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51.
R. J. Phillips D. C. Hickleton P. E. Boehmer P. T. Emmerson 《Molecular & general genetics : MGG》1997,254(3):319-329
To investigate the role that the individual subunits play in the ATP-dependent helicase activity of the RecBCD protein we
have investigated the ability of the RecB, RecC and RecD proteins to displace various 20-mer oligonucleotides annealed to
either end or to the centre of an oligonucleotide 60 bases long. The results show that the only subunit which can displace
the 20-mers in the absence of the other subunits is the RecB protein. Moreover, the 20-mer is displaced only if it is annealed
to the 60-mer at the 5′ end or the middle, suggesting that the RecB protein translocates along the 60-mer in the 3′ to 5′
direction, displacing annealed 20-mers as it proceeds. We have shown that reconstituted RecBC and RecBCD complexes displace
the 20-mers but, unlike RecB, they do not require a 3′-ended single-stranded region for helicase action, but can displace
the 20-mers from either end of the 60-mer. The level of helicase activity of the RecBC complex is considerably greater than
that of RecB alone, and the activity of the RecBCD complex appears to be greater still. This hierarchy of activity is also
shown by DNA binding studies, but is not reflected in the ATPase activities of the enzymes. We have also shown that the ability
of trypsin to cleave various sites on the RecB molecule is modified by the presence of ATP or ATP-γ-S, suggesting that conformational
changes may be induced in RecB upon ATP binding. We discuss a model for the ATP-driven, unidirectional motion of the RecB
translocase along single-stranded DNA. In this model, the RecB molecule binds to single-stranded DNA and then translocates
along it, one base at a time, in the 3′ to 5′ direction, by a `ratchet' mechanism in which repeated stretching and contraction
of the protein is coupled to ATP hydrolysis. The RecC protein in the RecBC complex is proposed to act as a `sliding clamp'
which increases processivity by preventing dissociation.
Received: 10 September 1996 / Accepted: 18 November 1996 相似文献
52.
AtRAD5A is a DNA translocase harboring a HIRAN domain which confers binding to branched DNA structures and is required for DNA repair in vivo
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Daniela Kobbe Andy Kahles Maria Walter Tobias Klemm Anja Mannuss Alexander Knoll Manfred Focke Holger Puchta 《The Plant journal : for cell and molecular biology》2016,88(4):521-530
DNA lesions such as crosslinks represent obstacles for the replication machinery. Nonetheless, replication can proceed via the DNA damage tolerance pathway also known as postreplicative repair pathway. SNF2 ATPase Rad5 homologs, such as RAD5A of the model plant Arabidopsis thaliana, are important for the error‐free mode of this pathway. We able to demonstrate before, that RAD5A is a key factor in the repair of DNA crosslinks in Arabidopsis. Here, we show by in vitro analysis that AtRAD5A protein is a DNA translocase able to catalyse fork regression. Interestingly, replication forks with a gap in the leading strand are processed best, in line with its suggested function. Furthermore AtRAD5A catalyses branch migration of a Holliday junction and is furthermore not impaired by the DNA binding of a model protein, which is indicative of its ability to displace other proteins. Rad5 homologs possess HIRAN (Hip116, Rad5; N‐terminal) domains. By biochemical analysis we were able to demonstrate that the HIRAN domain variant from Arabidopsis RAD5A mediates structure selective DNA binding without the necessity for a free 3′OH group as has been shown to be required for binding of HIRAN domains in a mammalian RAD5 homolog. The biological importance of the HIRAN domain in AtRAD5A is demonstrated by our result that it is required for its function in DNA crosslink repair in vivo. 相似文献
53.
Estelle Crozat Adrien Meglio Jean‐François Allemand Claire E Chivers Mark Howarth Catherine Vénien‐Bryan David J Sherratt 《The EMBO journal》2010,29(8):1423-1433
FtsK translocates dsDNA directionally at >5 kb/s, even under strong forces. In vivo, the action of FtsK at the bacterial division septum is required to complete the final stages of chromosome unlinking and segregation. Despite the availability of translocase structures, the mechanism by which ATP hydrolysis is coupled to DNA translocation is not understood. Here, we use covalently linked translocase subunits to gain insight into the DNA translocation mechanism. Covalent trimers of wild‐type subunits dimerized efficiently to form hexamers with high translocation activity and an ability to activate XerCD‐dif chromosome unlinking. Covalent trimers with a catalytic mutation in the central subunit formed hexamers with two mutated subunits that had robust ATPase activity. They showed wild‐type translocation velocity in single‐molecule experiments, activated translocation‐dependent chromosome unlinking, but had an impaired ability to displace either a triplex oligonucleotide, or streptavidin linked to biotin‐DNA, during translocation along DNA. This separation of translocation velocity and ability to displace roadblocks is more consistent with a sequential escort mechanism than stochastic, hand‐off, or concerted mechanisms. 相似文献
54.
Matthew J Harris Irwin M Arias 《Biochimica et Biophysica Acta (BBA)/Molecular and Cell Biology of Lipids》2003,1633(2):127-131
ATP8B1/FIC1 is a member of the Type IV P-type ATPase family, which function as ATP dependent aminophospholipid translocases (APLT). We identified two familial intrahepatic cholestasis type 1 (FIC1) homologues, ATP8B2 and ATP8B3, with 53% and 45% amino acid identity, respectively. The expression profile for each gene was determined using a 73-tissue human RNA expression array. The subfamily of FIC1-like proteins is expressed in a wide range of tissues. Given that mutations in FIC1 result in liver disease, these proteins may have important roles in other organs in which they are candidates for genetic and acquired diseases. 相似文献
55.
Cationic liposomes are used as efficient carriers for gene delivery into mammalian cells due to their ability to bind nucleic acids, adsorb onto the cell surface and fuse with negatively charged membranes. This last property enables the release and escape of their cargo from endosomal compartments. The efficiency of this fusion mainly depends on the surface charge of the target membranes. Here, we report that cells of two different lines, epithelial adenocarcinoma HeLa and lymphocytic leukemia Jurkat T, which externalize PS, are more susceptible to fusion with DOTAP liposomes than control cells. We compared the ability to undergo fusion of untreated and apoptotic cells. Apoptosis was induced by various pro-apoptotic agents and treatments, namely: incubation in the presence of MnCl(2), cytostatic drugs fludarabine and mitoxantrone, staurosporine and serum depletion in the case of HeLa cells. Jurkat T cells were treated similarly except apoptosis was additionally induced by incubation in the presence of 4% EtOH. Epithelial cells fused with the highest efficiencies of lipid mixing, when pretreated with staurosporine. Jurkat T cells were less susceptible to fusion, but they also displayed an increase in fusion efficiency after the induction of apoptosis. Alternatively, we treated the cells with metabolic inhibitors causing ATP-depletion in order to inactivate aminophospholipid translocase. After ATP-depletion, HeLa and Jurkat T cells fused with DOTAP liposomes with higher efficiencies than control cells. Our conclusion is that the lipid asymmetry of natural membranes may limit fusion with cationic liposomes. 相似文献
56.
G6P translocase (G6PT) is thought to play a crucial role in transducing intracellular signaling events in brain tumor-derived cancer cells. In this report, we investigated the contribution of G6PT to the control of U-87 brain tumor-derived glioma cell survival using small interfering RNA (siRNA)-mediated suppression of G6PT. Three siRNA constructs were generated and found to suppress up to 91% G6PT gene expression. Flow cytometry analysis of propidium iodide/annexin-V-stained cells indicated that silencing the G6PT gene induced necrosis and late apoptosis. The anticancer agent curcumin, also inhibited G6PT gene expression by more than 90% and triggered U-87 glioma cells death. Overexpression of recombinant G6PT rescued the cells from curcumin-induced cell death. Targeting G6PT expression may provide a new mechanistic rationale for the action of chemopreventive drugs and lead to the development of new anti-cancer strategies. 相似文献
57.
Brinkmann JF Pelsers MM van Nieuwenhoven FA Tandon NN van der Vusse GJ Glatz JF 《Molecular and cellular biochemistry》2006,284(1-2):127-134
Evidence is accumulating that the heavily glycosylated integral membrane protein fatty acid translocase (FAT/CD36) is involved
in the transport of long-chain fatty acids across the sarcolemma of heart muscle cells. The aim of this study was to analyse
the distribution between FAT/CD36 present in cardiac myocytes and endothelial cells. We therefore developed a method to purify
FAT/CD36 from total rat heart and isolated cardiomyocytes, and used the proteins as standards in an immunochemical assay.
Two steps, chromatography on wheat germ agglutinin-agarose and anion-exchange chromatography on Q-Sepharose fast flow, were
sufficient for obtaining the protein in a > 95% pure form. When used to isolate FAT/CD36 from total heart tissue, the FAT/CD36
yield of the method was 9% and the purification factor was 64. Purifying FAT/CD36 from isolated cardiomyocytes yielded the
same 88 kDa protein band on SDS-PAGE gels and reactivity of this band on western blots was comparable to that of the FAT/CD36
isolated from total hearts. Quantifying FAT/CD36 contents by western blotting showed that the amounts of FAT/CD36 that are
present in isolated cardiomyocytes (10 ± 3 μg/mg protein) and total hearts (14 ± 4 μg/mg protein) are of comparable magnitude.
Immunofluorescence labelling showed that at least a part of the FAT/CD36 present in the cardiomyocyte is associated with the
sarcolemma. This study established that FAT/CD36 is a relatively abundant protein in the cardiomyocyte. In addition, the further
developed purification procedure is the first method for isolating FAT/CD36 from rat heart and cardiomyocyte FAT/CD36. 相似文献
58.
Noji T Yamamoto T Saito K Fujimura-Kamada K Kondo S Tanaka K 《Biochemical and biophysical research communications》2006,344(1):323-331
Lem3p-Dnf1p is a putative aminophospholipid translocase (APLT) complex that is localized to the plasma membrane; Lem3p is required for Dnf1p localization to the plasma membrane. We have identified lem3 mutations, which did not affect formation or localization of the Lem3p-Dnf1p complex, but caused a synthetic growth defect with the null mutation of CDC50, a structurally and functionally redundant homologue of LEM3. Interestingly, these lem3 mutants exhibited nearly normal levels of NBD-labeled phospholipid internalization across the plasma membrane, suggesting that Lem3p may have other functions in addition to regulation of the putative APLT activity of Dnf1p at the plasma membrane. Similarly, deletion of the COOH-terminal cytoplasmic region of Dnf1p affected neither the localization nor the APLT activity of Dnf1p at the plasma membrane, but caused a growth defect in the cdc50Delta background. Our results suggest that the Lem3p-Dnf1p complex may play a role distinct from its plasma membrane APLT activity when it substitutes for the Cdc50p-Drs2p complex, its redundant partner in the endosomal/trans-Golgi network compartments. 相似文献
59.
Dhar MS Yuan JS Elliott SB Sommardahl C 《The Journal of nutritional biochemistry》2006,17(12):811-820
Mice carrying two pink-eyed dilution (p) locus heterozygous deletions represent a novel polygenic mouse model of type 2 diabetes associated with obesity. Atp10c, a putative aminophospholipid transporter on mouse chromosome 7, is a candidate for the phenotype. The phenotype is diet-induced. As a next logical step in the validation and characterization of the model, experiments to analyze metabolic abnormalities associated with these mice were carried out. Results demonstrate that mutants (inheriting the p deletion maternally) heterozygous for Atp10c are hyperinsulinemic, insulin-resistant and have an altered insulin-stimulated response in peripheral tissues. Adipose tissue and the skeletal muscle are the targets, and GLUT4-mediated glucose uptake is the specific metabolic pathway associated with Atp10c deletion. Insulin resistance primarily affects the adipose tissue and the skeletal muscle, and the effect in the liver is secondary. Gene expression profiling using microarray and real-time PCR show significant changes in the expression of four genes — Vamp2, Dok1, Glut4 and Mapk14 — involved in insulin signaling. The expression of Atp10c is also significantly altered in the adipose tissue and the soleus muscle. The most striking observation is the loss of Atp10c expression in the mutants, specifically in the soleus muscle, after eating the high-fat diet for 12 weeks. In conclusion, experiments suggest that the target genes and/or their cognate factors in conjunction with Atp10c presumably affect the normal translocation and sequestration of GLUT4 in both the target tissues. 相似文献
60.
Stephan Kutik David A. Stroud Nils Wiedemann Nikolaus Pfanner 《Biochimica et Biophysica Acta (BBA)/General Subjects》2009
Mitochondria and the nucleus are key features that distinguish eukaryotic cells from prokaryotic cells. Mitochondria originated from a bacterium that was endosymbiotically taken up by another cell more than a billion years ago. Subsequently, most mitochondrial genes were transferred and integrated into the host cell's genome, making the evolution of pathways for specific import of mitochondrial proteins necessary. The mitochondrial protein translocation machineries are composed of numerous subunits. Interestingly, many of these subunits are at least in part derived from bacterial proteins, although only few of them functioned in bacterial protein translocation. We propose that the primitive α-proteobacterium, which was once taken up by the eukaryote ancestor cell, contained a number of components that were utilized for the generation of mitochondrial import machineries. Many bacterial components of seemingly unrelated pathways were integrated to form the modern cooperative mitochondria-specific protein translocation system. 相似文献