ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.8181663

出版商:Wiley    

年代:1994

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.8181664

出版商:Wiley    

年代:1994

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/j.1530-6860.1994.tb93359.x

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

The AP‐1 transcription factor family consists of two groups of proteins, fos‐related antigens (fra) and jun proteins. These transcription factors are usually expressed at low basal levels but they can be dramatically induced in a variety of cell types by many different stimuli, in which the quantity of AP‐1 transcription factor and the DNA binding activity also rise. The quantity and DNA binding activity of transcription factors are not always at low levels. For example, early in brain development a high basal expression of AP‐1 DNA binding activity exists. Similarly, adult rat adrenal gland contains high levels of AP‐1 DNA binding activity whose regulation appears to be through post‐translational modification (i.e., phosphorylation). Thus, AP‐1 DNA binding activity is modulated in a developmental and tissue‐specific manner.—Pennypacker, K. R., Hong, J.‐S., McMillian, M. K. Pharmacological regulation of AP‐1 transcription factor DNA binding activity.FASEB J.8: 475‐478; 1994.

ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.8181665

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Theviable yellow Avymutation results in a mottled yellow mouse that is obese, slightly larger than its nonyellow sibs, and more susceptible to tumor formation in those tissues sensitized by the strain genome. The mutation exhibits variable expressivity resulting in a continuum of coat color phenotypes, from clear yellow to pseudoagouti. The mouseagoutiprotein is a paracrine signaling molecule that induces hair follicle melanocytes to switch from the synthesis of black pigment to yellow pigment. Molecular cloning studies indicate that the obesity and growth effects of theAvymutation result from ectopic expression of the normalagoutigene product. This review seeks to summarize the current state of knowledge regarding the obesity, stimulation of somatic growth, and enhancement of tumor formation caused by theAvymutation, and to interpret these pleiotropic effects in terms of the normal function of theagoutiprotein.—Yen, T. T., Gill, A. M., Frigeri, L. G., Barsh, G. S., and Wolff, G. L. Obesity, diabetes, and neoplasia in yellow Avy/‐ mice: ectopic expression of theagoutigene.FASEB J.8: 479‐488; 1994.

ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.8181666

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Many studies have used the intracerebral transplantation technique to study the neostriatum. Most of this work has been conducted in two well‐characterized animal models of striatal dysfunction: the rat model of Huntington's disease (striatal damage) and the rat model of Parkinson's disease (damage of dopaminergic nigrostriatal afferents). In animals with striatal damage, fetal striatal tissue implanted into the neostriatum (homotypic transplants) displays a remarkable anatomical and functional incorporation into the host brain. These homotypic grafts also induce a wide range of behavioral improvements in experimental animals. In contrast, fetal substantia nigra neurons implanted into the dopamine‐depleted neostriatum (heterotypic transplants) generally show a more restricted integration into the host brain and elicit fewer behavioral improvements. Nonetheless, the ability of grafted fetal neurons to survive, differentiate, and partially reconstruct an appropriate and functional neurocircuitry with host systems indicates that there are factors within the adult brain that promote neuronal development and regeneration. Such results have encouraged the clinical use of intracerebral grafts for the treatment of Parkinson's disease. Recent studies have emphasized the use of genetically modified cells and neural cell lines as alternative populations to study and repair the central nervous system.—Fisher, L. J., Gage, F. H. Intracerebral transplantation: basic and clinical applications to the neostriatum.FASEB J.8: 489‐496; 1994.

ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.8181667

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

The human immunodeficiency virus type 1 (HIV‐1) is the etiologic agent of AIDS. Replication of this virus requires the activity of a retrovirus encoded RNA‐dependent DNA polymerase, or reverse transcriptase (RT). HIV‐1 RT is required for the synthesis of the double‐stranded proviral DNA from the single‐stranded retroviral RNA genome. HIV‐1 RT has two subunits of 66 kDa and 51 kDa. The 66‐kDa subunit contains the DNA polymerase and RNase H domains whereas the 51‐kDa subunit, obtained by proteolytic maturation of the former subunit, has only the DNA synthetic activity. Two recently reported crystal structures of HIV‐1 RT have revealed the very asymmetric structure of this molecule. In addition to providing information concerning the mechanism of nucleic acid polymerization, biochemical and biophysical studies of this enzyme are providing key insights for the design of selective antiviral agents. The multiple activities displayed by reverse transcriptase in the replication of the retroviral genome ensure that this enzyme will remain at the forefront of antiviral strategies in the fight against AIDS and other retrovirus‐related pathologies.—Tarrago‐Litvak, L., Andréola, M.‐L., Nevinsky, G. A., Sarih‐Cottin, L., and Litvak, S. The reverse transcriptase of the human immunodeficiency virus type 1: from enzymology to therapeutic intervention.FASEB J.8: 497‐503; 1994.

ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.7514143

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

Neutrophil‐endothelial cell interactions are mediated by interacting sets of cell adhesion molecules (CAMs) and chemoattractant/activator molecules to form an “adhesion cascade.” The initial phase of inflammation, a transient slowing of neutrophils in postcapillary venules, is mediated by selectins. Subsequently, firm adhesion of neutrophils to the vessel wall occurs via interaction of the CD11/GD18 (β2) integrins to endothelial ligands such as intercellular adhesion molecule‐1 (ICAM‐1). This binding requires activation of CD11/GD18 by exposure of the neutrophil to a variety of activating/chemoattractant molecules, such as platelet‐activating factor or interleukin‐8. Finally, transmigration into tissues occurs, a process that requires both a chemotactic stimulus and engagement of platelet‐endothelial cell adhesion molecule‐1 (PECAM‐1). Several approaches have been used to probe the role of CAMs in vivo. These include the use of blocking antibodies, chimeric selectin‐immunoglobulin proteins, sialyl Lewisxoligosaccharides and peptides, along with the study of humans and animals with genetically determined adhesion deficiencies. These studies demonstrate that CAM blockade can effectively inhibit inflammation; however, there appear to be clear differences in the adhesion requirements for particular types of inflammation. By understanding the CAM/chemoattractant profiles involved in specific disease states, it may be possible to precisely and effectively target therapy to a wide variety of inflammatory diseases.—Albelda, S. M., Smith, C. W., Ward, P. A. Adhesion molecules and inflammatory injury.FASEB J.8: 504‐512; 1994.

ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.8181668

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

As used today, the word quinoprotein defines three distinct groups of enzymes. Before 1979, the structures of the essential, quinonoid oxidation‐reduction cofactors were a mystery for all these enzymes. The first proteins proven to harbor this type prosthetic group are those with noncovalently bound pyrroloquinoline quinone (PQQ). PQQ‐containing enzymes can be described as alcohol dehydrogenases, with the exception of a single protein, which is an amine dehydrogenase. More recently, it was discovered that copper‐containing amine oxidases contain 6‐hydroxydopa quinone, also known as topa quinone (TQ), whereas certain bacterial amine dehydrogenases require 2',4‐bitryptophan‐6,7‐dione (tryptophan tryptophylquinone, TTQ) for activity. These latter two quinones are formed, by unknown processes, from a specific tyrosyl residue for the amine oxidases, and from two widely separate tryptophyl residues in the polypeptide of the amine dehydrogenases.—McIntire, W. S. Quinoproteins.FASEB J.8: 513‐521; 1994.

ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.8181669

出版商:Wiley    

年代:1994

数据来源: WILEY

摘要:

The apical membrane of many tight epithelia contains Na+channels that are primarily characterized by their high affinity to the diuretic blocker amiloride. These channels mediate the first step of active Na+reabsorption essential for the maintenance of body salt and water homeostasis. They are regulated by mineralocorticoids, antidiuretic peptides, atrial natriuretic peptides, and other factors. The molecular events that mediate the hormonal actions are poorly understood. In addition, patch clamp studies have established that amiloride‐sensitive channels in different epithelia may differ in their regulatory mechanisms and biophysical properties. Several groups have reported the biochemical purification and/or molecular cloning of putative channel components. Of particular importance is the recent cloning of three cDNAs, whose coexpression inXenopusoocytes evokes a large amiloride‐blockable Na+specific conductance (Canesa et al. (1994)Nature (London), 367, 463‐467. This review summarizes existing data on properties, regulatory mechanisms, and diversity of amiloride‐blockable channels, describes the different putative channel components identified, and examines possible relationships among them.—Garty, H. Molecular properties of epithelial, amiloride‐blockable Na+channels.FASEB J.8: 0522‐0528; 1994.

ISSN:0892-6638    

DOI:10.1096/fasebj.8.8.8181670

出版商:Wiley    

年代:1994

数据来源: WILEY