Relevant bibliographies by topics / Calcium-binding proteins

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Calcium-binding proteins'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Calcium-binding proteins"

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Kerkut, G. A. "Calcium and calcium binding proteins." Comparative Biochemistry and Physiology Part A: Physiology 92, no. 1 (January 1989): 152. http://dx.doi.org/10.1016/0300-9629(89)90768-8.

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Mochida, Sumiko. "Calcium Channels and Calcium-Binding Proteins." International Journal of Molecular Sciences 24, no. 18 (September 19, 2023): 14257. http://dx.doi.org/10.3390/ijms241814257.

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Signals of nerve impulses are transmitted to excitatory cells to induce the action of organs via the activation of Ca2+ entry through voltage-gated Ca2+ channels (VGCC), which are classified based on their activation threshold into high- and low-voltage activated channels, expressed specifically for each organ [...]
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Heizmann, Claus W. "Intracellular Calcium-Binding Proteins." Journal of Cardiovascular Pharmacology 8 (1986): S7—S12. http://dx.doi.org/10.1097/00005344-198600088-00003.

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Maurer, Patrik, Erhard Hohenester, and Jürgen Engel. "Extracellular calcium-binding proteins." Current Opinion in Cell Biology 8, no. 5 (October 1996): 609–17. http://dx.doi.org/10.1016/s0955-0674(96)80101-3.

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Williams, R. J. P. "The calcium-binding proteins." Trends in Biochemical Sciences 16 (January 1991): 206. http://dx.doi.org/10.1016/0968-0004(91)90084-9.

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Michetti, Fabrizio. "The calcium-binding proteins." Giornale botanico italiano 127, no. 3 (January 1993): 470–73. http://dx.doi.org/10.1080/11263509309431029.

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Sohar, Istvan, John W. C. Bird, and Pamela B. Moore. "Calcium-dependent proteolysis of calcium-binding proteins." Biochemical and Biophysical Research Communications 134, no. 3 (February 1986): 1269–75. http://dx.doi.org/10.1016/0006-291x(86)90387-6.

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Lewit-Bentley, Anita, and Stéphane Réty. "EF-hand calcium-binding proteins." Current Opinion in Structural Biology 10, no. 6 (December 2000): 637–43. http://dx.doi.org/10.1016/s0959-440x(00)00142-1.

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Hutton, J. C. "Calcium-binding proteins and secretion." Cell Calcium 7, no. 5-6 (December 1986): 339–52. http://dx.doi.org/10.1016/0143-4160(86)90037-0.

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Hermann, A., T. L. Pauls, and C. W. Heizmann. "Calcium-binding proteins inAplysia neurons." Cellular and Molecular Neurobiology 11, no. 4 (August 1991): 371–86. http://dx.doi.org/10.1007/bf00711419.

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Dissertations / Theses on the topic "Calcium-binding proteins"

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Castiblanco, Alfonso Adriana Patricia. "Expression and purification of engineered calcium binding proteins." unrestricted, 2009. http://etd.gsu.edu/theses/available/etd-04212009-135436/.

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Thesis (M.S.)--Georgia State University, 2009.
Title from file title page. Jenny J. Yang, committee chair; Zhi-Ren Liu, Gangli Wang, Giovanni Gadda, committee members. Description based on contents viewed June 30, 2009. Includes bibliographical references (p. 116-119).
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Castiblanco, Alfonso Adriana Patricia. "Expression and purification of engineered calcium binding proteins /." unrestricted, 2006. http://etd.gsu.edu/theses/available/etd-04212009-135436/.

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Thesis (M.S.)--Georgia State University, 2009.
Jenny J. Yang, committee chair; Zhi-Ren Liu, Gangli Wang, Giovanni Gadda, committee members. Typescript. Includes bibliographical references (leaves 101-104). Also available via the World Wide Web.
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Prichard, Lisa. "The role of the IQ motif, a protein kinase C and calmodulin regulatory domain, in neuroplasticity, RNA processing, and RNA metabolism /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6302.

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Castiblanco, Adriana P. "Expression and Purification of Engineered Calcium Binding Proteins." Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/chemistry_theses/20.

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Previous studies in Dr. Yang’s laboratory have established a grafting, design, and subdomain approach in order to investigate the properties behind Ca2+-binding sites located in Ca2+-binding proteins by employing engineered proteins. These approaches have not only enabled us to isolate Ca2+-binding sites and obtain their Ca2+-binding affinities, but also to investigate conformational changes and cooperativity effects upon Ca2+ binding. The focus of my thesis pertains to optimizing the expression and purification of engineered proteins with tailored functions. Proteins were expressed in E. coli using different cell strains, vectors, temperatures, and inducer concentrations. After rigorous expression optimization procedures, proteins were further purified using chromatographic and/or refolding techniques. Expression and purification optimization of proteins is essential for further analyses, since the techniques used for these studies require high protein concentrations and purity. Evaluated proteins had yields between 5-70 mg/L and purities of 80-90% as confirmed by SDS-PAGE electrophoresis.
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Campbell, Joanne A. "Calcium-binding, low salt soluble human aortic proteins." Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388054.

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Maddox, Katherine. "A characterization of the calcium- and integrin-binding protein family." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 112 p, 2009. http://proquest.umi.com/pqdweb?did=1654487501&sid=7&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Gilchrist, James Stuart Charles. "Calcium regulation of calcium transport by sarcoplasmic reticulum." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30880.

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The sarcoplasmic reticulum (SR) of skeletal muscle is an intracellular membraneous network that, through the cyclical release and re-uptake of Ca²⁺ into and from, respectively, the cytoplasmic space, regulates myofilament shortening and, therefore, muscle contraction. SR derived from the terminal cisternae (HSR) demonstrates the property of Ca²⁺-induced Ca²⁺ release. Upon attainment of a threshold intralumenal Ca²⁺ load, application of a small pulse of extralumenal Ca²⁺ stimulates the release of a pool of intralumenal Ca²⁺ via the ligand gated Ca²⁺ permeable pore of the Ca²⁺ release channel/ryanodine receptor complex. It was hypothesised that intralumenal Ca²⁺ regulates the opening of the release channel. HSR vesicles were purified from skeletal and cardiac muscle by a novel technique. Structural characterisation of these membranes demonstrated an enrichment of harvested fractions in the Ca²⁺ release channel and the intralumenal Ca²⁺ binding protein, calsequestrin. In radiometric studies, skeletal HSR vesicles were shown to bind ryanodine with high capacity at both low and high affinity sites, with 2 fold stimulation of Ca²⁺ accumulation by the polyorganic cation Ca²⁺ channel blocker, ruthenium red. HSR vesicles passively loaded Ca²⁺. Passive loading of HSR vesicles with Ca²⁺ was found to be non-linearly dependent upon the concentration of Ca²⁺ within the loading medium. This suggested the presence of 2 intralumenal Ca²⁺ binding sites with different affinities for Ca²⁺. A spectroscopic dual-wavelength assay of Ca²⁺ release was developed that took advantage of peculiar spectral properties of the metallochromic sensitive dye Antipyrylazo III. In the presence of mM MgATP and mM Mg2+ the initial fast phase of HSR Ca²⁺ was well resolved. Evidence was presented that initial rapid uptake was associated with high affinity binding to an intralumenal compartment. Ca²⁺ -induced Caz+ release was shown to occur with a threshold loading of intralumenal Ca²⁺. The intralumenal Ca²⁺ threshold for Ca²⁺-induced Ca²⁺ release was decreased in the presence of ryanodine. Ryanodine induced Ca²⁺ release was also dependent upon the amount of intralumenal Ca²⁺. Ryanodine was also shown to inhibit sustained Ca²⁺-induced Ca²⁺ release by apparent inhibition of the binding of Ca²⁺ to intralumenal sites. These results suggested that junctional state transitions of the Ca²⁺ channel and calsequestrin were interdependent. Purified mM and mM Ca²⁺ activated neutral protease isoforms selectively cleaved the Ca²⁺ channel into 410 and 150kDa peptides with limited proteolysis. This was demonstrated in both HSR vesicles and the purified Ca²⁺ release channel. A novel 88kDa protein was also shown to be fragmented by both CANP isoforms. The identity of this prominent HSR associated protein remains obscure. CANP fragmentation of HSR protein elevated passive and active 4^Ca²⁺ loading in vesicles. This indicated that selective structural modification of the cytoplasmic portion of the release channel modified the comformational states of a intralumenal Ca²⁺ binding compartment in HSR vesicles. In spectroscopic studies, CANP proteolysis of HSR proteins increased the sensitivity to Ca²⁺ and ryanodine-induced Ca²⁺ release through decreases in the required intralumenal Ca²⁺ threshold for release. These functional alterations coincided with apparent single site cleavage of the release channel. Further proteolysis of the initial 410 and 150kDa peptides was without further significant effect upon function. Based upon the hypothesis that primary sequences rich in proline (P), glutamate (E), aspartate (D), serine (S) and threonine (T) (PEST regions) are recognition sites for CANP binding to substrates, a search for PEST regions within the Ca²⁺ channel was undertaken. It was tentatively proposed that two PEST regions near the N-terminal of the Caz release channel may represent sites close to the CANP cleavage site. The results of this work were discussed in relation to a possible role of Ca²⁺-induced Ca²⁺ release in regulating the patterning of Ca²⁺ cytosolic transients. The frequency and amplitude of cytosolic Ca²⁺ transients appear to be important in regulating protein expression. The requirement of intralumenal Ca²⁺-induced Ca²⁺ release may be a means by which the cyclical uptake and release of Ca²⁺ during muscle relaxation and contraction can be coordinated. This coordination may define the patterning of cytosolic Ca²⁺ transients. The increased sensitivity to Ca²⁺-induced Ca²⁺ release by HSR after CANP treatment may represent a means by which the patterning of cytosolic Ca²⁺ transients can be altered to effect changes in protein synthesis.
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Agah, Sayeh. "Parvalbumin stability and calcium affinity : the impact of the n-terminal domain /." Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?3164486.

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Ayar, Ahmet. "An investigation of calcium-induced calcium-release (CICR) in cultured rat sensory neurones." Thesis, University of Aberdeen, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285521.

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In this study the mechanisms of Ca2+-induced-Ca2+-release, effects of membrane depolarizations and the actions of pharmacological intracellular Ca2+-modulators were examined in cultured rat dorsal root ganglion (DRG) neurones. The whole cell configuration of the patch clamp technique was used to record action potentials, action potential after-potentials and voltage-activated calcium currents, (ICa), calcium-activated chloride currents, (ICI(Ca)), and non-selective cation currents, (ICAN), under current and voltage clamp recording conditions, respectively. A sub population of DRG neurones expressed action potential after-depolarizations and ICI(Ca) tail currents which were due to activation of Ca2+-activated Cl- channels as a result of Ca2+ entry. ICAN was dominantly activated due to Ca2+ release from intracellular stores evoked by pharmacological Ca2+-releasing agents such as caffeine, ryanodine and dihydrosphingosine. Calcium-activated conductances were identified by estimating reversal potentials of the activated currents, using selective pharmacological blockers and extracellular ionic replacement studies. Calcium-dependence of activated currents was also examined by using high concentration of intracellular Ca2+ buffer, EGTA, to prevent elevation of intracellular Ca2+-levels and by rapidly buffering raised intracellular Ca2+ using intracellular 'caged Ca2+ chelator', diazo-2. The involvement of intracellular Ca2+- stores was examined by performing experiments in Ca2+-free extracellular recording medium and pharmacologically inhibiting release of Ca2+ from intracellular stores, using dantrolene. Ryanodine had complex actions on DRG neurones, which reflected its ability to mobilize Ca2+, deplete Ca2+ stores, and inhibit Ca2+ release channels. Ryanodine inhibited action potential after-depolarizations and ICI(Ca) tail currents by interacting with intracellular stores and preventing amplification of Ca2+ signalling by CICR. It was found that CICR observed under physiological conditions in rat DRG neurones involves intracellular Ca2+ stores which were sensitive to ryanodine. In addition to ryanodine sensitivity these intracellular Ca2+ stores could be mobilized by caffeine and dihydrosphingosine.
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Skene, Robert J. "Crystallographic studies of calcium-binding proteins, aeromonas salmonicida surface array protein and calmodulin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ64978.pdf.

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Books on the topic "Calcium-binding proteins"

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Permyakov, Eugene A., and Robert H. Kretsinger. Calcium Binding Proteins. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470872390.

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Permi︠a︡kov, E. A. Calcium binding proteins. Hoboken, N.J: Wiley, 2010.

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P, Thompson Marvin, ed. Calcium-binding proteins. Boca Raton, FL: CRC Press, 1988.

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Gerday, Charles, L. Bolis, and R. Gilles, eds. Calcium and Calcium Binding Proteins. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73042-9.

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Heizmann, Claus W., ed. Novel Calcium-Binding Proteins. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8.

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J, Vogel Hans, ed. Calcium-binding protein protocols. Totowa, NJ: Humana Press, 2002.

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Heizmann, Claus W., ed. Calcium-Binding Proteins and RAGE. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-230-8.

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Evans, Lucy Jean Amanda. Aluminium and calcium binding proteins. Manchester: University of Manchester, 1992.

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Pauls, Thomas Lawrence. Metal-binding properties and cation-dependent conformational changes in rat parvalbumin wild-type and mutant proteins. Konstanz: Hartung-Gorre, 1995.

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Blum-Moonesinghe, Janaki Kumari. Expression of calcium-binding proteins in chemically transformed rat fibroblasts. Konstanz: Hartung-Gorre Verlag, 1993.

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Book chapters on the topic "Calcium-binding proteins"

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Balasubramanian, Doraivajan, and Yogendra Sharma. "Calcium-Binding Crystallins." In Novel Calcium-Binding Proteins, 361–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_20.

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Dwivedi, Meenakshi, and Joohong Ahnn. "Calcium-Binding Proteins." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_778-2.

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Yáñez, Matilde, José Gil-Longo, and Manuel Campos-Toimil. "Calcium Binding Proteins." In Advances in Experimental Medicine and Biology, 461–82. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2888-2_19.

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Dwivedi, Meenakshi, and Joohong Ahnn. "Calcium-Binding Proteins." In Encyclopedia of Cancer, 724–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_778.

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Wasserman, Robert H. "Calcium-Binding Proteins: Past, Present and Future." In Novel Calcium-Binding Proteins, 7–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_1.

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Kuźnicki, Jacek. "Calcyclin, from Gene to Protein." In Novel Calcium-Binding Proteins, 157–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_10.

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Murphy, L. C., Y. Gong, and R. E. Reid. "Cloning and Characterization of a cDNA Encoding a Highly Conserved Ca2+-Binding Protein, Identified by an Anti-Prolactin Receptor Antibody." In Novel Calcium-Binding Proteins, 169–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_11.

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Longbottom, David, and Veronica van Heyningen. "The Calgranulins, Members of the S-100 Protein Family: Structural Features, Expression, and Possible Function." In Novel Calcium-Binding Proteins, 191–223. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_12.

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Lagasse, Eric. "MRP8 and MRP14, Two Calcium-Binding Proteins Expressed During Myelopoiesis." In Novel Calcium-Binding Proteins, 225–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_13.

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Brüggen, Josef, and Nico Cerletti. "Distribution of the Calcium-Binding Proteins MRP-8 and MRP-14 in Normal and Pathological Conditions: Relation to the Cystic Fibrosis Antigen." In Novel Calcium-Binding Proteins, 237–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76150-8_14.

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Conference papers on the topic "Calcium-binding proteins"

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Steiner, Robert F., and Lynn Norris. "Fluorescence Dynamics Of Calcium-Binding Proteins." In OE LASE'87 and EO Imaging Symp (January 1987, Los Angeles), edited by E. R. Menzel. SPIE, 1987. http://dx.doi.org/10.1117/12.966939.

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KÖhlin, A., and J. Stenflo. "HIGH AFFINITY CALCIUM BINDING TO DOMAINES OF PROTEIN C THAT ARE HOMOLOGUS TO THE EPIDERMAL GROWTH FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643645.

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In addition to γ-carboxyglutamic acid (Gla)-dependent calcium binding all of the vitamin K-dependent plasma proteins, except prothrombin, have one or two high affinity calcium binding sites that do not require the Gla residues. A common denominator among these proteins (factors IX, X, protein C, protein Z and protein S) is that they have domaines that are homologus to the epidermal growth factor (EGF) precursor. In factors VII,IX,X, protein C and in protein Z the aminoterminal of two EGF homology regions contain one residue of β-hydroxyaspartic acid (Hya) whereas in protein S the aminoterminal EGF homology region contains Hya and the three following contain one β-hydroxyasparagine residue each.In an attempt to elucidate the role of the EGF homology regions in the Gla independent calcium binding we have isolated a tryptic fragment (residue 44-138) from the light chain of human protein C. The fragment was isolated using a monoclonal antibody that recognizes a calcium ion stabilized epitope that is expressed both in intact protein C and in protein C lacking the Gla domaine.The antibody bound the isolated EGF homology region in the presence of calcium ions but not in EDTA containing buffer. A calcium ion titration showed half maximal binding at approximately 200 μM Ca2+. The metal ion induced conformational change in the isolated fragment was also studied with affinity purified rabbit antibodies against Gla domainless protein C. Antibodies that bound in the presence of calcium ions and that could be eluted with EDTA recognized the metal ion induced conformational change in the isolated EGF homology domain. Our results suggest that one or both of the EGF homology regions are involved in the Gla-independent high affinity calcium binding in the vitamin K-dependent plasma proteins.
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"Calcium binding Proteins as Predictive Biomarkers for Vascular Disorders." In 3rd INTERNATIONAL CONFERENCE ON BIOLOGICAL RESEARCH AND APPLIED SCIENCE. Jinnah University for Women, Karachi,Pakistan, 2023. http://dx.doi.org/10.37962/ibras/2023/30.

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Church, W., T. Messier, P. Howard, J. Amiral, D. Meyer, and K. Mam. "A SHARED EPITOPE ON HUMAN PROTEIN C, FACTOR X, FACTOR VII, AND PROTTOBIN DEFINED BY A MONOCLONAL ANTIBODY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643937.

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A monoclonal antibody prepared against hunan protein C (HPC) was found to react with several other vitamin K-dependent blood proteins. Using a competitive inhibition solid-phase radioinminoassay with HPC, binding of 125I-HPC to the antibody was inhibited by purified prothrombin, Factor X, and Factor VII in addition to protein C. Other vitamin K-dependent proteins including Factor IX, protein S, and bone-GLA protein did not compete for binding of 125I-HPC to the antibody. The effect of calciun ion on the binding of antibody to 125I-HPC was examined in a solid-phase imnunoassay system with the antibody bound to rabbit anti-mouse inminoglobulin adsorbed to microtiter plates. In the presence of 5 mM calciun ion, radiolabeled protein C did not bind to the antibody; radiolabeled protein C did bind, however, in the presence of 5 nM EDTA suggesting that the epitope is expressed only after removal of calciun ion. The antibody bound to prothrombin and to decarboxylated prothrombin after adsorption of the antigens onto nitrocellulose indicating that the presence of GLA was not required for antibody binding. Iimunoblotting of proteins which were reduced, the peptides separated by SDS-PAGE, and transferred to nitrocellulose showed that the antibody reacts with a determinant found on the light chains of protein C and Factor X and with prothrombin Fragment 1. Comparison of the protein sequences of protein C light chain, Factor X light chain, Factor VII, and prothrombin Fragment 1 identified a segment of amino acid sequence that is highly conserved in all four proteins and might contain the antigenic site. The monoclonal antibody thus defines an antigenic determinant which is masked by calcium ion and is found on the surface of several related, yet different coagulation proteins. This antibody should prove useful in understanding the evolutionary relationships amongst the vitamin K-dependent proteins and also in understanding the effect of calcium ion on the structure of protein C, Factor X, prothrombin, Factor VII and possibly other related proteins. (Supported by NIH grant MHLBI HL35058)
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Timmons, Sheila, and Jack Hawiger. "REGULATION OF PLATELET RECEPTORS FOR FIBRINOGEN AND VON WILLEBRAND FACTOR BY PROTEIN KINASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644674.

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Positive and negative regulation of platelet receptors for adhesive proteins, fibrinogen (F) and von Willebrand Factor (vWF) determines whether binding of these ligands will or will not take place. We have shown previously that ADP stimulates and cyclic AMP inhibits binding of F and vWF to human platelets. Now we show that positive regulation of F and vWF binding to platelets via the glycoprotein 11b/1111a complex is dependent on platelet Protein Kinase C, a calcium- and phospholipid-dependent enzyme. A potent activator of Protein Kinase C, phorbol-12-myristoyl-13-acetate (PMA) induced saturable and specific binding of F and vWF which was inhibited by synthetic peptides, gamma chain .dodecapeptide (gamma 400-411) and RGDS. The phosphorylation of 47kDa protein (P47), a marker of Protein Kinase C activation in platelets, preceded binding of F and vWF induced with PMA as well as with ADP and thrombin. Sphingosine, an inhibitor of Protein Kinase C, blocked binding of F and vWF to platelets stimulated with PMA, ADP, and thrombin. Inhibition of binding was concentration-dependent and it was accompanied by inhibition of platelet aggregation. Thus, stimulation of Protein Kinase C is required for exposure of platelet receptors for adhesive proteins whereas inhibition of Protein Kinase C prevents receptorexposure. Protein Kinase C fulfills the role of an intraplatelet signal transducer, regulating receptors for adhesive proteins, and constitutes a target for pharmacologic modulation of the adhesive interactions of platelets.
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Lan, Jianqing, and Robert F. Steiner. "Studies of the interactions between calcium-binding proteins and phosphofructokinase using fluorescent probes." In OE/LASE '90, 14-19 Jan., Los Angeles, CA, edited by Joseph R. Lakowicz. SPIE, 1990. http://dx.doi.org/10.1117/12.17749.

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Koller, E., and F. Koller. "LIPOPROTEIN BINDING TOHUMAN PLATELETS IS LOCATED AT GPIIb/IIIa COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643702.

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Human Platelets possess specific binding sites for low density lipoproteins (LDL) and high density lipoproteins(HDL)(1). Binding of both classes of plasma lipoproteins, though competitive, has been shown by several groups to facilitate platelet activation.Isolated washed platelets occasionally aggregate upon addition of high concentrations of LDL even in the absence of known platelet activators. The proteins responsible for this binding have been visualized by ligand blotting (2). Both types of ligand specifically bind to two glycoproteins with molecular weights of 135 and 115 kD, respectively. The conditions of binding to these two proteins, however, markedly differ from those known for other lipoprotein receptors.Following extensive purification, these two species are still present at concentrations relative to each other that depend markedly on the conditions of purification. The purified, solubilized receptor was tested under various conditions, including in the absence and presence of calcium, after disulfide-reduction, and following chymotrypsin digestion. In parallel experiments, the same preparations were tested with respect to binding of fibrinogen, different lectins, and thealloantibody anti-PlAI . The results strongly support the assumption, that the two protein bands associated with lipoprotein binding are constituents of the GP-IIb/IIIa complex.These first results may have greatimplications for our understanding ofthe mechanism by which lipoproteins facilitate platelet stimulation.
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Monroe, D. M., D. W. Deerfield, D. L. Olson, T. N. Stewart, H. R. Roberts, R. G. Hiskey, and L. G. Pedersen. "BINDING OF CALCIUM TO HUMAN AND BOVINE FACTOR X." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643835.

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Human and bovine factor X contain 11 and 12 glutamyl residues respectively within the first forty amino terminal residues that are posttranslationally modified to y-carboxyglutamyl (Gla) residues. Calcium binding to these Gla residues and at other sites is critical for activity in factor X. We have measured calcium binding to human factor X by equilibrium dialysis for the first time. We have also re-examined calcium binding to bovine factor X in order to compare the two species. Factor X (10 μM) was incubated with 45Ca in 20 mM Tris (pH 7.5), 100 mM NaCl in a half cell separated by a 12-14000 molecular weight fast-equilib-rium disk membrane at 25°C for 24 hours. Four aliquots (100 μL each) were removed from each side of the cell and counted. Data were analyzed with a variety of models that allow for more than one class of binding site and for cooperativity among binding sites. Calcium binding to bovine factor X was best simulated by a model that assumes 1 very tight site, 3 cooperative tight sites, and 18 equivalent, non-interacting sites. Based on data from des(Gla)factor X, the first site is probably a high affinity non-Gla binding site. Our results differ from two previously published reports that indicated either 1 tight and 39 loose noncooperative sites (R.H. Yue & M.M. Gertler (1978) Thrombos. Haemostas. (Stuttg.) 40, 350) or 20 calcium binding sites with the first 4 being cooperative (M.J. Lindhout & H.C. Hemker (1978) Biochimica Biophysica Acta 533, 318). Our data on human factor X fit the same model as used for bovine factor X; however, coop-erativity is less in the 3 cooperative sites. Shown below are the first six thermodynamic equilibrium constants derived from a Scatchard analysis of binding data (values are M−1).Both proteins demonstrate the same total number of binding sites and essentially the same value for the first, tight binding site. Bovine factor X exhibits cooperativity, whereas human factor X has reduced cooperativity.
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Porcino, Caterina. "NEUROTROPHINS, TRK-RECEPTORS AND CALCIUM BINDING PROTEIN LOCALIZATION IN MECHANOSENSORY SYSTEMS AND RETINA OF NOTHOBRANCHIUS GUENTHERI." In Dubai International Conference on Research in Life-Science & Healthcare, 22-23 February 2024. Global Research & Development Services, 2024. http://dx.doi.org/10.20319/icrlsh.2024.4243.

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Neurotrophins are growth factors playing a crucial role in the survival, differentiation, development, and plasticity of neurons. They exert their effects by binding to specific receptors (Trks) in the central and peripheral nervous systems, including sensory organs. Calcium-binding proteins (CaBPs) are also present in these systems. They are involved in essential physiological functions related to calcium ions, such as nerve impulse transmission, neurogenesis, synaptic plasticity, and transmission. Further, CaBPs are supposed to be involved in neuron protection. Neurotrophins and CaBPs perform their roles in various vertebrates, including fish. Nonetheless, based on existing knowledge, there is no record of the presence of neurotrophins in the sensory organs of Nothobranchius guentheri. Due to its relatively short lifespan, N. guentheri has emerged as a valuable model for aging studies, holding significant relevance in the field of translational medicine. As a teleost, its sensory systems share several morphological and functional similarities with mammals, including humans. However, unlike mammals, fish sensory organs keep the regeneration capability. In light of this, the present research sought to identify the neurotrophin-receptor systems and calcium-binding proteins (CaBPs) in the mechanosensory organs and retina of N. guentheri. Utilizing immunoperoxidase, single, and double immunofluorescence methods, the investigation unveiled the localization of neurotrophins and CaBPs in the inner ear, neuromasts of the lateral line system, and retinal cells of N. guentheri. This newfound information indicates the influence of these proteins on the biology of N. guentheri, reinforcing its suitability as a model for aging studies. The implications of these findings could significantly contribute to research on age-related neurodegeneration within the realm of translational medicine.
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Dahiback, Bjorn, Ake Lundwall, Andreas Hillarp, Johan Malm, and Johan Stenflo. "STRUCTURE AND FUNCTION OF VITAMIN K-DEPENDENT PROTEIN S, a cofactor to activated protein C which also interacts with the complement protein C4b-binding protein." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642960.

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Protein S is a single chain (Mr 75.000) plasma protein. It is a cofactor to activated protein C (APC) in the regulation of coagulation factors Va and Villa. It has high affinity for negatively charged phospolipids and it forms a 1:1 complex with APC on phospholipid surfaces, platelets and on endothelial cells. Patients with heterozygous protein S deficiency have a high incidence of thrombosis. Protein S is cleaved by thrombin, which leads to a loss of calcium binding sites and of APC cofactor activity. Protein S has two to three high affinity (KD 20uM) calcium binding sites - unrelated to the Gla-region - that are unaffected by the thrombin cleavage. In human plasma protein S (25 mg/liter) circulates in two forms; free (approx. 40%) and in a 1:1 noncovalent complex (KD 1× 10-7M) with the complement protein C4b-binding protein (C4BP). C4BP (Mr 570.000) is composed of seven identical 70 kDa subunits that are linked by disulfide bonds. When visualized by electron microscopy, C4BP has a spiderlike structure with the single protein S binding site located close to the central core and one C4b-binding site on each of the seven tentacles. When bound to C4BP, protein S looses its APC cofactor activity, whereas the function-of C4BP is not directly affected by the protein S binding. Chymotrypsin cleaves each of the seven C4BP subunits close to the central core which results in the liberation of multiple 48 kDa “tentacte” fragments and the formation of a 160 kDa central core fragment. We have successfully isolated a 160 kDa central core fragment with essentially intact protein S binding ability.The primary structure of both bovine and human protein S has been determined and found to contain 635 and 634 amino acids, respectively, with 82 % homology to each other. Four different regions were distinguished; the N-terminal Gla-domain (position 1-45) was followed by a region which has two thrombin-sensitive bonds positioned within a disulfide loop. Position 76 to 244 was occupied by four repeats homologous to the epidermal growth factor (EGF) precursor. In the first EGF-domain a modified aspartic acid was identified at position 95, B-hydroxaspartic acid (Hya), and in corresponding positions in the three following EGF-domains (positions 136,178 and 217) we found B-hydroxyasparagine (Hyn). Hyn has not previously been identified in proteins. The C-terminal half of protein S (from position 245) shows no homology to the serine proteases but instead to human Sexual Hormon Binding Globulin (SHBG)(see separate abstract). To study the structure-function relationship we made eighteen monoclonal antibodies to human protein S. The effects of the monoclonals on the C4BP-protein S interaction and on the APC cofactor activity were analysed. Eight of the antibodies were calciumdependent, four of these were against the Gla-domain, two against the thrombin sensitive portion and two against the region bearing the high affinity calcium binding sites. Three of the monoclonals were dependent on the presence of chelating agents, EDTA or EGTA, and were probably directed against the high affinity calcium binding region. Three other monoclonals inhibited the protein S-C4BP interaction. At present, efforts are made to localize the epitopes to gain information about functionally important regions of protein S.
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Reports on the topic "Calcium-binding proteins"

1

Creutz, Carl E. Repair of Nerve Cell Membrance Damage by Calcium-Dependent, Membrane-Binding Proteins. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada596750.

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Creutz, Carl E. Repair of Nerve Cell Membrane Damage by Calcium-Dependent, Membrane-Binding Proteins. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada560549.

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3

Trewhella, J. The role of low frequency collective modes in biological function: Ligand binding and cooperativity in calcium-binding proteins. Office of Scientific and Technical Information (OSTI), November 2000. http://dx.doi.org/10.2172/768788.

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4

Wicker, Louise, Ilan Shomer, and Uzi Merin. Membrane Processing of Citrus Extracts: Effects on Pectinesterase Activity and Cloud Stability. United States Department of Agriculture, October 1993. http://dx.doi.org/10.32747/1993.7568754.bard.

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The U.S. team studied the role of cations and pH on thermolabile (TL-PE) and thermostable (TS-PE), permeation in ultrafiltration (UF) membranes, affinity to ion exchange membranes, mechanism of cation and pH activation, and effect on PE stability. An optimum pH and cation concentration exists for activity and UF permeation, which is specific for each cation type. Incomplete release of PE from a pectin complex resulted in low PE binding to cationic and anionic membranes. Incubation of PE at low pH increases the surface hydrophobicity, especially TL-PE, but the secondary structure of TL-PE is not greatly affected. The Israeli team showed that stable cloud colloidal constituents flocculate following the conversion of soluble to insoluble biopolymers. First, formation of pectic acid by pectinesterase activity is followed by the formation of calcium pectate gel. This process initiates a myriad of poorly defined reactions that result in juice clarification. Second, protein coagulation by heat resulted in flocculation of proteinacous bound cloud constituents, particularly after enzymatic pectin degradation. Pectinesterase activity is proposed to be an indirect cause for clarification; whereas binding of cloud constituents is the primary event in clarification by pectate gel and coagulated proteins. Understanding the mechanism of interaction of protein and pectic polymers is key to understanding cloud instability. Based on the above, it was hypothesized that the structure of pectin-protein coagulates plays a key role in cloud instability.
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Levy, Maggie, Raymond Zielinski, and Anireddy S. Reddy. IQD1 Function in Defense Responses. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7699842.bard.

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The main objective of the proposed research was to study IQD1's mechanism of action and elucidate its role in plant protection. Preliminary experiments suggest that IQD1 binds CaM in a Ca²⁺-dependent manner and functions in general defense responses. We propose to identify proteins and genes that interact with IQD1, which may provide some clues to its mechanism of action. We also plan to dissect IQD1's integration in defense pathways and to study and modulate its binding affinity to CaM in order to enhance crop resistance. Our specific objectives were: (1) Analysis of IQD1's CaM-binding properties; (2) Identification of IQD1 targets;(3) Dissection of IQD1 integration into defense signaling pathways. Analysis of IQD1's CaM-binding properties defined four potential classes of sequences that should affect CaM binding: one is predicted to raise the affinity for Ca²⁺-dependent interaction but have no effect on Ca²⁺-independent binding; a second is predicted to act like the first mutation but eliminate Ca²⁺-independent binding; a third has no predicted effect on Ca²⁺-dependent binding but eliminates Ca²⁺-independent binding; and the fourth is predicted to eliminate or greatly reduce both Ca²⁺-dependent and Ca²⁺-independent binding. Following yeast two hybrid analysis we found that IQD1 interact with AtSR1 (Arabidopsis thalianaSIGNALRESPONSIVE1), a calcium/calmodulin-binding transcription factor, which has been shown to play an important role in biotic and abiotic stresses. We tested IQD1 interaction with both N-terminal or C-terminal half of SR1. These studies have uncovered that only the N-terminal half of the SR1 interacts with the IQD1. Since IQD1 has an important role in herbivory, its interaction with SR1 suggests that it might also be involved in plant responses to insect herbivory. Since AtSR1, like IQD1, is a calmodulin-binding protein and the mutant showed increased sensitivity to a herbivore, we analyzed WT, Atsr1 and the complemented line for the levels of GS to determine if the increased susceptibility of Atsr1 plants to T. ni feeding is associated with altered GS content. In general, Atsr1 showed a significant reduction in both aliphatic and aromatic GS levels as compared to WT. In order to study IQD1's molecular basis integration into hormone-signaling pathways we tested the epistatic relationships between IQD1 and hormone-signaling mutants. For that purpose we construct double mutants between IQD1ᴼXᴾ and mutants defective in plant-hormone signaling and GS accumulation. Epitasis with SA mutant NahG and npr1-1 and JA mutant jar1-1 suggested IQD1 function is dependent on both JA and SA as indicated by B. cinerea infection assays. We also verified the glucosinolate content in the crosses siblings and found that aliphatic GSL content is reduced in the double transgenic plants NahG:IQD1ᴼXᴾ as compare to parental lines while the aliphatic GSL content in the npr1-1:IQD1ᴼXᴾ and jar1-1: IQD1ᴼXᴾ double mutants was intimidated to the parental lines. This suggests that GSL content dependency on SA is downstream to IQD1. As a whole, this project should contribute to the development of new defense strategies that will improve crop protection and reduce yield losses and the amount of pesticides required; these will genuinely benefit farmers, consumers and the environment.
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Locy, Robert D., Hillel Fromm, Joe H. Cherry, and Narendra K. Singh. Regulation of Arabidopsis Glutamate Decarboxylase in Response to Heat Stress: Modulation of Enzyme Activity and Gene Expression. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7575288.bard.

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Most plants accumulate the nonprotein amino acid, g-aminobutyric acid (GABA), in response to heat stress. GABA is made from glutamate in a reaction catalyzed by glutamate decarboxylase (GAD), an enzyme that has been shown by the Israeli PI to be a calmodulin (CaM) binding protein whose activity is regulated in vitro by calcium and CaM. In Arabidopsis there are at least 5 GAD genes, two isoforms of GAD, GAD1 and GAD2, are known to be expressed, both of which appear to be calmodulin-binding proteins. The role of GABA accumulation in stress tolerance remains unclear, and thus the objectives of the proposed work are intended to clarify the possible roles of GABA in stress tolerance by studying the factors which regulate the activity of GAD in vivo. Our intent was to demonstrate the factors that mediate the expression of GAD activity by analyzing the promoters of the GAD1 and GAD2 genes, to determine the role of stress induced calcium signaling in the regulation of GAD activity, to investigate the role of phosphorylation of the CaM-binding domain in the regulation of GAD activity, and to investigate whether ABA signaling could be involved in GAD regulation via the following set of original Project Objectives: 1. Construction of chimeric GAD1 and GAD2 promoter/reporter gene fusions and their utilization for determining cell-specific expression of GAD genes in Arabidopsis. 2. Utilizing transgenic plants harboring chimeric GAD1 promoter-luciferase constructs for isolating mutants in genes controlling GAD1 gene activation in response to heat shock. 3. Assess the role of Ca2+/CaM in the regulation of GAD activity in vivo in Arabidopsis. 4. Study the possible phosphorylation of GAD as a means of regulation of GAD activity. 5. Utilize ABA mutants of Arabidopsis to assess the involvement of this phytohormone in GAD activation by stress stimuli. The major conclusions of Objective 1 was that GAD1 was strongly expressed in the elongating region of the root, while GAD2 was mainly expressed along the phloem in both roots and shoots. In addition, GAD activity was found not to be transcriptionally regulated in response to heat stress. Subsequently, The Israeli side obtained a GAD1 knockout mutation, and in light of the objective 1 results it was determined that characterization of this knockout mutation would contribute more to the project than the proposed Objective 2. The major conclusion of Objective 3 is that heat-stress-induced changes in GAD activity can be explained by heat-stress-induced changes in cytosolic calcium levels. No evidence that GAD activity was transcriptionally or translationally regulated or that protein phosphorylation was involved in GAD regulation (objective 4) was obtained. Previously published data by others showing that in wheat roots ABA regulated GABA accumulation proved not to be the case in Arabidopsis (Objective 5). Consequently, we put the remaining effort in the project into the selection of mutants related to temperature adaptation and GABA utilization and attempting to characterize events resulting from GABA accumulation. A set of 3 heat sensitive mutants that appear to have GABA related mutations have been isolated and partially characterized, and a study linking GABA accumulation to growth stimulation and altered nitrate assimilation were conducted. By providing a better understanding of how GAD activity was and was not regulated in vivo, we have ruled out the use of certain genes for genetically engineering thermotolerance, and suggested other areas of endeavor related to the thrust of the project that may be more likely approaches to genetically engineering thermotolerance.
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O'Neill, Sharman, Abraham Halevy, and Amihud Borochov. Molecular Genetic Analysis of Pollination-Induced Senescence in Phalaenopsis Orchids. United States Department of Agriculture, 1991. http://dx.doi.org/10.32747/1991.7612837.bard.

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The project investigated the molecular genetic and biochemical basis of pollination-induced senescence of Phalaenopsis flowers. This experimental system offered unique advantages in that senescence is strictly regulated by pollination, providing the basis to experimentally initiate and synchronize senescence in populations of flowers. The postpollination syndrome in the Phalaenopsis orchid system was dissected by investigating the temporal and spatial regulation of ACC synthase gene expression. In the stigma, pollen-borne auxin induces the expression of the auxin-regulated ACC synthase (PS-ACS2) gene, resulting in ACC synthesis within 1 h following pollination. Newly formed ACC is oxidized by basal constitutive ACC oxidase to ethylene, which then induces the expression of the ethylene-regulated ACC synthase(PS-ACS1) and oxidase (ACO1) genes for further autocatalytic production of ethylene. It is speculated that during the 6-h period following pollination, emasculation leads to the production or release of a sensitivity factor that sensitizes the cells of the stigma to ethylene. ACC and ethylene molecules are translocated from the stigma to the labellum and perianth where ethylene induces the expression of PS-ACS1 and ACO1 resulting in an increased production of ACC and ethylene. Organ-localized ethylene is responsible for inrolling and senescence of the labellum and perianth. The regulation of ethylene sensitivity and signal transduction events in pollinated flowers was also investigated. The increase in ethylene sensitivity appeared in both the flower column and the perianth, and was detected as early as 4 h after pollination. The increase in ethylene sensitivity following pollination was not dependent on endogenous ethylene production. Application of linoleic and linoleic acids to Phalaenopsis and Dendrobium flowers enhanced their senescence and promoted ethylene production. Several major lipoxygenase pathway products including JA-ME, traumatic acid, trans-2-hexenal and cis-3-hexenol, also enhanced flower senescence. However, lipoxygenase appears to not be directly involved in the endogenous regulation of pollination-induced Phalaenopsis and Dendrobium flower senescence. The data suggest that short-chain saturated fatty acids may be the ethylene "sensitivity factors" produced following pollination, and that their mode of action involves a decrease in the order of specific regions i the membrane lipid bilayer, consequently altering ethylene action. Examination of potential signal transduction intermediates indicate a direct involvement of GTP-binding proteins, calcium ions and protein phosphorylation in the cellular signal transduction response to ethylene following pollination. Modulations of cytosolic calcium levels allowed us to modify the flowers responsiveness to ethylene.
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Rafaeli, Ada, Russell Jurenka, and Daniel Segal. Isolation, Purification and Sequence Determination of Pheromonotropic-Receptors. United States Department of Agriculture, July 2003. http://dx.doi.org/10.32747/2003.7695850.bard.

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Moths constitute a major group of pest insects in agriculture. Pheromone blends are utilised by a variety of moth species to attract conspecific mates, which is under circadian control by the neurohormone, PBAN (pheromone-biosynthesis-activating neuropeptide). Our working hypothesis was that, since the emission of sex-pheromone is necessary to attract a mate, then failure to produce and emit pheromone is a potential strategy for manipulating adult moth behavior. The project aimed at identifying, characterising and determining the sequence of specific receptors responsible for the interaction with pheromonotropic neuropeptide/s using two related moth species: Helicoverpa armigera and H. lea as model insects. We established specific binding to a membrane protein estimated at 50 kDa in mature adult females using a photoaffinity-biotin probe for PBAN. We showed that JH is required for the up-regulation of this putative receptor protein. In vitro studies established that the binding initiates a cascade of second messengers including channel opening for calcium ions and intracellular cAMP production. Pharmacological studies (using sodium fluoride) established that the receptor is coupled to a G-protein, that is, the pheromone-biosynthesis-activating neuropeptide receptor (PBAN-R) belongs to the family of G protein-coupled receptor (GPCR)'s. We showed that PBAN-like peptides are present in Drosophila melanogaster based on bioassay and immunocytochemical data. Using the annotated genome of D. melanogaster to search for a GPCR, we found that some were similar to neuromedin U- receptors of vertebrates, which contain a similar C-terminal ending as PBAN. We established that neuromedin U does indeed induce pheromone biosynthesis and cAMP production. Using a PCR based cloning strategy and mRNA isolated from pheromone glands of H. zea, we successfully identified a gene encoding a GPCR from pheromone glands. The full-length PBAN-R was subsequently cloned and expressed in Sf9 insect cells and was shown to mobilize calcium in response to PBAN in a dose-dependent manner. The successful progress in the identification of a gene, encoding a GPCR for the neurohormone, PBAN, provides a basis for the design of a novel battery of compounds that will specifically antagonize pheromone production. Furthermore, since PBAN belongs to a family of insect neuropeptides with more than one function in different life stages, this rationale may be extended to other physiological key-regulatory processes in different insects.
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9

Fromm, A., Avihai Danon, and Jian-Kang Zhu. Genes Controlling Calcium-Enhanced Tolerance to Salinity in Plants. United States Department of Agriculture, March 2003. http://dx.doi.org/10.32747/2003.7585201.bard.

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The specific objectives of the proposed research were to identify, clone and characterize downstream cellular target(s) of SOS3 in Arabidopsis thaliana, to analyze the Ca2+-binding characteristics of SOS3 and the sos3-1 mutant and their interactions with SOS3 cellular targets to analyze the SOS3 cell-specific expression patterns, and its subcellular localization, and to assess the in vivo role of SOS3 target protein(s) in plant tolerance to salinity stress. In the course of the study, in view of recent opportunities in identifying Ca2+ - responsive genes using microarrays, the group at Weizmann has moved into identifying Ca2+-responsive stress genes by using a combination of aqeuorin-based measurements of cytosolic Ca and analysis by DNA microarrays of early Ca-responsive genes at the whole genome level. Analysis of SOS3 (University of Arizona) revealed its expression in both roots and shoots. However, the expression of this gene is not induced by stress. This is reminiscent of other stress proteins that are regulated by post-transcriptional mechanisms such as the activation by second messengers like Ca. Further analysis of the expression of the gene using promoter - GUS fusions revealed expression in lateral root primordial. Studies at the Weizmann Institute identified a large number of genes whose expression is up-regulated by a specific cytosolic Ca burst evoked by CaM antagonists. Fewer genes were found to be down-regulated by the Ca burst. Among the up-regulated genes many are associated with early stress responses. Moreover, this study revealed a large number of newly identified Ca-responsive genes. These genes could be useful to investigate yet unknown Ca-responsive gene networks involved in plant response to stress.
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Nelson, Nathan, and Charles F. Yocum. Structure, Function and Utilization of Plant Photosynthetic Reaction Centers. United States Department of Agriculture, September 2012. http://dx.doi.org/10.32747/2012.7699846.bard.

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Light capturing and energy conversion by PSI is one of the most fundamental processes in nature. In the heart of these adaptations stand PSI, PSII and their light harvesting antenna complexes. The main goal of this grant proposal was to obtain by X-ray crystallography information on the structure of plant photosystem I (PSI) and photosystem II (PSII) supercomplexes. We achieved several milestones along this line but as yet, like several strong laboratories around the world, we have no crystal structure of plant PSII. We have redesigned the purification and crystallization procedures and recently solved the crystal structure of the PSI supercomplex at 3.3 Å resolution. Even though this advance in resolution appears to be relatively small, we obtained a significantly improved model of the supercomplex. The work was published in J. Biol. Chem. (Amunts et al., 2010). The improved electron density map yielded identification and tracing of the PsaK subunit. The location of an additional 10 ß-carotenes, as well as 5 chlorophylls and several loop regions that were previously uninterruptable have been modeled. This represents the most complete plant PSI structure obtained thus far, revealing the locations of and interactions among 17 protein subunits and 193 non-covalently bound photochemical cofactors. We have continued extensive experimental efforts to improve the structure of plant PSI and to obtain PSII preparation amenable to crystallization. Most of our efforts were devoted to obtain well-defined subcomplexes of plant PSII preparations that are amenable to crystallization. We studied the apparent paradox of the high sensitivity of oxygen evolution of isolated thylakoids while BBY particles exhibit remarkable resilience to the same treatment. The integrity of the photosystem II (PSII) extrinsic protein complement as well as calcium effects arise from the Ca2+ atom associated with the site of photosynthetic water oxidation were investigated. This work provides deeper insights into the interaction of PsbO with PSII. Sight-directed mutagenesis indicated the location of critical sites involved in the stability of the water oxidation reaction. When combined with previous results, the data lead to a more detailed model for PsbO binding in eukaryotic PSII.
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