ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958612

出版商:Wiley    

年代:1994

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958613

出版商:Wiley    

年代:1994

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/j.1530-6860.1994.tb93366.x

出版商:Wiley    

年代:1994

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958614

出版商:Wiley    

年代:1994

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958615

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

A few years after the identification of cyclin B‐cdc2 kinase as the universal factor that controls onset of M‐phase in eukaryotic cells, MPF (M‐phase promoting factor), it became evident that all transitions of the cell cycle are controlled through phosphorylation of specific targets due to changes in the activity of a variety of cyclin‐dependent kinases (cdks). These transitions include conversion of quiescent cells to a state of active proliferation, commitment to DNA replication, initiation of DNA replication, and entry into and exit from mitosis. Changes in the activity of cdks along the cell cycle depend not only on their association with a variety of cycling (including G1/S and G2/M cyclins) and on posttranslational modifications by phosphorylation‐dephosphorylation reactions, but also on specific protein inhibitors and on protein degradation.—Dorée, M., Galas, S. The cyclin‐dependent protein kinases and the control of cell division.FASEB J.8, 1114‐1121 (1994)

ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958616

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Transplantation of solid organs (heart, lung, liver, and kidney) from swine to humans would solve the current critical shortage of cadaver organs needed by patients with end‐stage disease of these organs. In addition, transplantation between distant species (discordant xenografting) will require an understanding of a number of unique immunologic features. Discordant xenografts are rejected within minutes to hours after transplantation. This rejection is due to natural immunity by recipients never before exposed to the xenografts. In some species combinations, this fulminant rejection is due to naturally occurring pre‐existing antibodies against the xenograft endothelium. In other species combinations, the xenograft activates the alternative pathway of complement. The swine to human species combination is the most clinically relevant. In this combination, natural human and private antibodies recognize alpha‐galactosyl residues of glycoproteins and glycolipids. Potential future therapeutic measures to prevent natural immunity include the genetic engineering of human complement inhibitors into swine cell membranes or genetic “knock out” of the enzymes responsible for placing alpha‐galactosyl residues on swine cell surfaces. There are also special considerations in acquired immunity against xenografts. Cytokines and adhesion molecules may not work across species lines. Xenograft antigens may have to be processed by host antigen‐presenting cells in order to effectively stimulate the immune system.—Lu, C. Y., Khair‐El‐Din, T., Dawidson, I. A., Butler, T. M., Brasky, K. M., Vazquez, M. A., Sicher, S. C. Xenotransplantation.FASEB J.8, 1122‐1130 (1994)

ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958617

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Even a moderate increase in the cellular cysteine supply elevates the intracellular glutathione (GSH) and glutathione disulfide (GSSG) levels and potentiates immunological functions of lymphocytes in vitro. At low GSSG levels, T cells cannot optimally activate the immunologically important transcription factor NFxB, whereas high GSSG levels inhibit the DNA binding activity of NFxB. The effects of GSSG are antagonized by reduced thioredoxin (TRX). As the protein tyrosine kinase activities p56lckand p59fynare activated in intact cells by hydrogen peroxide, they are likely targets for GSSG action. These redox‐regulated enzymes trigger signal cascades for NFxB activation and transduce signals from the T cell antigen receptor, from CD4 and CD8 molecules, and from the IL‐2 receptor β‐chain. The effector phase of cytotoxic T cell responses and IL‐2‐dependent functions are inhibited even by a partial depletion of the intracellular GSH pool. As signal transduction is facilitated by prooxidant conditions, we propose that the well‐known immunological consequences of GSH depletion ultimately may be results of the accompanying GSSG deficiency. As HIV‐infected patients and SIV‐infected rhesus macaques have, on the average, significantly decreased plasma cyst(e)ine and intracellular GSH levels, we also hypothesize that AIDS may be the consequence of a GSSG deficiency as well.—Dröge, W., Schulze‐Osthoff, K., Mihm, S., Galter, D., Schenk, H., Eck, H.‐P., Roth, S., Gmünder, H. Functions of glutathione and glutathione disulfide in immunology and immunopathology.FASEB J.8, 1131‐1138 (1994)

ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958618

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Memory processes and long‐term potentiation (LTP) are blocked at the time of their initiation by antagonists of glutamate NMDA or metabotropic receptors, by drugs that hinder the activity of carbon monoxide or the platelet‐activating factor, and by GABA type A receptor agonists. In the next 2 h, memory and LTP are accompanied by an enhancement of the activity of calcium/calmodulin‐dependent protein kinase II and of protein kinase C, and are blocked by inhibitors of these enzymes. At the time of expression, memory and LTP are blocked by antagonists of glutamate AMPA receptors. The effects of drugs on memory are seen upon their infusion into areas of the brain known to be responsible for the storage and retrieval of declarative memories (hippocampus, amygdala, medial septum, entorhinal cortex) and are both task‐ and structure‐specific. When put together with other pharmacologic findings, with lesion and recording studies, and with data on transgenic animals showing deficits of both memory and LTP, the data reviewed here lend strong support to the hypothesis that LTP in these brain areas underlies memory processes.—Izquierdo, I. Pharmacological evidence for a role of long‐term potentiation in memory.FASEB J.8, 1139‐1145 (1994)

ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958619

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Alcoholic myopathy is characterized by selective atrophy of type II fibers and affected subjects lose up to 20% of the entire musculature. Between one‐ and two‐thirds of all alcohol abusers are affected. In acute studies, defective rates of translation occur and type II fiber‐predominant muscles are more adversely affected than type I fiber‐predominant muscles. Furthermore, acetaldehyde is also a potent modulator of translation, and contractile and noncontractile proteins are affected equally. In chronic ethanol feeding there is rapid and sustained loss of ribosomal RNA. Recent attention has focused on the observation that total messenger RNA (mRNA) falls after ethanol consumption, but mRNA for specific myofibrillary contractile proteins are unaffected, implicating a role for translational modifications in the initial stages of the myopathy. Clinical studies have also shown that chronic alcohol abusers have defective rates of muscle protein synthesis and whole‐body protein metabolism. The modulations in transcription and translation are not mediated by availability of amino acids, the effects of endocrine dysfunction (cortisol and growth hormone), liver impairment, or malnutrition. Free radicals, however, may be contributory mediators. Receptor‐mediated events and the putative roles of growth factors are generally unexplored, though a distinguishing feature of acute ethanol administration is a reduction in circulating IGF‐I. Thus, ethanol may act directly on muscle, although other concordant processes may coexist.—Preedy, V. R., Peters, T. J., Patel, V. B., Miell, J. P. Chronic alcoholic myopathy: transcription and translation alterations.FASEB J.8, 1146‐1151 (1994)

ISSN:0892-6638    

DOI:10.1096/fasebj.8.14.7958620

出版商:Wiley    

年代:1994

数据来源: WILEY