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1
Recovery of the accumulation ability of thiomethyl-beta-galactoside in Escherichia coli after bacteriophage T4 infection.噬菌体T4感染后大肠杆菌中硫代甲基-β-半乳糖苷积累能力的恢复
J Virol. 1976 Feb;17(2):299-306. doi: 10.1128/JVI.17.2.299-306.1976.
2
Bacteriophage T4 inhibits colicin E2-induced degradation of Escherichia coli deoxyribonucleic acid. II. Inhibition by T4 ghosts and by T4 in the absence of protein synthesis.噬菌体T4抑制大肠杆菌素E2诱导的大肠杆菌脱氧核糖核酸降解。II. T4空壳及无蛋白质合成时T4的抑制作用
J Virol. 1973 Mar;11(3):386-98. doi: 10.1128/JVI.11.3.386-398.1973.
3
The biochemical and genetic basis for high frequency thiomethyl galactoside resistance in lambda,lambdadg lysogens of Escherichia coli.大肠杆菌λ噬菌体、λdg溶原菌中高频率硫代甲基半乳糖苷抗性的生化和遗传基础。
J Gen Microbiol. 1978 Feb;104(2):287-97. doi: 10.1099/00221287-104-2-287.
4
Effect of chloramphenicol and cyanide on the increase in UV resistance of intracellular bacteriophage T1.氯霉素和氰化物对细胞内噬菌体T1紫外线抗性增加的影响。
Microbios. 1978;20(80):125-31.
5
Injection of ultraviolet-damage-specific enzyme by T4 bacteriophage.T4噬菌体注射紫外线损伤特异性酶。
J Virol. 1973 Jul;12(1):1-8. doi: 10.1128/JVI.12.1.1-8.1973.
6
Metabolism of T4 bacteriophage ghost-infected cells: effect of bacteriophage and ghosts on the uptake of carbohydrates in Escherichia coli B.T4噬菌体空壳感染细胞的代谢:噬菌体及空壳对大肠杆菌B中碳水化合物摄取的影响
J Bacteriol. 1971 Jul;107(1):259-67. doi: 10.1128/jb.107.1.259-267.1971.
7
On the lack of host-cell reactivation of UV-irradiated phage T5 II. Further characterization of the repair inhibition exerted by T5 infection.
Mutat Res. 1976 Aug;36(2):135-46. doi: 10.1016/0027-5107(76)90002-6.
8
Inhibition of T4 bacteriophage multiplication by superinfecting ghosts and the development of tolerance after bacteriophage infection.超感染噬菌体空壳对T4噬菌体增殖的抑制作用及噬菌体感染后耐受性的发展。
J Virol. 1971 Jan;7(1):8-14. doi: 10.1128/JVI.7.1.8-14.1971.
9
Unfolding of the host genome after infection of Escherichia coli with bacteriophage T4.用噬菌体T4感染大肠杆菌后宿主基因组的解折叠
J Virol. 1974 Feb;13(2):548-50. doi: 10.1128/JVI.13.2.548-550.1974.
10
Excision of thymine dimers in vitro by extracts of bacteriophage-infected Escherichia coli.噬菌体感染的大肠杆菌提取物在体外对胸腺嘧啶二聚体的切除
J Virol. 1974 May;13(5):953-9. doi: 10.1128/JVI.13.5.953-959.1974.

本文引用的文献

1
RNA metabolism in Escherichia coli infected with bacteriophage T4. Inhibition of host ribosomal and soluble RNA synthesis by phage and effect of chloromycetin.感染噬菌体T4的大肠杆菌中的RNA代谢。噬菌体对宿主核糖体RNA和可溶性RNA合成的抑制作用以及氯霉素的影响。
J Mol Biol. 1962 May;4:376-87. doi: 10.1016/s0022-2836(62)80018-7.
2
Reversibility of inhibition of nucleic acids and protein synthesis by colicin K.大肠菌素K对核酸和蛋白质合成抑制作用的可逆性
Biochem Biophys Res Commun. 1962 May 4;7:306-9. doi: 10.1016/0006-291x(62)90196-1.
3
Comparative study of some properties of bacteriophage T4D irradiated with monochromatic ultraviolet light.用单色紫外线照射的噬菌体T4D某些特性的比较研究。
Virology. 1962 Nov;18:343-58. doi: 10.1016/0042-6822(62)90026-0.
4
The protein coats or ghosts of coli phage T2. II. The biological functions.大肠杆菌噬菌体T2的蛋白质外壳或空壳。II. 生物学功能。
J Gen Physiol. 1957 Nov 20;41(2):307-31. doi: 10.1085/jgp.41.2.307.
5
Acetylornithinase of Escherichia coli: partial purification and some properties.大肠杆菌的乙酰鸟氨酸酶:部分纯化及某些性质
J Biol Chem. 1956 Jan;218(1):97-106.
6
The action of T2 bacteriophage ghosts on Escherichia coli B.T2噬菌体空壳对大肠杆菌B的作用。
Can J Microbiol. 1955 Dec;1(9):757-74. doi: 10.1139/m55-090.
7
Mechanism of cell wall penetration by viruses. II. Demonstration of cyclic permeability change accompanying virus infection of Escherichia coli B cells.病毒穿透细胞壁的机制。II. 大肠杆菌B细胞受病毒感染时伴随的循环通透性变化的证明。
J Exp Med. 1955 Feb 1;101(2):151-75. doi: 10.1084/jem.101.2.151.
8
Mechanism of cell wall penetration by viruses. I. An increase in host cell permeability induced by bacteriophage infection.病毒穿透细胞壁的机制。I. 噬菌体感染诱导宿主细胞通透性增加。
J Exp Med. 1954 May 1;99(5):481-94. doi: 10.1084/jem.99.5.481.
9
Inhibition of T4 bacteriophage multiplication by superinfecting ghosts and the development of tolerance after bacteriophage infection.超感染噬菌体空壳对T4噬菌体增殖的抑制作用及噬菌体感染后耐受性的发展。
J Virol. 1971 Jan;7(1):8-14. doi: 10.1128/JVI.7.1.8-14.1971.
10
Breakdown and exclusion of superinfecting T-even bacteriophage in Escherichia coli.大肠杆菌中超级感染的T偶数噬菌体的分解与排除
J Virol. 1971 Dec;8(6):869-86. doi: 10.1128/JVI.8.6.869-886.1971.

噬菌体T4感染后大肠杆菌中硫代甲基-β-半乳糖苷积累能力的恢复

Recovery of the accumulation ability of thiomethyl-beta-galactoside in Escherichia coli after bacteriophage T4 infection.

作者信息

Saijo N, Okamoto K

出版信息

J Virol. 1976 Feb;17(2):299-306. doi: 10.1128/JVI.17.2.299-306.1976.

DOI:10.1128/JVI.17.2.299-306.1976
PMID:1255845
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC515421/
Abstract

Effects of UV-irridiated and unirradiated T4 phage infection on the beta-galactoside accumulation ability in Eschericia coli have been examined by the use of 14C-labeled thiomethyl-beta-galactoside (TMG). Under conditions where a synchronous adsorption of phage takes place, the cellular ability for TMG accumulation is found to be largely inhibited immediately after phage adsorption, but it recovers with time to a new level, which is dependent on the multiplicity of infection. When cells are infected with UV-irradiated T4 at the same multiplicity as that of unirradiated phage, the cellular accumulation ability is more severely inhibited and there is no recovery from the inhibition. The recovery process in T4-infected cells is mostly sensitive to puromycin. These results suggest that the initial inhibition of the TMG accumulation ability is probably caused by the adsorption of phage coats, and the subsequent restoration occurs through the action of a phage-directed protein(s). In the recovery process, no new transport system appears to be involved. The restored ability of TMG accumulation is resistant to the action of superinfecting UV phage. However, different mechanisms appear to be operating in T4-infected cells for the establishment of resistance to ghosts and for the recovery from the phage coat-induced inhibition.

摘要

通过使用¹⁴C标记的硫代甲基-β-半乳糖苷(TMG),研究了紫外线照射的和未照射的T4噬菌体感染对大肠杆菌中β-半乳糖苷积累能力的影响。在噬菌体同步吸附的条件下,发现噬菌体吸附后,细胞积累TMG的能力立即受到很大抑制,但随着时间的推移会恢复到一个新水平,这个新水平取决于感染复数。当用与未照射噬菌体相同感染复数的紫外线照射的T4噬菌体感染细胞时,细胞积累能力受到更严重的抑制,且抑制没有恢复。T4感染细胞中的恢复过程对嘌呤霉素最为敏感。这些结果表明,TMG积累能力的初始抑制可能是由噬菌体外壳的吸附引起的,随后的恢复是通过噬菌体指导的一种或多种蛋白质的作用发生的。在恢复过程中,似乎没有新的转运系统参与。恢复后的TMG积累能力对超感染的紫外线噬菌体的作用具有抗性。然而,在T4感染的细胞中,建立对噬菌体空壳的抗性和从噬菌体外壳诱导的抑制中恢复似乎涉及不同的机制。