FEBS Journal
1742-464X
1432-1033
Anh Quốc
Cơ quản chủ quản: Wiley-Blackwell Publishing Ltd , WILEY
Lĩnh vực:
Cell BiologyMolecular BiologyBiochemistry
Phân tích ảnh hưởng
Thông tin về tạp chí
The FEBS Journal is an international peer-reviewed Journal devoted to publication of high-quality papers reporting significant advances in the molecular life sciences. Acceptance decisions are based on the originality and quality of the research and its prospective interest to a wide readership. Papers submitted to The FEBS Journal should provide novel perspectives on a biologically relevant problem and be of interest to a broad readership. The scope of the Journal is broad and inclusive. We are particularly interested in papers in which state-of-the-art approaches are applied to bring novel insight into molecular and cellular mechanisms that underlie the functions of molecules, cells and organisms. The Journal also welcomes manuscripts of an interdisciplinary nature, including systems approaches that address fundamental concepts in molecular, cellular or organismal biology. The Journal does not accept papers that lack biological insight. Papers describing bioinformatic analysis, modelling or structural studies of specific systems or molecules should include experimental data. The FEBS Journal also publishes Reviews, Minireviews, Viewpoints and Snapshots on a wide range of topics. These pieces are specially commissioned by our Editorial team and are selected on the basis of their interest to a wide readership. In addition, the Journal publishes Special Issues that provide detailed insight into a specific scientific field.
Các bài báo tiêu biểu
The 58‐kDa microspherule protein (MSP58), a nucleolar protein, interacts with nucleolar protein p120 Proteinp120 is a proliferation‐related nucleolar protein which is detectable early in the G1 phase of the cell cycle and peaks early in the S phase. Most human malignant tumors contain much higher levels of protein p120 than normal resting cells. To identify p120‐associated protein(s), a yeast two‐hybrid screen was carried out using protein p120 as the bait. Two positive clones encoded portions of a novel protein, designated microspherule protein 58 kDa (MSP58). MSP58 mRNA is 1.9 kb and encodes an approximately 58‐kDa polypeptide of 462 amino acids as shown by Western blotting of HeLa nucleolar proteins. The mouse MSP58 homolog has 97 % amino acid similarity to human MSP58, but no MSP58 homolog was found in the yeast genome. The MSP58 N‐terminal region contains serine‐rich clusters and its C‐terminal region has a coiled‐coil domain. In insect Sf9 cells, recombinant p120 and MSP58 proteins associated with each other, confirming the results of the yeast two‐hybrid assay. Deletion mutations revealed that the binding of MSP58 to p120 required a previously unrecognized coiled‐coil domain within the N‐terminal region of p120 and the C‐terminal region of MSP58 protein. Immunofluorescence indicated that the MSP58 protein is localized in microspherules in the nucleolus. Anti‐MSP58 Ig labeled nucleolar ’caps' when HeLa cells were treated with actinomycin D. When the MSP58 protein was overexpressed in COS‐7 cells, the nucleolus became irregularly enlarged, which suggests that MSP58 may affect the size and shape of the nucleolus.
Tập 253 Số 3 - Trang 734-742 - 1998
The MgATP-Dependent Protein Phosphatase and Protein Phosphatase 1 Have Identical Substrate Specificities
Tập 115 Số 1 - Trang 197-205
Phosphorylation of the Type‐II Regulatory Subunit of Cyclic‐AMP‐Dependent Protein Kinase by Glycogen Synthase Kinase 3 and Glycogen Synthase Kinase 5 The regulatory (RII ) subunit of type‐II cyclic‐AMP‐dependent protein kinase from bovine heart is phosphorylated at a significant rate in vitro by glycogen synthase kinase 3 and glycogen synthase 5, but not by glycogen synthase kinase 4 or phosphorylase kinase. The regulatory (RI ) subunit of type‐I cyclic‐AMP‐dependent protein kinase from rabbit skeletal muscle is not phosphorylated by any of these four protein kinases. Glycogen synthase kinase 3 phosphorylates two serine residues on the RII subunit located 44 and 47 amino acids from the N terminus of the polypeptide chain. Glycogen synthase kinase 5 phosphorylates serine‐74 and serine‐76. These sites are distinct from the residue phosphorylated by the catalytic subunit of cyclic‐AMP‐dependent protein kinase (serine‐95). The RII subunit, as normally isolated, contains 1.5–1.8 mol alkali‐labile phosphate per subunit. At least 80% of this phosphate (∼ 1.3 mol/subunit) is located in the thermolytic peptide containing serine‐74 and serine‐76, demonstrating that phosphorylation of the RII subunit by glycogen synthase kinase 5 occurs in vivo. Only small amounts of phosphate (∼ 0.1 mol/subunit) are associated with the thermolytic peptides containing serine‐44/serine‐47 and serine‐95. The phosphorylation sites on the RII subunit are organised in a strikingly similar manner to those of glycogen synthase, the amino acid sequences in the immediate vicinity of the phosphorylation sites showing a particular resemblance. These include the presence of a number of proline residues near the sites phosphorylated by glycogen synthase kinase 3, five consecutive acidic residues C‐terminal to the sites phosphorylated by glycogen synthase kinase 5, and two adjacent arginine residues just N‐terminal to the sites phosphorylated by the catalytic subunit of cyclic‐AMP‐dependent protein kinase. Glycogen synthase kinase 5 is very similar or identical to the enzyme that has been variously termed casein kinase TS, casein kinase 2, casein kinase G, casein kinase N‐II or troponin‐T kinase. The biological role of this enzyme is reviewed.
Tập 127 Số 3 - Trang 473-481 - 1982
Purification of Glycogen Synthase Kinase 3 from Rabbit Skeletal Muscle.. Copurification with the Activating Factor (FA)of the (Mg-ATP) Dependent Protein Phosphatase.
Tập 119 Số 3 - Trang 443-451 - 1981
Inhibition of Rat-Liver Acetyl-Coenzyme-A Carboxylase by Palmitoyl-Coenzyme A. Formation of Equimolar Enzyme-Inhibitor Complex
Tập 89 Số 1 - Trang 33-41 - 1978
Chemical Modification of the Mitochodrial <i>bc<sub>1</sub></i> by <i>N,N′</i> ‐Dicyclohexylcarbodiimide Inhibits Proton Translocation We report here that N,N/i′‐dicyclohexylcarbodiimide (DCCD) decreases the H2e stoichiometry of the mytochrome bc 1 complex from 308 ± 0.2 (10) to 201 ± 0.1 (8) but has only a minimal effect on the H2e ratio of cytochrome oxidase under the relatively mild condition used. The veffect on the bc 1 complex connot be explained by uncoupling, by inhibition of electron transport or by selective mitochondrial damage. We conclude that DCCD is an inhibitor of proton translocation within ther bc 1 complex. There are three possible explanation of this effect: (a) DCCD could alter the pathway of electron flow, (b) DCCD could prevent one of the proton translocation reations but not electrton transport, (c) DCCD could prevent the couduction of the translocated proton to the external phase.
Tập 132 Số 3 - Trang 595-601 - 1983
Redox‐linked proton translocation in the <i>b–c</i><sub>1</sub> complex from beef‐heart mitochondria reconstituted into phospholipid vesicles Possible involvement of polypeptides of b–c 1 complex of beef‐heart mitochondria in its redox and protonmotive activity has been investigated, by means of chemical modification of amino acid residues in the soluble as well as in the phospholipid‐reconstituted b–c 1 complex. Treatment of the enzyme with tetranitromethane (C(NO2 )4 ) or with ethoxyformic anhydride (EFA), that modify reversibly tyrosyl and hystidyl residues respectively, resulted in a marked inhibition of electron transport from reduced quinols to cytochrome c . This was accompanied, in b–c 1 reconstituted into phospholipid vesicles, by a parallel inhibition of respiratory‐linked proton translocation; the H+ /e− stoichiometry remained unchanged. Treatment of b–c 1 complex with DCCD, that specifically modifies carboxylic groups of glutammic or aspartic residues caused a marked depression of proton translocation in b–c 1 vesicles, under conditions where the rate of electron flow in the coupled state, was enhanced. As a consequence the H+ /e− stoichiometry was lowered. SDS gel electrophoresis and [14 C]DCCD‐labelling of the polypeptides of the b–c 1 complex showed a major binding of 14 C‐DCCD to the 8‐kDa subunit of the complex and possible cross‐linking, induced by DCCD treatment, of polypeptide(s) in the 8‐kDa band and the 12‐kDa band, with the Fe‐S protein of the complex, with the appearance of a new polypeptide band with an apparent molecular mass of about 40 kDa. Involvement of polypeptides of low molecular mass, for which no functional role was so far described, and possibly of the Fe‐S protein in the redox‐linked proton translocation in b–c 1 complex is suggested.
Tập 137 Số 3 - Trang 413-420 - 1983
Redox‐linked proton translocation in the <i>b–c</i><sub>1</sub> complex from beef‐heart mitochondria reconstituted into phospholipid vesicles A study is presented of the characteristics of redox‐linked proton translocation in the b–c 1 complex isolated from beef‐heart mitochondria and reconstituted into phospholipid vesicles. Measurements of the H+ /e− stoichiometry, with three different methods, show that four protons are released from the vesicles per 2e− flowing from quinols to cytochrome c , two of these protons formally deriving from scalar oxidation of quinols by cytochrome c . This H+ /e− stoicheiometry is independent of the initial redox state of the b–c 1 complex (fully reduced or oxidized) and the rate of electron flow through the complex. It does not change in the pH range 6.0–7.2, but declines to 1.5 going with pH from 7.2–8.3. This decrease is accompanied by enhancement of the rate of electron flow in the coupled state. Collapse of ΔΨ effected by valinomycin addition to turning‐over b–c 1 vesicles resulted in substantial oxidation of cytochrome b ‐566 and comparable reduction of cytochrome c 1 , with little oxidation of cytochrome b ‐562. Nigericin alone had no effect on the steady‐state redox levels of b and c cytochromes. Its addition in the presence of valinomycin caused oxidation of b cytochromes but no change in the redox state of cytochrome c 1 . Valinomycin alone caused a marked enhancement of the rate of electron flow through the complex. Nigericin alone was ineffective, but caused further stimulation of electron flow when added in the presence of valinomycin. The data presented are discussed in terms of two mechanisms: the Q cycle and a model based on combination of protonmotive catalysis by special bound quinone and proton conduction along pathways in the apoproteins.
Tập 137 Số 3 - Trang 405-412 - 1983
Systems biology: experimental design Experimental design has a long tradition in statistics, engineering and life sciences, dating back to the beginning of the last century when optimal designs for industrial and agricultural trials were considered. In cell biology, the use of mathematical modeling approaches raises new demands on experimental planning. A maximum informative investigation of the dynamic behavior of cellular systems is achieved by an optimal combination of stimulations and observations over time. In this minireview, the existing approaches concerning this optimization for parameter estimation and model discrimination are summarized. Furthermore, the relevant classical aspects of experimental design, such as randomization, replication and confounding, are reviewed.
Tập 276 Số 4 - Trang 923-942 - 2009
Patterns of Amino Acids near Signal‐Sequence Cleavage Sites According to the signal hypothesis, a signal sequence, once having initiated export of a growing protein chain across the rough endoplasmic reticulum, is cleaved from the mature protein at a specific site. It has long been known that some part of the cleavage specificity resides in the last residue of the signal sequence, which invariably is one with a small, uncharged side‐chain, but no further specific patterns of amino acids near the point of cleavage have been discovered so far. In this paper, some such patterns, based on a sample of 78 eukaryotic signal sequences, are presented and discussed, and a first attempt at formulating rules for the prediction of cleavage sites is made.
Tập 133 Số 1 - Trang 17-21 - 1983