ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2253842

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

Fc receptors (FcR) are immunoglobulin‐binding molecules that enable antibodies to perform several biological functions by forming a link between specific antigen recognition and effector cells. FcRs are involved in regulating antibody production as well. Most FcRs belong to the immunoglobulin superfamily, and show structural homology with each other and with their ligands. Recent data on the structure of IgG binding FcRs obtained from monoclonal antibodies and gene cloning studies, as well as on ligand binding capacity and fine specificity of the receptor binding site (or sites), are reviewed. The binding capacity and fine specificity of receptor binding sites, as well as the structure and conformation of the immunoglobulin ligands, play important roles in triggering FcR‐mediated signals. In induction of signals, the interaction of the FcR with the CH2 domain of the IgGFc is decisive. The high‐affinity FcγRI possess one active binding site specific for contact residues that is located at the N‐proximal end of the CH2 domain and is able to mediate both binding and signal transfer. The low‐affinity FCγRIII has two active binding sites: the CH3 domain‐specific site, which mediates only binding; and the CH2 domain‐specific site, which is responsible for binding and signaling. Similarly, the low‐affinity FCγRII on resting B cells has one site for CH2 and another for CH3 binding. The expression, release, and fine specificity of FCγRII on B cells correlates with the cell cycle.—Gergely, J.; Sarmay, G. The two binding‐site models of human IgG binding Fcγ receptors.FASEB J.4: 3275–3283; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2253843

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

A combination of biochemical, structural, and morphological analyses during the last 2 decades has shown that the cytoplasm of a cell is not a disorganized mass of jelly but a highly structured cell compartment formed of a cytoskeleton, one of which principal components are the microtubules. More recently, studies have revealed that microtubule cytoskeleton is not only well organized but highly dynamic, and that microtubule dynamics may be responsible for several cell functions such as chromosome segregation, cell morphogenesis, or intracytoplasmic organization.—Avila, J. Microtubule dynamics.FASEB J.4: 3284–3290; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2253844

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

Ca2+influx into the nerve terminal is normally the trigger for the release of neurotransmitters. Many neurons possess presynaptic receptors whose activation results in changes in the quantity of neurotransmitter released by an action potential. This paper reviews studies that show that presynaptic receptors can regulate the activity of Ca2+channels in the nerve terminal, resulting in changes in the influx of Ca2+and in neurotransmitter release. Neurons possess several different types of voltage‐sensitive Ca2+channels. Ca2+influx through N‐type channels appears to trigger transmitter release in many instances. In other cases Ca2+influx through L channels can influence transmitter release. Neurotransmitters can inhibit N channels through a G protein‐mediated transduction mechanism. The G proteins are frequently pertussis toxin substrates. Inhibition of N channels appears to involve changes in their voltage dependence. Neurotransmitters can also regulate neuronal K+channels. Activation of these K+channels can lead to a reduction in Ca2+influx and neurotransmitter release; these effects are also mediated by G proteins. Thus neurotransmitters may often regulate both presynaptic Ca2+and K+channels. These two effects may be synergistic mechanisms for the regulation of Ca2+influx and neurotransmitter release.— Miller, R. J. Receptor‐mediated regulation of calcium channels and neurotransmitter release.FASEB J.4: 3291–3299; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.1979294

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

In recent years, numerous techniques have been developed to study renal microcirculation. These technical advances have provided new insight regarding the specificity of action of vasoconstrictor peptides (angiotensin II, arginine vasopressin, endothelin) and vasodilator peptides (bradykinin, atrial natriuretic peptide) at discrete sites within the renal vascular bed. Differential signal transduction mechanisms, particularly those related to calcium regulation, appear to mediate the renal vascular actions of these compounds, both in a segment‐specific and agonist‐specific manner. These observations substantiate the concept that regulation of intrarenal and intraglomerular dynamics is accomplished by selective changes in pre‐ and postglomerular resistance induced by different endogenous peptides. This microvascular selectivity allows precise regulation of glomerular and peritubular capillary function, and ultimately exerts great influence on the volume and composition of the final urine.—Carmines, P. K.; Fleming, J. T. Control of the renal microvasculature by vasoactive peptides.FASEB J.4: 3300–3309; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2147667

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

In adult individuals body weight is maintained at a relatively stable level for long periods. The set‐point theory suggests that body weight is regulated at a predetermined, or preferred, level by a feedback control mechanism. Information from the periphery is carried by an affector to a central controller located in the hypothalamus. The controller integrates and transduces the information into an effector signal that modulates food intake or energy expenditure to correct any deviations in body weight from set‐point. Evidence for involvement of various factors and physiological systems in the control of food intake and regulation of body weight and fat are reviewed within the context of a control model. Current working hypotheses include roles for nutrients, dietary composition and organoleptic properties, hormones, neural pathways, various brain nuclei, and many neurotransmitters in the regulation of food intake. It is concluded that regulation of body weight in relation to one specific parameter related to energy balance is unrealistic. It seems appropriate to assume that the level at which body weight and body fat content are maintained represents the equilibria achieved by regulation of many parameters.— Harris, R. B. S. Role of set‐point theory in regulation of body weight.FASEB J.4: 3310–3318; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2253845

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

Isoprenylation is a posttranslational modification that involves the formation of thioether bonds between cysteine and isoprenyl groups derived from pyrophosphate intermediates of the cholesterol biosynthetic pathway. Numerous isoprenylated proteins have been detected in mammalian cells. Those identified include K‐, N‐, and H‐p21ras,ras‐related GTP‐binding proteins such as G25K (Gp), nuclear lamin B and prelamin A, and the γ subunits of heterotrimeric G proteins. The modified cysteine is located in the fourth position from the carboxyl terminus in every protein where this has been studied. For p21ras, the last three amino acids are subsequently removed and the exposed cysteine is carboxylmethylated. Similar processing events may occur in lamin B and G protein 7 subunits, but the proteolytic cleavage in prelamin A occurs upstream from the modified cysteine. Lamin B and p21rasare modified by C15farnesyl groups, whereas other proteins such as the G protein 7 subunits are modified by C20geranylgeranyl chains. Separate enzymes may catalyze these modifications. The structural features that govern the ability of particular proteins to serve as substrates for isoprenylation by C15or C20groups are not completely defined, but studies of the p21rasmodification using purified farnesyl:protein transferase suggest that the sequence of the carboxyl‐terminal tetrapeptide is important. Isoprenylation plays a critical role in promoting the association of p21rasand the lamins with the cell membrane and nuclear envelope, respectively. Future studies of the role of isoprenylation in the localization and function ofras‐related GTP‐binding proteins and signal‐transducing G proteins should provide valuable new insight into the link between isoprenoid biosynthesis and cell growth.—Maltese, W. A. Posttranslational modification of proteins by isoprenoids in mammalian cells.FASEB J.4: 3319–3328; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2123808

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

Thioether methyltransferase was previously shown to catalyze the S‐adenosylmethionine‐dependent methylation of dimethyl selenide, dimethyl telluride, and various thioethers to produce the corresponding methyl onium ions. In this paper we show that the following thioethers are also substrates for this enzyme in vitro: 2‐hydroxyethyl ethyl sulfide, 2‐chloroethyl ethyl sulfide, thiodiglycol,t‐butyl sulfide, and isopropyl sulfide. To demonstrate thioether methylation in vivo, mice were injected with [methyl‐3H]methionine plus different thioethers, and extracts of lungs, livers, kidneys, and urine were analyzed by high‐performance liquid chromatography for the presence of [3H]methyl sulfonium ions. The following thioethers were tested, and all were found to be methylated in vivo: dimethyl sulfide, diethyl sulfide, methyl n‐propyl sulfide, tetrahydrothiophene, 2‐(methylthio)ethylamine, 2‐hydroxyethyl ethyl sulfide, and 2‐chloroethyl ethyl sulfide. This supports our hypothesis that the physiological role of thioether methyltransferase is to methylate seleno‐, telluro‐, and thioethers to more water‐soluble onium ions suitable for urinary excretion. Conversion of the mustard gas analog, 2‐chloroethyl ethyl sulfide, to the methyl sulfonium derivative represents a newly discovered mechanism for biochemical detoxification of sulfur mustards, as this conversion blocks formation of the reactive episulfonium ion that is the ultimate alkylating agent for this class of compounds.— Mozier, N. M.; Hoffman, J. L. Biosynthesis and urinary excretion of methyl sulfonium derivatives of the sulfur mustard analog, 2‐chloroethyl ethyl sulfide, and other thioethers.FASEB J.4: 3329–3333; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2253846

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

Mongolian gerbils,Meriones unguiculatus, when treated at intervals of 2–6 days with prednisolone tertiary butyl acetate, sustained infection with adultEchinococcus multilocularisin the small intestine, with the tapeworm exhibiting normal strobilation andeggproduction as in the natural canid host. Host age is critical for the survival of the tapeworm in normal gerbils; parasites survive for only 2 days in 20‐wk‐old animals, 4 days in 4‐wk‐old animals, but at least 7 days in 3‐wk‐old animals. The host age dependence in parasite recovery between days 28–37 postinfection was not affected by treatment from around the day of infection. Starting the treatment before infection (on day ‐17 relative to infection) remarkably improved the tapeworm's survival within the intestine of older animals. Eggs produced in this rodent model system 28 days postinfection were infective to rodents such as Mongolian gerbils and gray red‐backed voles,Clethrionomys rufocanus bedfordiae, by oral or intraperitoneal inoculation. TheE. multilocularis/Mongolian gerbil system can replace the natural canid hosts as a new way to obtain infective eggs and to analyze host‐parasite interactions. The development of an alternative definitive host for zoonotic tapeworms may accelerate experimentation in this field.—Kamiya, M.; Sato, H. Complete life cycle of the canid tapeworm,Echinococcus multilocularis, in laboratory rodents.FASEB J.4: 3334–3339; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2253847

出版商:Wiley    

年代:1990

数据来源: WILEY

摘要:

When BHK or HTC cells are cultured for 20 min with [U‐14C]glucose in the presence of agents that deplete reduced glutathione, DNA banded from the cells in cesium salt gradients containing guanidium HCl is radioactively labeled. This depletion‐dependent labeling required live cells. It was not caused by reactive contaminants in the radioactive glucose preparations, by carbohydrate or protein comigration into the DNA band, or by metabolism of glucose into deoxyribose. Labeling levels are similar whether depletion is achieved by oxidation (with the drug diamide) or by inhibition of synthesis (with methionine sulfoximine). A temporal association between GSH repletion and the appearance of D‐lactate, the putative unique product of GSH‐dependent glyoxylase action on pyruvaldehyde, suggests possible involvement of 3‐carbon dicarbonyls.—Shires, T. K., Tresnak, J., Kaminsky, M., Herzog, S. L.,andTruc‐Pham, B. DNA modification in vivo by derivatives of glucose: enhancement by glutathione depletion.FASEB J.4: 3340–3346; 1990.

ISSN:0892-6638    

DOI:10.1096/fasebj.4.15.2253848

出版商:Wiley    

年代:1990

数据来源: WILEY