of phospholipid metabolism in Haemophilus parainfluenzae with inhibitors of various cellular functions indicated that macromolecular synthesis and lipid metabolism can be dissociated at least for a short time. Two classes of inhibitors have relatively specific effects on cardiolipin (CL) metabolism. Pentachlorophenol and p-hydroxymercuribenzoate blocked CL synthesis but allowed CL hydrolysis to phosphatidic acid and phosphatidyl glycerol (PG); 3,3',4,5'-tetrachlorosalicylanilide (TCS) and carbonyl cyanide m-chlorophenylhydrazone (m-CCCP) blocked CL hydrolysis with the stoichiometric accumulation of CL. It appeared as if TCS and m-CCCP inhibited a vital activity coupled with the hydrolysis of CL by the highly active, CL-specific phospholipase D found in this organism. Because TCS and m-CCCP are thought to act by destroying the proton gradient thereby interrupting energy-dependent transport, it is possible that a highly active portion of the cellular CL could be coupled to some phase of this process.
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PMID:Consequences of the inhibition of cardiolipin metabolism in Haemophilus parainfluenzae. 513 31

The principal lipids associated with the electron transport membrane of Haemophilus parainfluenzae are phosphatidylethanolamine (78%), phosphatidylmonomethylethanolamine (0.4%), phosphatidylglycerol (18%), phosphatidylcholine (0.4%), phosphatidylserine (0.4%), phosphatidic acid (0.2%), and cardiolipin (3.0%). Phospholipids account for 98.4% of the extractible fatty acids. There are no glycolipids, plasmalogens, alkyl ethers, or lipo amino acid esters in the membrane lipids. Glycerol phosphate esters derived from the phospholipids by mild alkaline methanolysis were identified by their staining reactions, mobility on paper and ion-exchange column chromatography, and by the molar glycerol to phosphate ratios. Eleven diacyl phospholipids can be separated by two-dimensional thin-layer chromatography. Each lipid served as a substrate for phospholipase D, and had a fatty acid to phosphate ratio of 2:1. Each separated diacyl phospholipid was deacylated and the glycerol phosphate ester was identified by paper chromatography in four solvent systems. Of the 11 separated phospholipids, 3 were phosphatidylethanolamines, 2 were phosphatidylserines, and 2 were phosphatidylglycerols. Phosphatidylcholine, cardiolipin, and phosphatidic acid were found at a single location. Phosphatidylmonomethylethanolamine was found with the major phosphatidylethanolamine. Three distinct classes of phospholipids are separable according to their relative fatty acid compositions. (i) The trace lipids consist of two phosphatidylethanolamines, two phosphatidylserines, phosphatidylcholine, phosphatidic acid, and a phosphatidylglycerol. Each lipid represents less than 0.3% of the total lipid phosphate. These lipids are characterized by high proportions of the short (C(10) to C(14)) and long (C(19) to C(22)) fatty acids with practically no palmitoleic acid. (ii) The major phospholipids (93% of the lipid phosphate) are phosphatidylethanolamine, phosphatidylmonomethylethanolamine, and phosphatidylglycerol. These lipids contain a low proportion of the short (<C(14)) and long (>C(19)) fatty acids. Palmitic and palmitoleic acids represent over 80% of the total fatty acids. (iii) The fatty acid composition of the cardiolipin is intermediate between the other two classes. Both palmitoleic and the longer fatty acids represent a significant proportion of the total fatty acid.
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PMID:Lipid composition of the electron transport membrane of Haemophilus parainfluenzae. 568 94

There are several bacterial polysaccharides (PSs) which contain a terminal lipid moiety. It has been postulated that these terminal lipid moieties anchor the PSs to the outer membrane of the bacteria. Our studies have shown that incubation of native PS from group C Neisseria meningitidis or Haemophilus influenzae type b with isolated outer membrane vesicles results in association of a portion of the PS with the vesicles. Removal of the terminal lipid from the PS by treatment with phospholipase A2 or phospholipase D eliminates this association. In other studies, it was shown that delipidated PSs are not suitable as solid-phase antigens in a currently used enzyme-linked immunosorbent assay (ELISA). Measurement of antibody units in the reference sera by using delipidated PSs as antigens in an ELISA yielded negligible absorbance compared with native PSs when methylated human serum albumin was used to coat the PSs to the plate. Nevertheless, phospholipase A2 and phospholipase D treatment did not noticeably affect antigenic epitopes, since soluble group C PS without the terminal lipid bound antibody as effectively as the native PS did, as measured by a competitive inhibition assay. Both hydrophobic and electrostatic interactions are important for the binding of group C N. meningitidis PS to the ELISA plate, while charge interactions seem to be sufficient for binding the more negatively charged H. influenzae type b PS.
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PMID:Involvement of phospholipid end groups of group C Neisseria meningitidis and Haemophilus influenzae type b polysaccharides in association with isolated outer membranes and in immunoassays. 830 May 24