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PubMed1982

Oral lecithin and linoleic acid in Friedreich's ataxia: III. Biochemical results.

Lecithin and safflower oil brought about the same changes in serum LAD activity and kinetics in patients with Friedreich's Ataxia as in controls when results of this double-blind crossover study were analyzed according to group assignation. According to functional stages, pretrial LAD activity decreased with advancing severity while Km for lipoamide increased. Lecithin and safflower oil supplements corrected the elevated Km for lipoamide but produced a further reduction in LAD activity. These changes may have been due to the increased intake of linoleic acid, a precursor of lipoic acid, which is present in high percentage in both lecithin and safflower oil. Results of the biochemical study thus agreed with the clinical data gathered during the course of the one-year trial in suggesting that linoleic acid may well have been the active factor through which biochemical and clinical improvement was previously observed in patients with Friedreich's Ataxia supplemented with lecithin.

Administration, Oral↗
PubMed2002

Solution structure and dynamics of the lipoic acid-bearing domain of human mitochondrial branched-chain alpha-keto acid dehydrogenase complex.

The lipoyl-bearing domain (LBD) of the transacylase (E2) subunit of the branched-chain alpha-keto acid dehydrogenase complex plays a central role in substrate channeling in this mitochondrial multienzyme complex. We have employed multidimensional heteronuclear NMR techniques to determine the structure and dynamics of the LBD of the human branched-chain alpha-keto acid dehydrogenase complex (hbLBD). Similar to LBD from other members of the alpha-keto acid dehydrogenase family, the solution structure of hbLBD is a flattened beta-barrel formed by two four-stranded antiparallel beta-sheets. The lipoyl Lys(44) residue resides at the tip of a beta-hairpin comprising a sharp type I beta-turn and the two connecting beta-strands 4 and 5. A prominent V-shaped groove formed by a surface loop, L1, connecting beta 1- and beta 2-strands and the lipoyl lysine beta-hairpin constitutes the functional pocket. We further applied reduced spectral density functions formalism to extract dynamic information of hbLBD from (15)N-T(1), (15)N-T(2), and ((1)H-(15)N) nuclear Overhauser effect data obtained at 600 MHz. The results showed that residues surrounding the lipoyl lysine region comprising the L1 loop and the Lys(44) beta-turn are highly flexible, whereas beta-sheet S1 appears to display a slow conformational exchange process.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed2006

Antioxidant down-regulates interleukin-18 expression in asthma.

An alteration in the balance between a T-helper type 2 cell (Th2) response and a Th1 response may predispose to the development of bronchial asthma. Interleukin-18 (IL-18) has an ability to promote both Th1 and Th2 responses, depending on the surrounding cytokine environment. Reactive oxygen species (ROS) play a crucial role in the pathogenesis of airway inflammation and hyperresponsiveness. Recent studies have demonstrated that antioxidants are able to reduce airway inflammation and hyperreactivity in animal models of asthma. In this study, we used a C57BL/6 mouse model of allergic asthma to examine the effects of antioxidants on the regulation of IL-18 expression. Our present study with ovalbumin-induced murine model of asthma revealed that ROS production in cells from bronchoalveolar lavage fluids was increased and that administration of L-2-oxothiazolidine-4-carboxylic acid or alpha-lipoic acid reduced the increased levels of ROS, the increased expression of IL-18 protein and mRNA, airway inflammation, and bronchial hyperresponsiveness. Our results also showed that antioxidants down-regulated a transcription factor, nuclear factor-kappaB (NF-kappaB), activity. These results indicate that antioxidants may reduce IL-18 expression in asthma by inhibiting the activity of NF-kappaB and suggest that ROS regulate the IL-18 expression.

Animals↗
PubMed2003

Activation of JNK in sensory neurons protects against sensory neuron cell death in diabetes and on exposure to glucose/oxidative stress in vitro.

Diabetes activates all three groups of MAP kinases in sensory ganglia. Inhibition of this activation for the ERK and p38 groups prevents nerve damage, and agents that improve neuronal function in diabetic rats-antioxidants and aldose reductase inhibitors-also inhibit activation of ERK and p38 in dorsal root ganglia (DRG). However, these same treatments consistently increase activation of JNK. Thus, in DRG from rats with streptozotocin (STZ)-induced diabetes of 12-week duration, the p54/56 isoforms of JNK were activated by 2.75 compared to controls (P <.05). In DRG from diabetic rats treated with a gamma-linolenic acid and alpha-lipoic acid diester (GLA/LA), the activity of the p54/56 isoform was 3.75 that of controls and the p46 isoform was also increased to 1.75 that of controls (both P <.05 compared to both controls and untreated diabetics). We therefore tested the hypothesis that JNK activation is protective. Exposure of rats to diabetes increased activation of JNK in DRG, but treatment with GLA/LA increased this effect (P <.05). Specific inhibition of JNK in primary cultures of DRG neurons using a peptide inhibitor of JNK (JNKi1, 159-600-R100, 7.5 micro M, Alexis Biochemicals) increased the release of LDH and reduced MTT staining; both findings indicate an increase in neuronal damage. Taken together these findings indicate that multiple isoforms of JNK were activated in sensory neurons of diabetic rats, probably by a combination of raised glucose and oxidative stress, and that this activation of JNK serves to protect the neurons from damage.

Animals↗
PubMed2002

Oxidative stress in humans training in a cold, moderate altitude environment and their response to a phytochemical antioxidant supplement.

OBJECTIVE: This study examined the effectiveness of an antioxidant mixture containing vitamin E, beta-carotene, ascorbic acid, selenium, alpha-lipoic acid, N-acetyl 1-cysteine, catechin, lutein, and lycopene to reduce oxidative stress in US Marines undergoing 24 days of cold-weather field training at a moderate altitude. METHODS: Forty physically active male volunteers (ages 18-40) were randomly assigned to a treatment (antioxidant) group (n = 21) or a control (placebo) group (n = 19). Breath pentane (BP), serum lipid hydroperoxides (LPO), urine malondialdehyde (MDA), urine 8-hydroxy deoxyguanosine (8-OHdG), ferric-reducing ability of plasma (FRAP), and serum and urine oxygen radical absorption capacity (ORAC) were measured as indicators of oxidative stress and antioxidant status. Urine was sampled at days 0, 12, and 24. Serum and breath were sampled on days 0 and 24. RESULTS: Both groups exhibited increased levels of oxidative stress after 24 days of field training, as indicated by an increased LPO, pentane, and 8-OHdG. There was no significant difference between the treatment and placebo groups at day 24; however, there was some indication that test subjects with initially low antioxidant capacity (ORAC) may have benefited from the antioxidant supplement. CONCLUSIONS: An increased level of oxidative stress was associated with high levels of physical exertion of training in a cold environment at moderate altitude. The antioxidant mixture tested did not attenuate the mean oxidative stress levels in the entire group of test subjects, but it may have reduced the oxidative stress of some individuals with low initial antioxidant status.

Adaptation, Physiological↗
PubMedDate not supplied

[Effect of the B-group vitamin complex on the blood content of saturated and unsaturated fatty acids in patients with ischemic heart disease and hypertension].

Gas-liquid chromatography was used to study the blood content of saturated and unsaturated fatty acids, under the influence of the functionally-associated vitamin-B complex, in 45 patients with coronary heart disease and essential hypertension. The vitamins were given daily in the following doses: thiamine diphosphate 50 mg, riboflavine 40 mg, calcium pantothenate 200 mg, nicotinic acid 200 mg and lipoic acid 50 mg. Favourable shifts leading to positive clinical effects were recorded in the fatty acid metabolism after 10-day taking the vitamin-B complex: the content of unsaturated (linoleic and arachidonic) fatty acids increased while that of saturated (stearic and palmitic) fatty acids decreased.

Aged↗
PubMed1998

Future prevention and treatment of diabetic neuropathy.

This review orders the likely components of the pathogenesis of diabetic neuropathy into vertical (temporal) and horizontal dimensions. It is argued that the effects of hyperglycaemia are transduced to neuronal dysfunction via at least three secondary biochemical disturbances--the sorbitol (polyol) pathway, non-enzymatic glycation of proteins and oxidative stress--and that there are clear interactions between them. Because of these interactions, interference with one of these biochemical transducers could either worsen or attenuate the effects of the others. Examples of these alternatives are given. It is suggested that the prime goal for pharmacological intervention should be a combined attack on all three sources of disturbance. Interventions further on in the sequence of pathogenesis are also considered, and the arguments for the use of neurotrophic factors are persuasive because of their selectivity for different neuronal phenotypes, even though side-effects may be inevitable. Finally, a novel conjugate of gamma-linolenic acid and alpha-lipoic acid is considered as an agent with the potential to correct effects arising from more than one pathway of disorder in experimental diabetic neuropathy. The preliminary results with this agent have been encouraging.

Diabetic Neuropathies↗
PubMed1995

Pyruvate: ferredoxin oxidoreductase from the sulfate-reducing Archaeoglobus fulgidus: molecular composition, catalytic properties, and sequence alignments.

Archaeoglobus fulgidus is a hyperthermophilic sulfate-reducing archaeon. In this communication we describe the purification and properties of pyruvate: ferredoxin oxidoreductase from this organism. The catabolic enzyme was purified 250-fold to apparent homogeneity with a yield of 16%. The native enzyme had an apparent molecular mass of 120 kDa and was composed of four different subunits of apparent molecular masses of 45, 33, 25, and 13 kDa, indicating an alpha beta gamma delta structure. Per mol, the enzyme contained 0.8 mol thiamine pyrophosphate, 9 mol non-heme iron, and 8 mol acid-labile sulfur. FAD, FMN, lipoic acid, and copper were not found. The purified enzyme showed an apparent Km for coenzyme A of 0.02 mM, for pyruvate of 0.3 mM, and for clostridial ferredoxin of 0.01 mM, an apparent Vmax of 64 U/mg (at 65 degrees C) with a pH optimum near 7.5 and an Arrhenius activation energy of 75 kJ/mol (between 30 and 70 degrees C). The temperature optimum was above 90 degrees C. At 90 degrees C, the enzyme lost 50% activity within 60 min in the presence of 2 M KCl. The enzyme did not catalyze the oxidation of 2-oxoglutarate, indolepyruvate, phenylpyruvate, glyoxylate, and hydroxypyruvate. The N-terminal amino acid sequences of the four subunits were determined. The sequence of the alpha-subunit had similarities to the N-terminal amino acid sequence of the alpha-subunit of the heterotetrameric pyruvate: ferredoxin oxidoreductase from Pyrococcus furiosus and from Thermotoga maritima, and unexpectedly, to the N-terminal amino acid sequence of the homodimeric pyruvate:ferredoxin oxidoreductase from proteobacteria and from cyanobacteria. No sequence similarities were found, however, between the alpha-subunits of the enzyme from A. fulgidus and the heterodimeric pyruvate:ferredoxin oxidoreductase from Halobacterium halobium.

Amino Acid Sequence↗
PubMed2006

Protective role of eicosapentaenoate-lipoate (EPA-LA) derivative in combating oxidative hepatocellular injury in hypercholesterolemic atherogenesis.

The aim of the present study is to evaluate the effect of eicosapentaenoic acid (EPA), dl-alpha-lipoic acid (LA) and eicosapentaenoate-lipoate (EPA-LA) derivative on the atherogenic disturbances in hypercholesterolemic atherogenic animals. Eight groups of male Wistar rats were employed in this study, wherein four groups were fed with a high cholesterol diet (rat chow supplemented with 4% cholesterol and 1% cholic acid; HCD) for 30 days, among which, three groups of rats were also treated with either EPA (35 mg/kg body weight/day, oral gavage), LA (20 mg/kg body weight/day, oral gavage) or EPA-LA derivative (50 mg/kg body weight/day, oral gavage) commencing from 16th day of the experimental period. The remaining four groups served as control and EPA, LA and EPA-LA derivative treated drug controls. Abnormal increases in the levels of malondialdehyde, protein carbonyl and 8-hydroxy-2-deoxyguanosine, as well as depressed antioxidants status, were observed in hepatic tissue of HCD fed rats. HCD induced abnormal elevation in the activities of hepatic lactate dehydrogenase, aminotransferases and alkaline phosphatase (ALP) and was accompanied by increased hepatic cholesterol level and altered fatty changes in the histology of liver. These changes were restored partially in the EPA and LA administered groups. However, the combined derivative EPA-LA almost ameliorated the hypercholesterolemic-oxidative changes in the HCD fed rats. The results of this study present oxidative injury induced by hypercholesterolemic diet and administration of the combination treatment of EPA-LA afforded sound protection against lipemic-oxidative injury.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2005

Attenuation of serum lipid abnormalities and cardiac oxidative stress by eicosapentaenoate-lipoate (EPA-LA) derivative in experimental hypercholesterolemia.

BACKGROUND: Dietary cholesterol plays an important role in development of atherogenesis and cardiovascular disease. We explored the lipemic-oxidative injury in the hypercholesterolemic atherogenic animals. The effects of eicosapentaenoic acid (EPA), dl-alpha-lipoic acid (LA) and eicosapentaenoate-lipoate derivative (EPA-LA) were tested for their efficacy in controlling the atherogenic disturbances. METHODS: Four groups of male Wistar rats were fed with a high cholesterol diet (rat chow supplemented with 4% cholesterol and 1% cholic acid; HCD) for 30 days. Of these groups, 3 groups of rats were treated with either EPA (oral gavage, 35 mg/kg body weight/day), LA (oral gavage, 20 mg/kg body weight/day) or EPA-LA derivative (oral gavage, 50 mg/kg body weight/day) from 16th day to 30th day of the experimental period. RESULTS: HCD induced abnormal increase in lipid peroxidation and serum cholesterol, triglyceride, LDL and VLDL, and a decreased HDL concentration. Altered activity of cardiac and serum creatine kinase, accompanied by a depressed cardiac enzymatic and nonenzymatic antioxidants defense system were observed in HCD fed rats. These changes were partially restored in the EPA and LA treated groups, however, their combined derivative EPA-LA more effectively restored the altered parameters near to that of control (P<0.05). CONCLUSION: Lipid abnormalities and oxidative injury were induced by a hypercholesterolemic diet. Administration of the combination treatment of EPA-LA afforded protection against the lipemic-oxidative injury.

Animals↗
PubMed2006

Oxidative renal injury and lipoprotein oxidation in hypercholesterolemic atherogenesis: Role of eicosapentaenoate-lipoate (EPA-LA) derivative.

Hypercholesterolemia, an independent risk factor for increased oxidative renal injury, is associated with the formation of oxidized low-density lipoprotein. Production of reactive oxygen species and nitrogen species have been implicated in diet-induced hypercholesterolemia, principally as means of oxidising low-density lipoproteins. This in turn initiates the accumulation of cholesterol in macrophages, which sets key event in the initiation of atherosclerosis. The aim of the present work is to evaluate the effects of eicosapentaenoic acid (EPA), DL alpha-lipoic acid (LA) and eicosapentaenoate-lipoate derivative (EPA-LA) in controlling the atherogenic disturbances. Four groups of male Wistar rats were fed with a high cholesterol diet (rat chow supplemented with 4% cholesterol and 1% cholic acid; HCD) for 30 days. Among them, 3 groups of rats were treated with either EPA (35 mg/kg body weight/day, oral gavage), LA (20 mg/kg body weight/day, oral gavage) or EPA-LA derivative (50 mg/kg body weight/day, oral gavage) from 16th day to 30th day of the experimental period. Abnormal increase in the levels of reactive oxygen species, 3-nitrotyrosine, malondialdehyde and protein carbonyl as well as an elevation in the activities of xanthine oxidase, lactate dehydrogenase, alkaline phosphatase and acid phosphatase was observed in renal tissue of HCD fed rats. HCD fed rats also showed an increased susceptibility of the apo B-containing lipoproteins to in vitro oxidation. These changes were restored partially in the EPA and LA administered groups. However, the combined derivative EPA-LA almost ameliorated the hypercholesterolemic-oxidative changes in the HCD fed rats.

Animals↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMedDate not supplied

Functional characterization of sodium-dependent multivitamin transporter in MDCK-MDR1 cells and its utilization as a target for drug delivery.

The objective of this research is to characterize a sodium-dependent multivitamin transporter (SMVT) in MDCK-MDR1 cells (Madin-Darby canine kidney cells transfected with the human MDR1 gene) and to investigate the feasibility of utilizing the MDCK-MDR1 cell line as an in vitro model to study the permeability of biotin-conjugated prodrugs of anti-HIV protease inhibitors. Mechanism of [3H]biotin uptake and transport was delineated. Transepithelial permeability of the biotin-conjugated prodrug, i.e., biotin-saquinavir, was also studied. Reverse transcription polymerase chain reaction (RT-PCR) was carried out to confirm the existence of SMVT in MDCK-MDR1 cells. Biotin uptake was Na+, pH, and temperature dependent, but energy independent. Uptake of biotin was found to be saturable with a Km of 13.0 microM, Vmax 21.5 of pmol min-1 (mg of protein)-1, and Kd of 0.12 microL min-1 (mg of protein)-1. Both apical and basal uptake and transepithelial transport of [3H]biotin showed that SMVT localized predominantly on the apical membrane of MDCK-MDR1 cells. [3H]Biotin uptake was inhibited by excess unlabeled biotin and its structural analogues, i.e., desthiolbiotin and valeric acid, and other vitamins such as lipoic acid and pantothenic acid, but not by acetic acid, benzoic acid, biotin methyl ester, and biocytin. Biotin-saquinavir caused lowering of [3H]biotin uptake, which indicates that it is recognized by SMVT. Apical to basal transport of [3H]biotin was also significantly inhibited in the presence of excess biotin or biotin-saquinavir. Transepithelial transport studies of biotin-saquinavir in MDCK-MDR1, wild type MDCK, and Caco-2 cells revealed that permeability of biotin-saquinavir was similar in all three cell lines. A band of SMVT mRNA at 862 bp was identified by RT-PCR. A sodium-dependent multivitamin transporter, SMVT, responsible for biotin uptake and transport, was identified and functionally characterized in MDCK-MDR1 cells. Therefore, the MDCK-MDR1 cell line may be utilized as an in vitro model to study the permeability of biotin-conjugated prodrugs such as HIV protease inhibitors.

Animals↗
PubMed1997

Antioxidants and cataract: (cataract induction in space environment and application to terrestrial aging cataract).

The effect of several antioxidants and cysteine-elevating precursor drugs (prodrugs) was tested on lens damage occurring after in vitro exposure to low levels of 60Co-gamma-irradiation, to simulate in vitro the exposure to radiation in vivo of (1) astronauts (2) jet crews (3) military radiation accident personnel. Tocopherol (100 microM), ascorbic acid (1 mM), R-alpha-lipoic acid (1 mM), and taurine (0.5 mM) protected against radiation-associated protein leakage. MTCA and ribocysteine protected lenses against opacification, LDH and protein leakage, indicating that antioxidants and prodrugs of cysteine appear to offer protection against lens damage caused by low level radiation.

Animals↗
PubMed1996

Catalytic properties, molecular composition and sequence alignments of pyruvate: ferredoxin oxidoreductase from the methanogenic archaeon Methanosarcina barkeri (strain Fusaro).

Methanosarcina barkeri (strain Fusaro) was grown on pyruvate as methanogenic substrate [Bock, A. K., Prieger-Kraft, A. & Schönheit, P. (1994) Arch. Microbiol. 161, 33-46]. The first enzyme of pyruvate catabolism, pyruvate oxidoreductase, which catalyzes oxidation of pyruvate to acetyl-CoA was purified about 90-fold to apparent electrophoretic homogeneity. The purified enzyme catalyzed the CoA-dependent oxidation of pyruvate with ferredoxin as an electron acceptor which defines the enzyme as a pyruvate: ferredoxin oxidoreductase. The deazaflavin, coenzyme F420, which has been proposed to be the physiological electron acceptor of pyruvate oxidoreductase in methanogens, was not reduced by the purified enzyme. In addition to ferredoxin and viologen dyes, flavin nucleotides served as electron acceptors. Pyruvate: ferredoxin oxidoreductase also catalyzed the oxidation of 2-oxobutyrate but not the oxidation of 2-oxoglutarate, indolepyruvate, phenylpyruvate, glyoxylate, 3-hydroxypyruvate and oxaloacetate. The apparent Km values of pyruvate:ferredoxin oxidoreductase were 70 microM for pyruvate, 6 microM for CoA and 30 microM for clostridial ferredoxin. The apparent Vmax with ferredoxin was about 30 U/mg (at 37 degrees C) with a pH optimum of approximately 7. The temperature optimum was approximately 60 degrees C and the Arrhenius activation energy was 40 kJ/mol (between 30 degrees C and 60 degrees C). The enzyme was extremely oxygen sensitive, losing 90% of its activity upon exposure to air for 1 h at 0 degrees C. Sodium nitrite inhibited the enzyme with a Ki of about 10 mM. The native enzyme had an apparent molecular mass of approximately 130 kDa and was composed of four different subunits with apparent molecular masses of 48, 30, 25, and 15 kDa which indicates that the enzyme has an alpha beta gamma delta structure. The enzyme contained 1 mol/mol thiamine diphosphate, and about 12 mol/mol each of non-heme iron and acid-labile sulfur. FAD, FMN and lipoic acid were not found. The N-terminal amino acid sequences of the four subunits were determined. The sequence of the alpha-subunit was similar to the N-terminal amino acid sequence of the alpha-subunit of the heterotetrameric pyruvate:ferredoxin oxidoreductases of the hyperthermophiles Archaeoglobus fulgidus, Pyrococcus furiosus and Thermotoga maritima and of the mesophile Helicobacter pylori, and to the N-terminal amino acid sequence of the homodimeric pyruvate:ferredoxin oxidoreductase from proteobacteria and from cyanobacteria. No sequence similarities were found, however, between the alpha-subunit of the M. barkeri enzyme and the heterodimeric pyruvate:ferredoxin oxidoreductase of the archaeon Halobacterium halobium.

Amino Acid Sequence↗
PubMed1992

Methylation of FrzCD, a methyl-accepting taxis protein of Myxococcus xanthus, is correlated with factors affecting cell behavior.

Myxococcus xanthus, a nonflagellated gliding bacterium, exhibits multicellular behavior during vegetative growth and fruiting body formation. The frizzy (frz) genes are required to control directed motility for these interactions. The frz genes encode proteins that are homologous to all of the major enteric chemotaxis proteins, with the exception of CheZ. In this study, we characterized FrzCD, a protein which is homologous to the methyl-accepting chemotaxis proteins from the enteric bacteria. FrzCD, unlike the other methyl-accepting chemotaxis proteins, was found to be localized primarily in the cytoplasmic fraction of cells. FrzCD migrates as a ladder of bands on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, reflecting heterogeneity due to methylation or demethylation and to deamidation. FrzCD was shown to be methylated in vivo when cells were exposed to yeast extract or Casitone and demethylated when starved in buffer. We used the methylation state of FrzCD as revealed by Western blot (immunoblot) analyses to search for stimuli that are recognized by the frz signal transduction system. Common amino acids, nucleotides, vitamins, and sugars were not recognized, but certain lipids and alcohols were recognized. For example, the saturated fatty acids capric acid and lauric acid stimulated FrzCD methylation, whereas a variety of other saturated fatty acids did not. Lauryl alcohol and lipoic acid also stimulated methylation, as did phospholipids containing lauric acid. In contrast, several short-chain alcohols, such as isoamyl alcohol, and some other solvents caused demethylation. The relatively high concentrations of the chemicals required for a response may indicate that these chemicals are not the relevant signals recognized by M. xanthus in nature. Isoamyl alcohol and isopropanol also had profound effects on the behavior of wild-type cells, causing them to reverse continuously. Cells of frzB, frzF, and frzG mutants also reversed continuously in the presence of isoamyl alcohol, whereas cells of frzA, frzCD, or frzE mutants did not. On the basis of the data presented, we propose a model for the frz signal transduction pathway in M. xanthus.

Bacterial Proteins↗