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Articles 301 - 311 of 311
Full-Text Articles in Microbiology
The Seca Subunit Of Escherichia Coli Preprotein Translocase Is Exposed To The Periplasm, Jerry Eichler, William Wickner
The Seca Subunit Of Escherichia Coli Preprotein Translocase Is Exposed To The Periplasm, Jerry Eichler, William Wickner
Dartmouth Scholarship
SecA undergoes conformational changes during translocation, inserting domains into and across the membrane or enhancing the protease resistance of these domains. We now show that some SecA bound at SecYEG is accessible from the periplasm to a membrane-impermeant probe in cells with a permeabilized outer membrane but an intact plasma membrane.
Cyclic Amp And Its Receptor Protein Negatively Regulate The Coordinate Expression Of Cholera Toxin And Toxin-Coregulated Pilus In Vibrio Cholerae, Karen Skorupski, Ronald K. Taylor
Cyclic Amp And Its Receptor Protein Negatively Regulate The Coordinate Expression Of Cholera Toxin And Toxin-Coregulated Pilus In Vibrio Cholerae, Karen Skorupski, Ronald K. Taylor
Dartmouth Scholarship
Insertion mutations in two Vibrio cholerae genes, cya and crp, which encode adenylate cyclase and the cyclic AMP (cAMP) receptor protein (CRP), respectively, derepressed the expression of a chromosomal cholera toxin (CT) promoter-lacZ fusion at the nonpermissive temperature of 37 degrees C. In the classical biotype strain O395, the crp mutation increased the production of both CT and toxin-coregulated pilus (TCP) in vitro under a variety of growth conditions not normally permissive for their expression. The most dramatic increase in CT and TCP was observed with the crp mutant in Luria-Bertani (LB) medium pH 8.5, at 30 degrees C. El …
Activation Of The Human Thymidine Kinase (Tk) Promoter By Simian Virus 40 Large T Antigen Requires Both The T Antigen Prb Family-Binding Domain And Tk Promoter Sequences Resembling E2f-Binding Sites., Michelle M. Anderson, Jun Chen, Charles N. Cole, Susan E. Conrad
Activation Of The Human Thymidine Kinase (Tk) Promoter By Simian Virus 40 Large T Antigen Requires Both The T Antigen Prb Family-Binding Domain And Tk Promoter Sequences Resembling E2f-Binding Sites., Michelle M. Anderson, Jun Chen, Charles N. Cole, Susan E. Conrad
Dartmouth Scholarship
Infection of quiescent cells with the DNA tumor virus simian virus 40 induces expression of the cellular thymidine kinase (TK) gene a minimum of 10- to 20-fold, and this induction depends upon the viral protein large T antigen (T-Ag). To define both human TK promoter elements and T-Ag functional domains required for transcriptional induction, we have established a system in which stable Rat-1 transfectants harboring TK promoter-luciferase hybrid genes are infected with recombinant adenoviruses expressing either wild-type or mutant forms of T-Ag and luciferase expression is measured as an indicator of promoter activity. The results show that (i) a 135-bp …
Antibody To The Ligand For Cd40 (Gp39) Inhibits Murine Aids-Associated Splenomegaly, Hypergammaglobulinemia, And Immunodeficiency In Disease-Susceptible C57bl/6 Mice., Kathy A. Green, Karen M. Crassi, Jon D. Laman, Arjan Schoneveld, Rendall R. Strawbridge, Teresa M. Foy, Randolph J. Noelle, William R. Green
Antibody To The Ligand For Cd40 (Gp39) Inhibits Murine Aids-Associated Splenomegaly, Hypergammaglobulinemia, And Immunodeficiency In Disease-Susceptible C57bl/6 Mice., Kathy A. Green, Karen M. Crassi, Jon D. Laman, Arjan Schoneveld, Rendall R. Strawbridge, Teresa M. Foy, Randolph J. Noelle, William R. Green
Dartmouth Scholarship
Infection of genetically susceptible C57BL/6 mice with the LP-BM5 isolate of murine retroviruses cause profound splenomegaly, hypergammaglobulinemia, lymphadenopathy, and an immunodeficiency syndrome which includes the development of terminal B-cell lymphomas. Because many of these and the other manifestations of LP-BM5 virus-induced disease are similar to those seen in AIDS, this syndrome has been named murine AIDS, or MAIDS. Previous reports have shown that the onset of MAIDS depends on the presence of both CD41 T cells and B cells and have suggested that CD41 T-cell-B-cell interactions are important to disease pathogenesis. Here, we assessed the possibility that interactions between CD40 …
A Tef-1-Independent Mechanism For Activation Of The Simian Virus 40 (Sv40) Late Promoter By Mutant Sv40 Large T Antigens., Paul Casaz, Phillip W. Rice, Charles N. Cole, Ulla Hansen
A Tef-1-Independent Mechanism For Activation Of The Simian Virus 40 (Sv40) Late Promoter By Mutant Sv40 Large T Antigens., Paul Casaz, Phillip W. Rice, Charles N. Cole, Ulla Hansen
Dartmouth Scholarship
Simian virus 40 (SV40) large tumor antigen (T antigen) stimulates the activity of the SV40 late promoter and a number of cellular and other viral promoters. We have characterized the ability of T antigens with mutations in the DNA-binding domain and within the N-terminal 85 residues to activate the SV40 late promoter. T antigens lacking both nonspecific and sequence-specific DNA-binding activities were able to induce the late promoter. Mutations within the N-terminal 85 residues of T antigen diminished activation by less than twofold. Activation by wild-type and most of the mutant T antigens required intact binding sites for the cellular …
A Novel Translational Regulation Function For The Simian Virus 40 Large-T Antigen Gene., Prithi Rajan, Sathyamagalam Swaminathan, Jiyue Zhu, Charles N. Cole
A Novel Translational Regulation Function For The Simian Virus 40 Large-T Antigen Gene., Prithi Rajan, Sathyamagalam Swaminathan, Jiyue Zhu, Charles N. Cole
Dartmouth Scholarship
Cells use the interferon-induced, double-stranded-RNA-dependent protein kinase PKR as a defense against virus infections. Upon activation, PKR phosphorylates and thereby inactivates the protein synthesis initiation factor eIF-2, resulting in the cessation of protein synthesis. Viruses have evolved various strategies to counteract this cellular defense. In this paper, we show that simian virus 40 (SV40) large-T antigen can antagonize the translational inhibitory effect resulting from the activation of PKR in virus-infected cells. Unlike the situation with other virus-host cell interactions, SV40 large-T antigen does not block the activation of PKR, suggesting that SV40 counteracts the cellular antiviral response mediated by PKR …
Adoptive Transfer Of Polyclonal And Cloned Cytolytic T Lymphocytes (Ctl) Specific For Mouse Aids-Associated Tumors Is Effective In Preserving Ctl Responses: A Measure Of Protection Against Lp-Bm5 Retrovirus-Induced Immunodeficiency., William R. Green, Kathy A. Green, Karen M. Crassi
Adoptive Transfer Of Polyclonal And Cloned Cytolytic T Lymphocytes (Ctl) Specific For Mouse Aids-Associated Tumors Is Effective In Preserving Ctl Responses: A Measure Of Protection Against Lp-Bm5 Retrovirus-Induced Immunodeficiency., William R. Green, Kathy A. Green, Karen M. Crassi
Dartmouth Scholarship
Cytolytic T lymphocytes (CTL) can be raised against C57BL/6 B-cell lymphomas from mice with LP-BM5 murine leukemia virus-induced AIDS (MAIDS). Adoptive transfer of polyclonal anti-MAIDS tumor CTL or two CTL clones specific for the B6-1710 MAIDS lymphoma caused preservation of major histocompatibility complex-restricted and allogeneic CTL responses, which may be interpreted as indices of protection from LP-BM5 murine leukemia virus-induced immunodeficiency.
Molecular Cloning Of Infectious Ecotropic Murine Leukemia Virus Ak7 From An Emv-14-Positive Akxl-5 Mouse And The Resistance Of Ak7 To Recognition By Cytotoxic T Lymphocytes., Hillary D. White, William R. Green, Nuria R. Giné
Molecular Cloning Of Infectious Ecotropic Murine Leukemia Virus Ak7 From An Emv-14-Positive Akxl-5 Mouse And The Resistance Of Ak7 To Recognition By Cytotoxic T Lymphocytes., Hillary D. White, William R. Green, Nuria R. Giné
Dartmouth Scholarship
The AKXL-5 recombinant inbred mouse strain is positive for the endogenous ecotropic murine leukemia virus emv-14, the only emv present in its germ line. emv-14 is of particular interest because spleen cells expressing emv-14 virus escape recognition by anti-AKR/Gross virus-specific cytotoxic T lymphocytes. We report here the isolation and characterization of a replication-competent emv clone, pAK7, derived from an AKXL-5 mouse. This clone is novel in that it encodes a variant ecotropic murine leukemia virus that, when expressed in SC.Kb target cells, fails to be recognized efficiently by anti-AKR/Gross virus cytotoxic T lymphocytes. The pAK7 clone can therefore be used …
Cytolytic T Lymphocytes Specific For Tumors And Infected Cells From Mice With A Retrovirus-Induced Immunodeficiency Syndrome., Jennifer G. Erbe, Kathy A. Green, Karen M. Crassi, Herbert C. Morse, W R. Green
Cytolytic T Lymphocytes Specific For Tumors And Infected Cells From Mice With A Retrovirus-Induced Immunodeficiency Syndrome., Jennifer G. Erbe, Kathy A. Green, Karen M. Crassi, Herbert C. Morse, W R. Green
Dartmouth Scholarship
LP-BM5 retrovirus complex-infected C57BL/6 mice develop immunodeficiency, somewhat analogous to AIDS, termed murine AIDS (MAIDS). After secondary stimulation with syngeneic B-cell lymphomas from LP-BM5-infected mice, C57BL/6 mice produced vigorous CD8+ cytotoxic T lymphocytes specific for MAIDS-associated tumors. An anti-LP-BM5 specificity was suggested because spleen and lymph node cells from LP-BM5-infected mice served as target cells in competition assays, and cells from LP-BM5, but not ecotropic, virus-infected mice functioned as secondary in vitro stimulators to generate cytotoxic T lymphocytes to MAIDS tumors.
The Growth Of Simian Virus 40 (Sv40) Host Range/Adenovirus Helper Function Mutants In An African Green Monkey Cell Line That Constitutively Expresses The Sv40 Agnoprotein., Terryl P. Stacy, Michele Chamberlain, Susan Carswell, Charles N. Cole
The Growth Of Simian Virus 40 (Sv40) Host Range/Adenovirus Helper Function Mutants In An African Green Monkey Cell Line That Constitutively Expresses The Sv40 Agnoprotein., Terryl P. Stacy, Michele Chamberlain, Susan Carswell, Charles N. Cole
Dartmouth Scholarship
The simian virus 40 T-antigen carboxy-terminal mutants, dlA2459 and dlA2475, are cell line and temperature dependent for growth and plaque formation in monkey kidney cells. Although these mutants did form plaques on BSC-1 cells at 37 degrees C, they were about fivefold less efficient for plaque formation than wild-type simian virus 40. These mutants did not grow in CV-1 cells and did not synthesize agnoprotein in those cells. CV-1 cells which constitutively express the agnoprotein were permissive for mutant plaque formation. However, late mRNAs, virion proteins, and progeny virion yields did not accumulate to wild-type levels during mutant infection of …
Mechanism Of Escape Of Endogenous Murine Leukemia Virus Emv-14 From Recognition By Anti-Akr/Gross Virus Cytolytic T Lymphocytes., Hillary D. White, Michael D. Robbins, William R. Green
Mechanism Of Escape Of Endogenous Murine Leukemia Virus Emv-14 From Recognition By Anti-Akr/Gross Virus Cytolytic T Lymphocytes., Hillary D. White, Michael D. Robbins, William R. Green
Dartmouth Scholarship
It was previously shown that spleen cells from endogenous ecotropic murine leukemia virus emv-14+ AKXL-5 mice fail to stimulate an anti-AKR/Gross virus cytolytic T-lymphocyte (CTL) response in a mixed lymphocyte culture with primed C57BL/6 responder spleen cells, whereas spleen cells from AKXL strains carrying the very similar emv-11 provirus do stimulate a response (Green and Graziano, Immunogenetics 23:106-110, 1986). We wished to determine whether the lack of response with AKXL-5 spleen cells was at the level of recognition between effector cell and target cell and whether the relevant mutation was within the emv-14 provirus. It is shown here that EMV-negative …