共查询到20条相似文献,搜索用时 15 毫秒
1.
《Hydrobiologia》1995,302(2):177-178
Announcement
Eight International Symposium of the Biology of the Turbellaria 相似文献2.
Vincenzo Maione Francesca Cantini Mirko Severi Lucia Banci 《Biochimica et Biophysica Acta (BBA)/General Subjects》2018,1862(9):1980-1987
Background
The CIA2A protein, in complex with CIAO1, has been proposed to be exclusively implicated in the maturation of cytosolic aconitase. However, how the CIA2A-CIAO1 complex generates active aconitase is still unknown and the available structural information has not provided any crucial insights into the molecular function of CIA2A.Methods
In this work we have characterized the Fe/S cluster binding properties of CIA2A and of the CIA2A-CIAO1 complex via NMR, UV???vis absorption and EPR spectroscopies and we have investigated how the Fe/S cluster is transferred to inactive aconitase/IRP1 protein.Results
We found that an heterotrimeric species formed by two molecules of CIA2A and one of CIAO1 can bind one [4Fe-4S] cluster and that residue Cys90 of CIA2A is one of the cluster ligand. The holo trimeric complex is able to transfer the [4Fe-4S] cluster to apo-IRP1 thus generating the active form of aconitase.Conclusions and general significance
These findings, which highlight a functional role for CIA2A-CIAO1 complex in aconitase maturation, raises a broad interest and can have a high impact on the community studying metal trafficking and iron?sulfur protein biogenesis. The present study can provide solid bases for further investigation of the molecular mechanisms involving also other CIA machinery proteins. 相似文献3.
Tiina Nieminen Pyry I. Toivanen Nina Rintanen Tommi Heikura Suvi Jauhiainen Kari J. Airenne Kari Alitalo Varpu Marjomäki Seppo Ylä-Herttuala 《Biochimica et Biophysica Acta (BBA)/General Subjects》2014
Background
Vascular endothelial growth factors (VEGFs) are potential therapeutic agents for treatment of ischemic diseases. Their angiogenic effects are mainly mediated through VEGF receptor 2 (VEGFR2).Methods
Receptor binding, signaling, and biological efficacy of several VEGFR2 ligands were compared to determine their characteristics regarding angiogenic activity and vascular permeability.Results
Tested VEGFR2 ligands induced receptor tyrosine phosphorylation with different efficacy depending on their binding affinities. However, the tyrosine phosphorylation pattern and the activation of the major downstream signaling pathways were comparable. The maximal angiogenic effect stimulated by different VEGFR2 ligands was dependent on their ability to bind to co-receptor Neuropilin (Nrp), which was shown to form complexes with VEGFR2. The ability of these VEGFR2 ligands to induce vascular permeability was dependent on their concentration and VEGFR2 affinity, but not on Nrp binding.Conclusions
VEGFR2 activation alone is sufficient for inducing endothelial cell proliferation, formation of tube-like structures and vascular permeability. The level of VEGFR2 activation is dependent on the binding properties of the ligand used. However, closely similar activation pattern of the receptor kinase domain is seen with all VEGFR2 ligands. Nrp binding strengthens the angiogenic potency without increasing vascular permeability.General significance
This study sheds light on how different structurally closely related VEGFR2 ligands bind to and signal via VEGFR2/Nrp complex to induce angiogenesis and vascular permeability. The knowledge of this study could be used for designing VEGFR2/Nrp ligands with improved therapeutic properties. 相似文献4.
A. Jerome-Morais S. Bera W. Rachidi P.H. Gann A.M. Diamond 《Biochimica et Biophysica Acta (BBA)/General Subjects》2013
Background
Significant data supports the health benefits of selenium although supplementation trials have yielded mixed results. GPx-1, whose levels are responsive to selenium availability, is implicated in cancer etiology by human genetic data. Selenium's ability to alter the phosphorylation of the H2AX, a histone protein that functions in the reduction of DNA damage by recruiting repair proteins to the damage site, following exposure to ionizing radiation and bleomycin was investigated.Methods
Human cell lines that were either exposed to selenium or were transfected with a GPx-1 expression construct were exposed to ionizing radiation or bleomycin. Phosphorylation of histone H2AX was quantified by flow cytometry and survival by the MTT assay. Phosphorylation of the Chk1 and Chk2 checkpoint proteins was quantified by western blotting.Results
In colon-derived cells, selenium increases GPx-1 and attenuated H2AX phosphorylation following genotoxic exposures while the viability of these cells was unaffected. MCF-7 cells and transfectants that express high GPx-1 levels were exposed to ionizing radiation and bleomycin, and H2AX phosphorylation and cell viability were assessed. GPx-1 increased H2AX phosphorylation and viability following the induction of DNA damage while enhancing the levels of activated Chk1 and Chk2.Conclusions
Exposure of mammalian cells to selenium can alter the DNA damage response and do so by mechanisms that are dependent and independent of its effect on GPx-1.General significance
Selenium and GPx-1 may stimulate the repair of genotoxic DNA damage and this may account for some of the benefits attributed to selenium intake and elevated GPx-1 activity. 相似文献5.
《Antonie van Leeuwenhoek》1992,62(4):245-245
Editorial
Recent developments in the biology and systematics of the Lipomycetaceae 相似文献6.
7.
Stefanie Nowak Antonella Di Pizio Anat Levit Masha Y. Niv Wolfgang Meyerhof Maik Behrens 《Biochimica et Biophysica Acta (BBA)/General Subjects》2018,1862(10):2162-2173
Background
In humans, bitterness perception is mediated by ~25 bitter taste receptors present in the oral cavity. Among these receptors three, TAS2R10, TAS2R14 and TAS2R46, exhibit extraordinary wide agonist profiles and hence contribute disproportionally high to the perception of bitterness. Perhaps the most broadly tuned receptor is the TAS2R14, which may represent, because of its prominent expression in extraoral tissues, a receptor of particular importance for the physiological actions of bitter compounds beyond taste.Methods
To investigate how the architecture and composition of the TAS2R14 binding pocket enables specific interactions with a complex array of chemically diverse bitter agonists, we carried out homology modeling and ligand docking experiments, subjected the receptor to point-mutagenesis of binding site residues and performed functional calcium mobilization assays.Results
In total, 40 point-mutated receptor constructs were generated to investigate the contribution of 19 positions presumably located in the receptor's binding pocket to activation by 7 different TAS2R14 agonists. All investigated positions exhibited moderate to pronounced agonist selectivity.Conclusions
Since numerous modifications of the TAS2R14 binding pocket resulted in improved responses to individual agonists, we conclude that this bitter taste receptor might represent a suitable template for the engineering of the agonist profile of a chemoreceptive receptor.General significance
The detailed structure-function analysis of the highly promiscuous and widely expressed TAS2R14 suggests that this receptor must be considered as potentially frequent target for known and novel drugs including undesired off-effects. 相似文献8.
《Entomological Review》2009,89(9):1207-1208
Memory
In Memory of the Editor Editorial Board of The Entomologicheskoe Obozrenie 相似文献9.
10.
Group of the pupils 《Human physiology》2005,31(4):490-491
Chronicle
On the 100th Anniversary of the Birth of G.V. Gershuni 相似文献11.
Takafumi Kawai Hideki AbeKen-ichi Wakabayashi Yoshitaka Oka 《Biochimica et Biophysica Acta (BBA)/General Subjects》2009,1790(12):1681-1688
Background
The olfactory nonsensory cells contribute to the maintenance of normal functions of the olfactory epithelium (OE). Specifically, the ciliated nonsensory cells of teleosts play important roles in the odorant detection by OE in aqueous environment. Their cilia show strong beating activities and cause water flow at the OE surface, making the detection of odorants by OE more efficient. Because intracellular Ca2+ level has been reported to play an important role in ciliary beating, the ciliary beating activity may be regulated by intracellular Ca2+ dynamics of these ciliated nonsensory cells.Methods
We performed Ca2+ imaging experiments to analyze the Ca2+ dynamics in acutely dissociated OE cells of the goldfish. Furthermore, we examined the contribution of the Ca2+ dynamics to the ciliary beating frequency (CBF) at the surface of the intact OE.Results
Olfactory nonsensory cells showed both spontaneous intracellular Ca2+ oscillations and propagating intercellular Ca2+ waves. Application of 2-aminoethoxydiphenylborate (2-APB), which antagonizes IP3-induced Ca2+ release from intracellular stores suppressed these Ca2+ oscillations. Furthermore, 2-APB application to the intact OE lamellae resulted in the decrease of CBF at the surface of the OE.Conclusions
These results indicate that spontaneous intracellular calcium oscillations persistently up-regulate the ciliary beating at the surface of the OE in teleosts.General significance
Ciliary beating activity at the surface of OE can be regulated by the Ca2+ dynamics of olfactory nonsensory cells. Because this ciliary movement causes inflow of external fluid into the nostril, this regulation is suggested to influence the efficiency of odorant detection by OE. 相似文献12.
Background
Guinea pigs are considered to be genetically adapted to a high altitude environment based on the consistent finding of a high oxygen affinity of their blood.Methodology/Principal Findings
The crystal structure of guinea pig hemoglobin at 1.8 Å resolution suggests that the increased oxygen affinity of guinea pig hemoglobin can be explained by two factors, namely a decreased stability of the T-state and an increased stability of the R2-state. The destabilization of the T-state can be related to the substitution of a highly conserved proline (P44) to histidine (H44) in the α-subunit, which causes a steric hindrance with H97 of the β-subunit in the switch region. The stabilization of the R2-state is caused by two additional salt bridges at the β1/β2 interface.Conclusions/Significance
Both factors together are supposed to serve to shift the equilibrium between the conformational states towards the high affinity relaxed states resulting in an increased oxygen affinity. 相似文献13.
Satomi Nadanaka Hiroshi Kitagawa 《Biochimica et Biophysica Acta (BBA)/General Subjects》2018,1862(4):791-799
Background
Heparan sulfate proteoglycans are ubiquitously expressed on cell surfaces and in extracellular matrices, and are engaged in heparin-binding growth factor-related signal transduction. Thus, changes in the amounts, structures, and chain lengths of heparan sulfate have profound effects on aspects of cell growth controlled by heparin-binding growth factors such as FGF2. Exostosin glycosyltransferases (EXT1, EXT2, EXTL1, EXTL2, and EXTL3) control heparan sulfate biosynthesis, and the expression levels of their genes regulate the amounts, chain lengths, and sulfation patterns of heparan sulfate. Unlike EXT1, EXT2, and EXTL3, EXTL2 functions chain termination of heparan sulfate. Here, we examined the importance of EXTL2 in FGF2-dependent signaling.Methods
We investigated heparan sulfate biosynthesis and FGF2 signaling using four cell lines, EXT1-deficient cells, EXT2-, EXTL2-, or EXTL3-knockdown cells, by HPLC, qRT-PCR, flow cytometry, and western blotting.Results
Reduced expression of either EXT1, EXT2, or EXTL3 decreased heparan sulfate biosynthesis, and consequently suppressed the FGF2-dependent proliferation of mouse L fibroblasts. In contrast, although knockdown of EXTL2 increased the amounts of heparan sulfate, FGF2-dependent proliferation was significantly inhibited because the increased heparan sulfate enhanced the incorporation of FGF2 into the cells.Conclusions
EXTL2 controls FGF2 signaling through regulation of heparan sulfate biosynthesis in a manner distinct from that of other exostosins.General significance
This study provides new insights into the regulatory mechanisms of FGF2 signaling by EXTL2. 相似文献14.
Background
Epidemiological and experimental evidence that support the correlation between Type 2 diabetes mellitus (T2D) and increased risks of colorectal cancer formation have led us to hypothesize the existence of molecular crosstalk between insulin and canonical Wnt signaling pathways. Insulin was shown to stimulate Wnt target gene expression, utilizing the effector of the Wnt signaling pathway. Whether insulin affects expression of components of Wnt pathway has not been extensively examined.Methods
cDNA microarray was utilized to assess the effect of insulin on gene expression profile in the rat intestinal non-cancer IEC-6 cell line, followed by real-time RT-PCR, Western blotting and reporter gene analyses in intestinal cancer and non-cancer cells.Results
Insulin was shown to alter the expression of a dozen of Wnt pathway related genes including TCF-4 (= TCF7L2) and frizzled- (Fzd-4). The stimulatory effect of insulin on TCF-4 expression was then confirmed by real-time RT-PCR, Western blotting and luciferase reporter analyses, while the activation on Fzd-4 was confirmed by real-time PCR.General significance
Our observations suggest that insulin may crosstalk with the Wnt signaling pathway in a multi-level fashion, involving insulin regulation of the expression of Wnt target genes, a Wnt receptor, as well as mediators of the Wnt signaling pathway. 相似文献15.
Masami Watanabe 《Neurochemical research》2003,28(7):1063-1144
Abstract List
Abstracts of Communications of the 45th Annual Meeting of the Japanese Society for Neurochemistry 相似文献16.
17.
《Molecular Biology》2011,45(4):691-692
Chronicle
On the 75th anniversary of the birth of L. L. Kiselev 相似文献18.
《Neurochemical research》2000,25(7):983-1066
Summary List
Abstracts of Communications of the 1999 Meeting of the Japanese Society for Neurochemistry (JSN) 相似文献19.
Lynda Blayney Konrad Beck Ewan MacDonald Leon D'Cruz Michail Nomikos Julia Griffiths Angelos Thanassoulas George Nounesis F. Anthony Lai 《Biochimica et Biophysica Acta (BBA)/General Subjects》2013
Background
This study was designed to determine whether the cardiac ryanodine receptor (RyR2) central domain, a region associated with catecholamine polymorphic ventricular tachycardia (CPVT) mutations, interacts with the RyR2 regulators, ATP and the FK506-binding protein 12.6 (FKBP12.6).Methods
Wild-type (WT) RyR2 central domain constructs (G2236to G2491) and those containing the CPVT mutations P2328S and N2386I, were expressed as recombinant proteins. Folding and stability of the proteins were examined by circular dichroism (CD) spectroscopy and guanidine hydrochloride chemical denaturation.Results
The far-UV CD spectra showed a soluble stably-folded protein with WT and mutant proteins exhibiting a similar secondary structure. Chemical denaturation analysis also confirmed a stable protein for both WT and mutant constructs with similar two-state unfolding. ATP and caffeine binding was measured by fluorescence spectroscopy. Both ATP and caffeine bound with an EC50 of ~ 200–400 μM, and the affinity was the same for WT and mutant constructs. Sequence alignment with other ATP binding proteins indicated the RyR2 central domain contains the signature of an ATP binding pocket. Interaction of the central domain with FKBP12.6 was tested by glutaraldehyde cross-linking and no association was found.Conclusions
The RyR2 central domain, expressed as a ‘correctly’ folded recombinant protein, bound ATP in accord with bioinformatics evidence of conserved ATP binding sequence motifs. An interaction with FKBP12.6 was not evident. CPVT mutations did not disrupt the secondary structure nor binding to ATP.General significance
Part of the RyR2 central domain CPVT mutation cluster, can be expressed independently with retention of ATP binding. 相似文献20.