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1. |
A monoclonal antibody recognizes an epitope common to an avian‐specific nuclear antigen and to cytokeratins |
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Journal of Cellular Biochemistry,
Volume 24,
Issue 1,
1984,
Page 1-14
Richard M. Franklin,
Lyman R. Emmons,
Rebecca P. Emmons,
Osamu Kai,
Anna Oommen,
J. Richard Pink,
Anne‐Marie Rijnbeek,
Marianne Schnetzler,
Leena Tuderman,
Eeva Vainio,
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摘要:
AbstractX3, a monoclonal antibody of unusual specificity, is described. This antibody reacts with one or more cytokeratin polypeptides and also reacts with an avian (chicken, quail) nuclear antigen that appears to be present in all cell types (chicken) tested, although with variable staining pattern and intensity. This antigen is distinct from the cytokeratins but does have an epitope in common with this class of proteins. It disappears from the nucleus during the early stages of cell division and reappears during anaphase as a granular cytoplasmic structure. In late telophase the antigen is relocated in the nucleus. This antigen, which we have designated as avian‐specific nuclear antigen (AVNA), is not associated with chromatin or ribonucleoproteins. From immunoblotting experiments on chicken fibroblast nuclei, AVNA is probably a complex composed of one or several polypeptides, one of which has a molecular weight of approximately 60 kD. The proteins were identified as nuclear matrix proteins rather than pore complex‐lamina proteins by immunoblotting experiments on the purified nuclear matrix of chicken erythrocytes. The major polypeptide had a molecular weight of 60 kD and the minor polypeptide a molecular weight of 69
ISSN:0730-2312
DOI:10.1002/jcb.240240102
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1984
数据来源: WILEY
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2. |
Modulation by retinyl acetate of microfilament bundle formation in C3H/10T1/2 cells |
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Journal of Cellular Biochemistry,
Volume 24,
Issue 1,
1984,
Page 15-25
Lawrence J. Mordan,
Sek‐Wen Hui,
John S. Bertram,
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摘要:
AbstractRetinyl acetate has been previously shown to inhibit carcinogen‐induced neoplastic transformation in 10T1/2 cells and to accentuate many aspects of the nontransformed phenotype. Scanning electron microscopy of logarithmic phase 10T1/2 cells treated for 3 days with 0.3 μg/ml retinyl acetate revealed that this treatment caused extensive flattening of cells to the plastic substrate. In contrast the tumor promoter tetradecanoyl phorbol acetate, which antagonizes the antineoplastic activity of retinyl acetate, caused cell rounding and completely inhibited the action of retinyl acetate on cell morphology. During this same time course, the formation of microfilament bundles was also found to be modulated by retinyl acetate. Transmission electron micrographs of unsectioned peripheral regions of flattened cells showed that while the unit density of microfilament bundles was not influenced, the thickness of bundles, particularly those with a diameter of 100 nm or more, was increased by retinyl acetate. Tetradecanoyl phorbol acetate had little effect on microfilament bundle diameters but did partially antagonize the action of retinyl acetate. To determine if this increase was associated with an increase in total actin/cell, total cell proteins, and proteins not extractable by glycerol‐triton extraction, were subjected to sodium dodecylsulfate/ polyacrylamide gel electrophoresis. It was found that while total cellular actin was not increased by retinyl acetate, the proportion of nonextractable actin (which includes microfilament bundles) increased from 65% to 88% of total actin. This increase was not inhibited by inhibitors of protein or RNA synthesis. These studies again demonstrate that retinyl acetate accentuates the nontransformed phenotype of 10T1/2 cells: it is hypothesized that these actions are related to the antineoplastic activity of retin
ISSN:0730-2312
DOI:10.1002/jcb.240240103
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1984
数据来源: WILEY
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3. |
The ubiquitin‐mediated proteolytic pathway and mechanisms of energy‐dependent intracellular protein degradation |
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Journal of Cellular Biochemistry,
Volume 24,
Issue 1,
1984,
Page 27-53
Aaron Ciechanover,
Daniel Finley,
Alexander Varshavsky,
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摘要:
AbstractIn this review we briefly describe the lysosomal system, consider the evidence for multiplicity of protein degradation pathways in vivo, discuss in detail the ubiquitin‐mediated pathway of intracellular ATP‐dependent protein degradation, and also the possible significance of ubiquitin‐histone conjugates in chromatin. For detailed discussions of the various characteristics and physiological roles of intracellular protein breakdown, the reader is referred to earlier reviews [1–7] and reports of recent symposia [8–10]. Information on the ubiquitin system prior to 1981 was described in an earlier review [11]. Hershko has briefly reviewed more recent informa
ISSN:0730-2312
DOI:10.1002/jcb.240240104
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1984
数据来源: WILEY
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4. |
The chloroplast envelope: Is it homologous with the double membranes of mitochondria and gram‐negative bacteria? |
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Journal of Cellular Biochemistry,
Volume 24,
Issue 1,
1984,
Page 55-68
Kenneth Keegstra,
Margaret Werner‐Washburne,
Kenneth Cline,
Jaen Andrews,
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ISSN:0730-2312
DOI:10.1002/jcb.240240105
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1984
数据来源: WILEY
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5. |
Differential protein insertion into developing photosynthetic membrane Regions of Rhodopseudomonas sphaeroides |
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Journal of Cellular Biochemistry,
Volume 24,
Issue 1,
1984,
Page 69-77
Gordon S. Inamine,
Patricia A. Reilly,
Robert A. Niederman,
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摘要:
AbstractPrevious studies have suggested that much of the B800‐850 light‐harvesting bacteriochlorophylla‐protein complex is inserted directly into the intracytoplasmic photosynthetic membrane of Rhodopseudomonas sphaeroides. In contrast, the B875 light‐harvesting and reaction center complexes are assembled preferentially at peripheral sites of photosynthetic membrane growth initiation. The basis for this apparent site‐specific polypeptide insertion was examined during the inhibition of RNA and protein syntheses. The pulse labeling of polypeptides at the membrane growth initiation sites was significantly less sensitive to inhibition by rifampicin, chloramphenicol, or kasugamycin than in the intfacytoplasmic or outer membranes. This suggests increased stability for the translation machinery at these membrane invagination sites. Similar differential effects in polypeptide insertion were observed during inhibition of bacteriochlorophyll synthesis through deprival of δ‐aminolevulinate to R sphaeroides mutant H‐5, which requires this porphyrin precursor. The pulse‐labeling patterns observed during the inhibition of both RNA and pigment syntheses were consistent with the uncoupling of polypeptide insertion into the membrane invagination sites from their growth and maturation into intracytop
ISSN:0730-2312
DOI:10.1002/jcb.240240106
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1984
数据来源: WILEY
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6. |
Release and purification of trypanosoma brucei variant surface glycoprotein |
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Journal of Cellular Biochemistry,
Volume 24,
Issue 1,
1984,
Page 79-90
George A. M. Cross,
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摘要:
AbstractConditions affecting the solubilization of variant surface glycoprotein (VSG) from Trypanosoma brucei have been investigated. The results obtained form the basis for a convenient and efficient method for VSG purification. VSG release from the cell surface was temperature‐dependent, following osmotic lysis at 0 °C, and was inhibited by low concentrations of Zn2+but not by tosyl‐lysine chloromethyl‐ketone (TLCK), phenylmethylsulfonylfluoride (PMSF), or iodoacetamide. These and other results eliminated the possibility that release was due to proteolytic cleavage of the C‐terminal hydrophobic tail present on newly synthesized VSG. Bolton and Hunter reagent reacted with several components on livi
ISSN:0730-2312
DOI:10.1002/jcb.240240107
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1984
数据来源: WILEY
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7. |
Genetic control of resistance to murine malaria |
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Journal of Cellular Biochemistry,
Volume 24,
Issue 1,
1984,
Page 91-102
Mary Stevenson,
Suzanne Lemieux,
Emil Skamene,
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摘要:
AbstractStrain variation in the level of resistance to malaria was investigated in inbred mice after infection with Plasmodium chabaudi. Following intraperitoneal infection with the typing dose of parasitized erythrocytes, mice of 11 inbred strains could be separated using survival time as the criterium into resistant and susceptible groups. Genetic analysis of F1hybrid and backcross progeny derived from one of the most resistant (B10.A) and from the most susceptible (A/J) strains as parents suggested that host resistance in this strain combination was genetically controlled by a dominant, non‐H‐2‐linked, autosomal gene or closely linked genes. Analysis of the mechanisms of resistance to P chabaudi showed (1) phenotypic expression of the resistance gene was apparent within 6 days of infection as a significant difference between resistant and susceptible mice in the level of parasitemia; (2) the level of host NK cell activity wasnotrelated to the level of host resistance to malaria; (3) compared with susceptible A/J mice, resistant B1O.A hosts had an augmented erythropoietic response during the course of malaria as well as during phenylhydrazine‐induced anemia and (4) treatment with BCG or P acnes resulted in an equal degree of protection, measured by parasitemia and survival, in both resistant and susceptib
ISSN:0730-2312
DOI:10.1002/jcb.240240108
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1984
数据来源: WILEY
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8. |
Masthead |
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Journal of Cellular Biochemistry,
Volume 24,
Issue 1,
1984,
Page -
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PDF (118KB)
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ISSN:0730-2312
DOI:10.1002/jcb.240240101
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1984
数据来源: WILEY
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