Academic literature on the topic 'Proteins – Metabolism'

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Journal articles on the topic "Proteins – Metabolism"

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Rostom, Hussam, and Brian Shine. "Basic metabolism: proteins." Surgery (Oxford) 36, no. 4 (April 2018): 153–58. http://dx.doi.org/10.1016/j.mpsur.2018.01.009.

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Shine, Brian, and Hussam Rostom. "Basic metabolism: proteins." Surgery (Oxford) 39, no. 1 (January 2021): 1–6. http://dx.doi.org/10.1016/j.mpsur.2020.11.003.

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Bidlack, Wayne R. "Proteins of Iron Metabolism." Journal of the American College of Nutrition 21, no. 3 (June 2002): 290–91. http://dx.doi.org/10.1080/07315724.2002.10719225.

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Pietrangelo, Antonello. "Proteins of iron metabolism." Gastroenterology 125, no. 6 (December 2003): 1906. http://dx.doi.org/10.1053/j.gastro.2003.08.039.

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Hamuro, Lora L., and Narendra S. Kishnani. "Metabolism of biologics: biotherapeutic proteins." Bioanalysis 4, no. 2 (January 2012): 189–95. http://dx.doi.org/10.4155/bio.11.304.

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Csaki, Lauren S., and Karen Reue. "Lipins: Multifunctional Lipid Metabolism Proteins." Annual Review of Nutrition 30, no. 1 (July 2010): 257–72. http://dx.doi.org/10.1146/annurev.nutr.012809.104729.

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Shahverdiyeva, I. J., A. H. Orujov, and U. H. Azizova. "IRON METABOLISM PROTEINS DURING PREGNANCY." Biological Markers in Fundamental and Clinical Medicine (collection of abstracts) 3, no. 1 (November 7, 2019): 90–91. http://dx.doi.org/10.29256/v.03.01.2019.escbm61.

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Christians, Uwe. "Transport Proteins and Intestinal Metabolism." Therapeutic Drug Monitoring 26, no. 2 (April 2004): 104–6. http://dx.doi.org/10.1097/00007691-200404000-00002.

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Xu, Li, Linkang Zhou, and Peng Li. "CIDE Proteins and Lipid Metabolism." Arteriosclerosis, Thrombosis, and Vascular Biology 32, no. 5 (May 2012): 1094–98. http://dx.doi.org/10.1161/atvbaha.111.241489.

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Kuhnert, Franziska, Urte Schlüter, Nicole Linka, and Marion Eisenhut. "Transport Proteins Enabling Plant Photorespiratory Metabolism." Plants 10, no. 5 (April 27, 2021): 880. http://dx.doi.org/10.3390/plants10050880.

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Photorespiration (PR) is a metabolic repair pathway that acts in oxygenic photosynthetic organisms to degrade a toxic product of oxygen fixation generated by the enzyme ribulose 1,5-bisphosphate carboxylase/oxygenase. Within the metabolic pathway, energy is consumed and carbon dioxide released. Consequently, PR is seen as a wasteful process making it a promising target for engineering to enhance plant productivity. Transport and channel proteins connect the organelles accomplishing the PR pathway—chloroplast, peroxisome, and mitochondrion—and thus enable efficient flux of PR metabolites. Although the pathway and the enzymes catalyzing the biochemical reactions have been the focus of research for the last several decades, the knowledge about transport proteins involved in PR is still limited. This review presents a timely state of knowledge with regard to metabolite channeling in PR and the participating proteins. The significance of transporters for implementation of synthetic bypasses to PR is highlighted. As an excursion, the physiological contribution of transport proteins that are involved in C4 metabolism is discussed.
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Dissertations / Theses on the topic "Proteins – Metabolism"

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Ainsworth, Julia. "Comparison of p53 and MAGI-3 regulation mediated by the E6 protein from high-risk human papillomavirus types 18 and 33." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112368.

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The HPV E6-p53 interaction is well-understood, but not for all high-risk HPV types. In addition, HPV E6 p53-independent functions are gaining recognition for their importance in cellular transformation but require clarification. Thus, the aim of this study was two-fold: (1) to gain insight into the p53-E6 interaction for high-risk HPV-33 and, (2) to explore how high-risk HPV E6 proteins targets cellular MAGI-3 for degradation.
In vivo and in vitro results indicated that E6 from HPV types 18 and 33 interacted similarly with p53 although, variants of the HPV-33 E6 prototype demonstrated interesting disparities. Of note was HPV-33 E6 variant 2, which degraded p53 more efficiently than prototype HPV-33 E6 and HPV-18 E6. The E6 protein from HPV types 18 and 33 also potently degraded MAGI-3 via a different pathway than that used for p53. Specifically, proteasome inhibition did not interfere with MAGI-3 degradation and MAGI-3 was not ubiquitinated in the presence of the E6 protein.
Therefore, the results described herein enhance our understanding of high-risk HPV type 33 E6 and the E6-MAGI-3 interaction.
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Ring, Giselle Natasha. "Identification and characterization of TMEM 85, a novel suppressor of bax-mediated cell death in yeast." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112352.

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The ability to evade apoptosis is an acquired characteristic associated with many normal and pathophysiological processes. TMEM 85 represents a novel transmembrane domain containing human protein isolated in our previous screen for Bax suppressors, but whose function is currently unknown. Using viability and growth assays, we confirmed that TMEM 85 is anti-apoptotic. Four unique human cDNA sequences containing regions distinct from and of perfect identity to our cDNA were present in the database. Analysis of TMEM 85 suggests that it consists of five exons, alternatively spliced to produce at least four different mRNA's and proteins (TMEM 85v1-v4). RT-PCR analysis using RNA isolated from mice and humane tissues show that all transcripts are expressed. Yeast contain an orthologue of the human TMEM 85v1 protein, YGL213C. Surprisingly, the viability assay indicated that mutants lacking YGL231c do not show a hyper-responsive apoptotic phenotype, however its overexpression shows that it is nevertheless anti-apoptotic. Using a yeast strain expressing chromosomally TAP-tagged YGL231c, we found no up-regulation of the endogenous gene due to stress. The deletion mutant is also known to expresses a synthetically lethal phenotype in the presence of alpha-synuclein. While expression of alpha-synuclein caused significant death in both the wild type and deletion mutants, TMEM 85v2 was unable to exhibit a protective role. These findings demonstrate the complexity of the TMEM 85 gene and its anti-apoptotic function in both yeast and human.
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Smits, Callum, and n/a. "Structures of the pro-survival protein A1 in complex with BH3-domain peptides." University of Otago. Department of Biochemistry, 2007. http://adt.otago.ac.nz./public/adt-NZDU20071218.131743.

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Protein:protein interactions are central to the regulation of the intrinsic programmed cell death (apoptosis) pathway. Opposing members of the Bcl-2 family of proteins, which have distinct sequence features, interact with each other on the outer mitochondrial membrane to regulate apoptosis. Pro-survival proteins such as Bcl-2, Bcl-x[L], Bcl-w, Mcl-1 and A1 protect cells from apoptosis and contain up to four regions of homology to Bcl-2 (Bcl-2 homology domains 1 - 4, BH1-4). Pro-apoptotic BH3-only proteins such as Bim, Puma, Noxa, Bad, Bmf, and Bid promote apoptosis by interacting with and inactivating pro-survival proteins, and contain just the BH3-domain. The pro-apoptotic proteins Bax and Bak are essential for apoptosis and contain three regions of homology to Bcl-2 (the BH1-, BH2- and BH3-domains). In this study, two different sets of interactions involving pro-survival proteins were investigated. Initially, the pro-apoptotic protein Bnip3 was examined to determine if it was a mitochondrial anchor for the pro-survival protein Bcl-w. Secondly, to characterise the interactions between a pro-survival protein and different BH3-domains, structures were solved of the pro-survival protein A1 in complex with four different BH3-domains. In the structure of Bcl-w, the hydrophobic C-terminus is bound to its own BH3-domain binding groove. This location of the C-terminus is consistent with the observation that Bcl-w is only loosely associated with the outer mitochondrial membrane in healthy cells. Upon interaction of Bcl-w with a BH3-domain, Bcl-w becomes tightly associated with the mitochondrial membrane, presumably due to displacement of the C-terminal residues by the BH3-only protein. In healthy cells it has been suggested that Bcl-w is associated with the membrane due to an interaction with an unidentified membrane protein, which preliminary experiments suggested may be Bnip3. Protein interaction experiments performed in vitro and in vivo did not reveal an interaction between Bnip3 and Bcl-w. It was originally thought that each pro-apoptotic BH3-only protein could interact with all pro-survival proteins. However, it has recently become clear that there is selectivity within the pathway suggesting functional groupings. Bim and Puma behave as originally predicted and can interact with all pro-survival proteins and are potent killers. In contrast, Noxa and Bad interact with distinct subsets of pro-survival proteins. Noxa only binds Mcl-1 and A1, while Bad binds Bcl-2, Bcl-x[L] and Bcl-w. As a result, either Noxa or Bad acting alone is a weak killer, but together they are potent. Other BH3-only proteins bind tightly to some pro-survival proteins and weakly to others. The diversity that exists between BH3-domain sequences precludes sequence-based identification of the determinants of specificity. In this study, crystal structures of A1:Puma BH3-domain, A1:Bmf BH3-domain, A1:Bak BH3-domain and A1:Bid BH3-domain complexes have been solved. Differences identified between these structures explain some of the variation in affinities observed in pro-survival protein:BH3-domain complexes. These observations, in combination with published data, suggest that BH3-domains bind weakly when the optimal interactions with conserved residues cannot be formed. Additionally, differences were observed in the A1:Bak BH3-domain structure that may be functionally important for the regulation of Bak.
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Spathaky, Jane Mary. "A novel method for the isolation of genes encoding peroxisomal matrix proteins." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361693.

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Charest-Marcotte, Alexis 1984. "Functional interaction between PROX1, ERR[alpha] and PGC-1[alpha] in the control of energy metabolism." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111571.

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Nuclear receptors play crucial roles in the transcriptional regulation of many biological processes such as development and cellular differentiation. ERRalpha is known, along with coactivator PGC-1alpha, to playa central role in the control of energy metabolism in cardiac and skeletal muscle. They activate the expression of many genes involved in mitochondrial oxidative metabolism. Here we identified PROX1, a factor that was previously shown to broadly influence metabolism, as a regulator of this pathway. Indeed, PROX1 interacts in vitro and in vivo with both ERRalpha and PGC-1alpha. To provide more insight on the hepatic functions of ERRalpha and PROX1, we performed ChIP-on-chip using mouse liver, identifying a large number of ERRalpha and PROX1 genomic targets and reinforcing their role in energy metabolism. Over 40% of the target genes were found to be common to both factors and we observed that PROX1 could be recruited to ERRalpha binding sites and act as a negative regulator o fthe ERRalpha/POC-1alpha pathway.
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Rossi, Merja. "Investigating cell type specific metabolism using GFP as a reporter protein." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:0c418362-63e7-496d-9ff6-584a0c54c127.

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Metabolic flux analysis (MFA) is a powerful technique for quantifying the intracellular fluxes in central carbon metabolism. It relies on detection of stable isotope labelling from metabolites such as amino acids derived from protein. Current standard techniques are, however, unable to distinguish between different cell types in heterogeneous tissue. The aim of the thesis was to address this problem by developing and validating a strategy using green fluorescent protein (GFP) with cell type specific expression as a reporter protein for investigating the fluxes in specific cell types in the Arabidopsis thaliana root. The fundamental difficulty in applying a reporter protein strategy in a multicellular organism arises from the limited amount of recombinant protein expressed by the cells. The main novel contributions of the work in this thesis are threefold. First, a robust protocol for purification of GFP from the roots of Arabidopsis seedlings and for detection of reliable mass isotopomer distributions from the amino acids derived from GFP are described. Secondly, the reporter protein strategy is validated in this biological system with a focus on showing the data obtained by the use of the reporter protein is equal to that normally obtained from the total protein fraction. To expand on this, stable isotope labelling in isolated root hair cells is explored. These cells are easily isolated and show potential as a model system for cell type specific metabolism. Finally, the experimental data provide evidence for the feasibility of measuring data from specific cell types with appropriate mass spectrometric techniques. Analysis of cell type specific gene expression in this system suggests differences in the primary metabolism of different cell types cannot be ruled out without further investigation. Based on small scale in silico modelling described in this thesis, new solutions capable of providing data on sub-populations of cells are required, if central metabolism of the cell types differs significantly.
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Faubert, Amélie. "Towards the identification of cellular and molecular regulators of hematopoietic stem cell self-renewal." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103195.

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Self-renewal is central to the expansion of normal and cancerous stem cells. Its understanding is therefore critical for future advances in transplantation-based therapies and cancer treatment. Although the molecular machinery controlling stem cell self-renewal remains poorly defined, a number of genes important to this process have recently been identified. Two prominent genes in this group are Hoxb4 and Bmi1. Members of our group led the way to demonstrate important regulatory functions of these genes in hematopoietic stem cell (HSC) self-renewal and expansion.
The major goal of my thesis project is to dissect mechanisms that regulate self-renewal of HSCs. Our starting hypothesis was that HSC activity is regulated by complementary and independent self-renewal mechanisms: self-renewal of expansion and self-renewal of maintenance (Chapters 1-2). In order to further verify this theory, we have analyzed the genetic interaction between Hoxb4 and Bmi1. While Hoxb4 overexpression triggers HSC expansion, Bmi1 proper expression is essential to sustain long-term stem cell activity. We have also demonstrated that Hoxb4 and Bmi1 regulate distinct gene targets, likely suggesting a complementary and independent function for these two regulators in HSC activity (Chapter 3).
The second part of this thesis highlights efforts that were made in order to get a better understanding of self-renewal mechanisms. We have identified potential new regulators of stem cell activity by characterizing a stem cell leukemia population (Chapter 4) and by assessing the expression of asymmetrical distributed factors (Chapter 5) and selected nuclear factors of the Hematopoietic Stem Cell Nuclear Factor Database (Chapter 6) in stem cell-enriched sub-fractions.
This project will lead to a better understanding of the cellular basis regulating self-renewal of both normal and cancer stem cells and potentially to the future identification of new self-renewal determinants.
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Dzikaitė, Vijolė. "Studies of proteins in heme and iron metabolism /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-762-2/.

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Cervantes-Laurean, Daniel. "Preparation and Characterization of Model Conjugates for the Study of Proteins Modified by ADP-ribose." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc935701/.

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Modification of proteins by ADP-ribose has been shown to be a versatile modification with respect to the amino acid side chain. The results described here will allow the study of the biological importance of ADP-ribose glycation and also allow differentiation on crude extracts between enzymatic modifications from protein ADP-ribose glycation that can occur due to the presence of NAD glycohydrolases.
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Buscarlet, Manuel. "The neural progenitor to neuron transition : role and regulation of GrouchoTLE proteins." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115670.

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Groucho/transducin-like Enhancer of split (Gro/TLE) family proteins are corepressors found as part of multiple transcriptional complexes that play significant roles during many developmental processes, including neurogenesis. This thesis sought to characterize the molecular mechanisms underlying the biological activity of Gro/TLE1. More specifically, the aim was to clarify the contribution of different transcriptional cofactors, as well as phosphorylation events induced by cofactor binding, to Gro/TLE1 ability to inhibit neuronal differentiation from proliferating neural progenitor cells.
By characterizing specific point mutations within the C-terminal domain of Gro/TLE1, we were able to selectively impair binding of Gro/TLE1 to different classes of DNA-binding proteins and then assess the effect of those mutations on Gro/TLE1 anti-neurogenic function. These studies showed that the inhibition of cerebral cortex (cortical) neuron differentiation by Gro/TLE1 requires interaction with transcription factors that use short tetrapeptide sequences, WRP(W/Y), to recruit Gro/TLE1. In contrast, interactions with proteins that either interact with the C-terminal domain of Gro/TLE1 using a different type of binding sequence, termed engrailed homology 1 (Eh1) motif, or bind to the N-terminal part of the protein, are not required for Gro/TLE1 anti-neurogenic function.
Using a similar strategy based on mutation analysis, we characterized point mutations that block the hyperphosphorylation of Gro/TLE1 induced by transcription cofactor binding ("cofactor-activated phosphorylation") without impairing cofactor binding and transcriptional corepression ability. These mutations map at phosphorylatable serine residues, Ser-286, Ser-289, and Ser298. Mutation of those residues to alanine blocks/reduces both cofactor-activated phosphorylation and anti-neurogenic activity of Gro/TLE1, demonstrating that cofactor-activated phosphorylation is required for that function. Tandem mass spectroscopy analysis showed further that Ser-286 is phosphorylated. Taken together, these findings characterize the role of cofactor-activated phosphorylation and identify residues important for this mechanism.
Our studies also showed that homeodomain-interacting protein kinase 2 (HIPK2) mediates phosphorylation of Gro/TLE1 when the latter is complexed with transcriptional partners of the WRP(W/Y) motif family. However, HIPK2 is not involved in Gro/TLE1 cofactor-activated phosphorylation. Rather, HIPK2--mediated phosphorylation is antagonistic to the latter and decreases the ability of Gro/TLE1 to interact and repress transcription with WRP(W/Y) motif proteins.
Taken together, these results improve significantly our understanding of the mechanisms underlying the anti-neurogenic function of Gro/TLE1. This information provides new insight into the regulation of mammalian neuronal development and, possibly, other developmental processes controlled by Gro/TLE proteins.
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Books on the topic "Proteins – Metabolism"

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F, Hudson B. J., ed. Biochemistry of food proteins. London: Elsevier Applied Science, 1992.

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Welle, Stephen. Human protein metabolism. New York: Springer, 1999.

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Coffee, Carole. Metabolism. Madison, Wis: Fencecreek, 1999.

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-D, Bock H., ed. Protein metabolism in farm animals: Evaluation, digestion, absorption, and metabolism. Oxford [England]: Oxford University Press, 1989.

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Doherty, Fergus J. Intracellular protein degradation. Oxford: IRL Press, 1992.

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C, Glatz Jan F., and Vusse, G. J. van der., eds. Cellular fatty-acid binding proteins. Dordrecht: Kluwer Academic Publishers, 1990.

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1933-, Sugano Michihiro, and Beynen Anton C. 1953-, eds. Dietary proteins, cholesterol, metabolism and atherosclerosis. Basel: Karger, 1990.

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R, Räihä Niels C., Nestlé Nutrition Services, and Nestlé Nutrition Workshop (33rd : 1993 : Magaliesburg, South Africa), eds. Protein metabolism during infancy. [Vevey, Switzerland]: Nestlé Nutrition Services, 1994.

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I, Zabolotnyĭ D., ed. Molecular pathology of proteins. Hauppauge, NY: Nova Science Publishers, 2009.

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Haian, Fu, ed. Protein-protein interactions: Methods and applications. Totowa, N.J: Humana Press, 2004.

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Book chapters on the topic "Proteins – Metabolism"

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Millichip, Mark, Frances Jackson, Gareth Griffiths, Arthur Tatham, Alex Drake, Peter Shewry, and Keith Stobart. "Oil Body Proteins." In Plant Lipid Metabolism, 561–63. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-015-8394-7_157.

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Parry, Martin A. J., Steven P. Colliver, Pippa J. Madgwick, and Matthew J. Paul. "Manipulation of Photosynthetic Metabolism." In Recombinant Proteins from Plants, 229–49. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-60327-260-5_17.

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Mason, Robert W. "Lysosomal Metabolism of Proteins." In Subcellular Biochemistry, 159–90. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5833-0_6.

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Benson, M. D., B. Kluve-Beckerman, J. J. Liepnieks, J. R. Murrell, D. Hanes, and T. Uemichi. "Metabolism of Amyloid Proteins." In Novartis Foundation Symposia, 104–18. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514924.ch7.

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Fürst, W., A. Vogel, M. Lee-Vaupel, E. Conzelmann, and K. Sandhoff. "Glycosphingolipid Activator Proteins." In Enzymes of Lipid Metabolism II, 315–38. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5212-9_44.

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Kersten, Sander. "Angiopoietin-Like Proteins and Lipid Metabolism." In Cellular Lipid Metabolism, 237–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00300-4_9.

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Li, Su-Chen, and Yu-Teh Li. "Activator Proteins (Protein Cofactors) for the Catabolism of Glycosphingolipids." In Enzymes of Lipid Metabolism II, 307–14. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5212-9_43.

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Tamura, Yuki. "Heat Shock Response and Metabolism in Skeletal Muscle." In Heat Shock Proteins, 41–52. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03952-3_3.

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Chang, T. Y., Cathy Chang, Oneil Lee, and Jonathan Cruz. "ACAT Genes and Proteins in Humans." In Lipoprotein Metabolism and Atherogenesis, 124–29. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_26.

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Izumi, Tohru, Haruo Hanawa, Makihiko Saeki, and Makoto Kodama. "Cardiac Contractile Proteins and Autoimmune Myocarditis." In Cellular Function and Metabolism, 67–71. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3078-7_10.

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Conference papers on the topic "Proteins – Metabolism"

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Smith, Robert Lane. "Mechanical Loading and Articular Cartilage Metabolism." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2520.

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Abstract Articular cartilage provides diarthrodial joints with a loading-bearing surface that ensures functional motility. The physical characteristics of articular cartilage originate with the highly organized matrix of extracellular macromolecules that provide structural elements to the tissue. The matrix specialization rests with specific proteins produced by the cartilage cells, the chondrocytes that undergo extensive post-translational modification through addition of sulfated glycosaminoglycan and oligosaccharides. The matrix proteins fall into three major categories, the collagens, the proteoglycans and the glycoproteins, with each group contributing unique properties to cartilage form and function.
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Sauvant, D., and P. Nozière. "The rumen protein balance as a key trait to model ruminant responses to dietary proteins." In 6th EAAP International Symposium on Energy and Protein Metabolism and Nutrition. The Netherlands: Wageningen Academic Publishers, 2019. http://dx.doi.org/10.3920/978-90-8686-891-9_142.

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Berndtsson, E., A.-L. Nynäs, W. Newson, M. Langton, R. Andersson, E. Johansson, and M. E. Olsson. "21. The underutilised side streams of broccoli and kale – valorisation via proteins and phenols." In 6th EAAP International Symposium on Energy and Protein Metabolism and Nutrition. The Netherlands: Wageningen Academic Publishers, 2019. http://dx.doi.org/10.3920/978-90-8686-892-6_21.

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Chiang, T. M., R. J. H. Wojcikiewicz, A. H. Kang, and J. N. Fain. "PHOSPHORYLATION OF THE OUTER SURFACE OF PLATELETS ENHANCES THE EFFECTS OF COLLAGEN ON PLATELET AGGREGATION, ATP RELEASE, CALCIUM TRANSLOCATION AND PHOSPHOINOSITIDE HYDROLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644477.

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We have recently isolated and purified from human plasma two isomeric forms of protein kinase, both of which can phosphorylate the outer surface proteins of human platelets. One of the proteins phosphorylated is the platelet collagen receptor. The phosphorylation of the outer surface proteins of human platelets increased their functional responsiveness to collagen. Collagen-stimulated platelet aggregation, release of ATP and calcium translocation were all enhanced by pretreatment with plasma protein kinase in the presence of ATP. The mechanism by which phosphorylated platelets become hypersensitive to collagen is not established. In the present study, we have used [3H]myo-inositol-labeled human platelets to investigate the possible role of phosphoinositide metabolism in mediating this hypersensitivity. Formation of inositol mono-, bis-, and trisphosphate in response to collagen was more pronounced in phosphorylated platelets than controls. these results indicate that enhanced phosphoinositide hydrolysis in phosphorylated platelets correlate with the increased functional responses to collagen.
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Jander, Georg. "Manipulation of plant metabolism by proteins and small molecules in aphid saliva." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93762.

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Stricker-Shaver, Janice, Benedikt Fabry, Libo Yu-Taeger, Elisabeth Singer, Lisa Stanek, Carsten Calaminus, Bernd J. Pichler, Lamya S. Shihabuddin, Olaf Riess, and Huu Phuc Nguyen. "A50 Hypothalamic suppression of mutant huntingtin restored proteins involved in energy metabolism." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.48.

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Jovičić Milić, Sandra S., Marko Antonijević, Đorđe S. Petrović, Verica V. Jevtić, and Danijela Lj Stojković. "Investigation of the anticancer activity of 2-amino-6-methylbenzothiazole and corresponding Pd(II) complex using molecular docking simulations." In 2nd International Conference on Chemo and Bioinformatics. Institute for Information Technologies, University of Kragujevac, 2023. http://dx.doi.org/10.46793/iccbi23.535jm.

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In our prior investigations, it has been established that compound di(2-amino-6-methylbenzothiazole)dichloridopalladate(II) (C1) exhibits promising efficacy in inhibiting the growth of colon carcinoma, thereby demonstrating potential as an anticancer agent. To elucidate the underlying mechanism of action against cancer, a comprehensive investigation involving DNA binding analysis and a series of assays to evaluate the inhibitory potential of compound C1 against key proteins involved in cancer metabolism were conducted. The significant inhibitory potential of C1 towards Bcl-2, Ki-67, and CDK-4 was determined. In order to investigate the underlying mechanism behind the anticancer properties and to assess the inhibition of various proteins involved in different metabolic pathways of C1, molecular docking simulations were conducted. The investigation revealed that the observed lack of similarity between the experimental outcomes and the inhibition of Bcl-2 and CDK-4 by C1 and 2-amino-6-methylbenzothiazole (L1) suggests that the metabolic pathways involving these proteins do not contribute to the anticancer properties of C1. The observed correlation between the inhibition of Ki-67 and the experimental outcomes was found to be significant. The inhibition of Ki-67 in cell cycle regulation is a promising approach to the development of anticancer drugs. Further research is required to explore the potential application of C1 as a Ki-67 inhibitor.
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Palm, Wilhelm, Youngkyu Park, Kevin Wright, Natalya N. Pavlova, David A. Tuveson, and Craig B. Thompson. "Abstract B43: The utilization of extracellular proteins as nutrients is suppressed by mTORC1." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-b43.

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Cunha, Heloíza Rabêlo, Johann Victor Neves de Souza, Ana Luzia Ferreira Farias, Patrick de Castro Cantuária, and Sheylla Susan Moreira da Silva de Almeida. "Obtaining alcoholic extract from leaves from species Sapindus Saponarial. (sapindaceae) for phytochemical analysis." In II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-020.

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Abstract Phytochemical analysis aims to know the secondary metabolites. According to Simões et. al. (2010), metabolism is the set of chemical reactions that are continuously occurring in each cell, being divided into primary and secondary. Beings and general m have primary metabolism (carbohydrates, lipids, proteins, and nucleic acids). Plants, micro-organisms and a few animals also have secondary metabolism (whose products, although not necessarily essential for the producing organism, guarantee advantages for their survival and the perpetuation of their species, in its ecosystem). Such metabolites can trigger reactions in the body, which according to dosage can be toxic or beneficial, which is why there is interest in the study of plant extracts (FRANCO et al., 2021).
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Diniz, Clebiana Alves e. silva, Poliana Silva de Brito, Tainan de Andrade Rocha, Suzana Maria de Oliveira Costa Meneses, and Julia Maria Pacheco Lins Magalhães. "Elderly people with diabetes: an analysis of the factors that are associated with lower limb amputation." In II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-028.

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Abstract Population aging has been occurring extremely rapidlyin developing countries, implying a higher prevalence of chronic-degenerative diseases (NCDs,s). Among these, diabetes mellitus stands out, a syndrome characterized by a chronic state of hyperglycemia and disorders in the metabolism of carbohydrates, lipids and proteins, associated with absolute or relative insulin deficiency and/or its action in the body.
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Reports on the topic "Proteins – Metabolism"

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Corscadden, Louise, and Anjali Singh. Metabolism And Measurable Metabolic Parameters. ConductScience, December 2022. http://dx.doi.org/10.55157/me20221213.

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Metabolism is the sum of chemical reactions involved in sustaining the life of organisms.[1] It constantly provides your body with the energy to perform essential functions. The process is categorized into two groups:[2] Catabolism: It’s the process of breaking down molecules to obtain energy. For example, converting glucose to pyruvate by cellular respiration. Anabolism: It’s the process of synthesis of compounds required to run the metabolic process of the organisms. For example, carbohydrates, proteins, lipids, and nucleic acids.[2] Metabolism is affected by a range of factors, such as age, sex, muscle mass, body size, and physical activity affect metabolism or BMR (the basal metabolic rate). By definition, BMR is the minimum amount of calories your body requires to function at rest.[2] Now, you have a rough idea about the concept. But, you might wonder why you need to study it. What and how metabolic parameters are measured to determine the metabolism of the organism? Find the answer to all these questions in this article.
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Blumwald, Eduardo, and Avi Sadka. Citric acid metabolism and mobilization in citrus fruit. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7587732.bard.

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Accumulation of citric acid is a major determinant of maturity and fruit quality in citrus. Many citrus varieties accumulate citric acid in concentrations that exceed market desires, reducing grower income and consumer satisfaction. Citrate is accumulated in the vacuole of the juice sac cell, a process that requires both metabolic changes and transport across cellular membranes, in particular, the mitochondrial and the vacuolar (tonoplast) membranes. Although the accumulation of citrate in the vacuoles of juice cells has been clearly demonstrated, the mechanisms for vacuolar citrate homeostasis and the components controlling citrate metabolism and transport are still unknown. Previous results in the PIs’ laboratories have indicated that the expression of a large number of a large number of proteins is enhanced during fruit development, and that the regulation of sugar and acid content in fruits is correlated with the differential expression of a large number of proteins that could play significant roles in fruit acid accumulation and/or regulation of acid content. The objectives of this proposal are: i) the characterization of transporters that mediate the transport of citrate and determine their role in uptake/retrieval in juice sac cells; ii) the study of citric acid metabolism, in particular the effect of arsenical compounds affecting citric acid levels and mobilization; and iii) the development of a citrus fruit proteomics platform to identify and characterize key processes associated with fruit development in general and sugar and acid accumulation in particular. The understanding of the cellular processes that determine the citrate content in citrus fruits will contribute to the development of tools aimed at the enhancement of citrus fruit quality. Our efforts resulted in the identification, cloning and characterization of CsCit1 (Citrus sinensis citrate transporter 1) from Navel oranges (Citrus sinesins cv Washington). Higher levels of CsCit1 transcripts were detected at later stages of fruit development that coincided with the decrease in the juice cell citrate concentrations (Shimada et al., 2006). Our functional analysis revealed that CsCit1 mediates the vacuolar efflux of citrate and that the CsCit1 operates as an electroneutral 1CitrateH2-/2H+ symporter. Our results supported the notion that it is the low permeable citrateH2 - the anion that establishes the buffer capacity of the fruit and determines its overall acidity. On the other hand, it is the more permeable form, CitrateH2-, which is being exported into the cytosol during maturation and controls the citrate catabolism in the juice cells. Our Mass-Spectrometry-based proteomics efforts (using MALDI-TOF-TOF and LC2- MS-MS) identified a large number of fruit juice sac cell proteins and established comparisons of protein synthesis patterns during fruit development. So far, we have identified over 1,500 fruit specific proteins that play roles in sugar metabolism, citric acid cycle, signaling, transport, processing, etc., and organized these proteins into 84 known biosynthetic pathways (Katz et al. 2007). This data is now being integrated in a public database and will serve as a valuable tool for the scientific community in general and fruit scientists in particular. Using molecular, biochemical and physiological approaches we have identified factors affecting the activity of aconitase, which catalyze the first step of citrate catabolism (Shlizerman et al., 2007). Iron limitation specifically reduced the activity of the cytosolic, but not the mitochondrial, aconitase, increasing the acid level in the fruit. Citramalate (a natural compound in the juice) also inhibits the activity of aconitase, and it plays a major role in acid accumulation during the first half of fruit development. On the other hand, arsenite induced increased levels of aconitase, decreasing fruit acidity. We have initiated studies aimed at the identification of the citramalate biosynthetic pathway and the role(s) of isopropylmalate synthase in this pathway. These studies, especially those involved aconitase inhibition by citramalate, are aimed at the development of tools to control fruit acidity, particularly in those cases where acid level declines below the desired threshold. Our work has significant implications both scientifically and practically and is directly aimed at the improvement of fruit quality through the improvement of existing pre- and post-harvest fruit treatments.
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Hanke, Andreas. Regulation of DNA Metabolism by DNA-Binding Proteins Probed by Single Molecule Spectroscopy. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada459264.

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Anderson, Olin D., Gad Galili, and Ann E. Blechl. Enhancement of Essential Amino Acids in Cereal Seeds: Four Approaches to Increased Lysine Content. United States Department of Agriculture, October 1998. http://dx.doi.org/10.32747/1998.7585192.bard.

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Cereal seeds are the basis of the human diet, and their amino acid composition is thus of major nutritional and economic importance. Currently, deficiencies in essential amino acids are addressed, when possible, by additionalprotein sources or by supplementing animal feed with non-cereal protein or synthetic amino acids. A number of strategies have been suggested to make cereal flours more complete and balanced sources of amino acids, although systematic examination of such strategies is rare. This project proposed to begin such a systematic examination using four complementary and parallel approaches to increasing wheat seed lysine: 1) Modifying endogenous wheat seed proteins for increased lysine composition. 2) Overexpression of naturally occurring high-lysine proteins in the wheat endosperm. 3) Ectopic expression of proteins in the wheat endosperm. 4) Alteration of free lysine levels in the wheat endosperm. The results of these studies are expected to be wheat lines with increased lysine content and will establish a clearer understanding of the approaches most likely to enhance cereal seed protein quality. Progress is reported for all four objectives, with a significant foundation for further work on two of the objectives (modification of wheat storage proteins and lysine metabolism). Plans for continuing work on all four objectives are briefly outlined.
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Wolf, Shmuel, and William J. Lucas. Involvement of the TMV-MP in the Control of Carbon Metabolism and Partitioning in Transgenic Plants. United States Department of Agriculture, October 1999. http://dx.doi.org/10.32747/1999.7570560.bard.

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The function of the 30-kilodalton movement protein (MP) of tobacco mosaic virus (TMV) is to facilitate cell-to-cell movement of viral progeny in infected plants. Our earlier findings have indicated that this protein has a direct effect on plasmodesmal function. In addition, these studies demonstrated that constitutive expression of the TMV MP gene (under the control of the CaMV 35S promoter) in transgenic tobacco plants significantly affects carbon metabolism in source leaves and alters the biomass distribution between the various plant organs. The long-term goal of the proposed research was to better understand the factors controlling carbon translocation in plants. The specific objectives were: A) To introduce into tobacco and potato plants a virally-encoded (TMV-MP) gene that affects plasmodesmal functioning and photosynthate partitioning under tissue-specific promoters. B) To introduce into tobacco and potato plants the TMV-MP gene under the control of promoters which are tightly repressed by the Tn10-encoded Tet repressor, to enable the expression of the protein by external application of tetracycline. C) To explore the mechanism by which the TMV-MP interacts with the endogenous control o~ carbon allocation. Data obtained in our previous project together with the results of this current study established that the TMV-MP has pleiotropic effects when expressed in transgenic tobacco plants. In addition to its ability to increase the plasmodesmal size exclusion limit, it alters carbohydrate metabolism in source leaves and dry matter partitioning between the various plant organs, Expression of the TMV-MP in various tissues of transgenic potato plants indicated that sugars and starch levels in source leaves are reduced below those of control plants when the TMV-MP is expressed in green tissue only. However, when the TMV-MP was expressed predominantly in PP and CC, sugar and starch levels were raised above those of control plants. Perhaps the most significant result obtained from experiments performed on transgenic potato plants was the discovery that the influence of the TMV-MP on carbohydrate allocation within source leaves was under developmental control and was exerted only during tuber development. The complexity of the mode by which the TMV-MP exerts its effect on the process of carbohydrate allocation was further demonstrated when transgenic tobacco plants were subjected to environmental stresses such as drought stress and nutrients deficiencies, Collectively, these studies indicated that the influence of the TMV-MP on carbon allocation L the result of protein-protein interaction within the source tissue. Based on these results, together with the findings that plasmodesmata potentiate the cell-to-cell trafficking of viral and endogenous proteins and nucleoproteins complexes, we developed the theme that at the whole plant level, the phloem serves as an information superhighway. Such a long-distance communication system may utilize a new class of signaling molecules (proteins and/or RNA) to co-ordinate photosynthesis and carbon/nitrogen metabolism in source leaves with the complex growth requirements of the plant under the prevailing environmental conditions. The discovery that expression of viral MP in plants can induce precise changes in carbon metabolism and photoassimilate allocation, now provide a conceptual foundation for future studies aimed at elucidating the communication network responsible for integrating photosynthetic productivity with resource allocation at the whole-plant level. Such information will surely provide an understanding of how plants coordinate the essential physiological functions performed by distantly-separated organs. Identification of the proteins involved in mediating and controlling cell-to-cell transport, especially at the companion cell-sieve element boundary, will provide an important first step towards achieving this goal.
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Blumwald, Eduardo, and Avi Sadka. Sugar and Acid Homeostasis in Citrus Fruit. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697109.bard.

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Citrus fruit quality standards have been determined empirically, depending on species and on the particular growing regions. In general, the TSS (total soluble solids) to total acidity (TA) ratio determines whether citrus fruit can be marketed. Soluble sugars account for most of the TSS during harvest while TA is determined almost solely by the citric acid content, which reaches levels of 1-5% by weight in many cultivated varieties. Acid and sugar homeostasis in the fruit is critical for the management of existing cultivars, the development of new cultivars, the improvement of pre- and post-harvest strategies and the control of fruit quality and disorders. The current proposal (a continuation of a previous proposal) aimed at: (1) completing the citrus fruit proteome and metabolome, and establish a citrus fruit functional database, (2) further characterization of the control of fruit acidity by studying the regulation of key steps affecting citrate metabolism, and determine the fate of citrate during acid decline stage, and (3) Studying acid and sugar homeostasis in citrus fruits by characterizing transport mechanisms across membranes. These aims were completed as the following: (1) Our initial efforts were aimed at the characterization and identification of citric acid transporters in citrus juice cells. The identification of citrate transporters at the vacuole of the citrus juice cell indicated that the steady-state citrate cytosolic concentration and the action of the cytosolic aconitase were key elements in establishing the pH homeostat in the cell that regulates the metabolic shift towards carbon usage in the fruit during the later stages of fruit development. We focused on the action of aconitase, the enzyme mediating the metabolic use of citric acid in the cells, and identified processes that control carbon fluxes in developing citrus fruits that control the fruit acid load; (2) The regulation of aconitase, catalyzing a key step in citrate metabolism, was further characterized by using two inhibitors, citramalte and oxalomalte. These compounds significantly increased citrate content and reduced the enzyme’s activity. Metabolite profiling and changes of amino-acid metabolizing enzymes in oxalomalate- treated cells suggested that the increase in citrate, caused by aconitase inhibition, induces amino acid synthesis and the GABA shunt, in accordance with the suggested fate of citrate during the acid decline stage in citrus fruit. (3) We have placed a considerable amount of time on the development of a citrus fruit proteome that will serve to identify all of the proteins in the juice cells and will also serve as an aid to the genomics efforts of the citrus research community (validating the annotation of the fruit genes and the different ESTs). Initially, we identified more than 2,500 specific fruit proteins and were able to assign a function to more than 2,100 proteins (Katz et al., 2007). We have now developed a novel Differential Quantitative LC-MS/MS Proteomics Methodology for the identification and quantitation of key biochemical pathways in fruits (Katz et al., 2010) and applied this methodology to identify determinants of key traits for fruit quality (Katz et al., 2011). We built “biosynthesis maps” that will aid in defining key pathways associated with the development of key fruit quality traits. In addition, we constructed iCitrus (http://wiki.bioinformatics.ucdavis.edu/index.php/ICitrus), a “functional database” that is essentially a web interface to a look-up table that allows users to use functional annotations in the web to identify poorly annotated citrus proteins. This resource will serve as a tool for growers and field extension specialists.
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Ghanim, Murad, Joe Cicero, Judith K. Brown, and Henryk Czosnek. Dissection of Whitefly-geminivirus Interactions at the Transcriptomic, Proteomic and Cellular Levels. United States Department of Agriculture, February 2010. http://dx.doi.org/10.32747/2010.7592654.bard.

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Our project focuses on gene expression and proteomics of the whitefly Bemisia tabaci (Gennadius) species complex in relation to the internal anatomy and localization of expressed genes and virions in the whitefly vector, which poses a major constraint to vegetable and fiber production in Israel and the USA. While many biological parameters are known for begomovirus transmission, nothing is known about vector proteins involved in the specific interactions between begomoviruses and their whitefly vectors. Identifying such proteins is expected to lead to the design of novel control methods that interfere with whitefly-mediated begomovirus transmission. The project objectives were to: 1) Perform gene expression analyses using microarrays to study the response of whiteflies (B, Q and A biotypes) to the acquisition of begomoviruses (Tomato yellow leaf curl (TYLCV) and Squash leaf curl (SLCV). 2) Construct a whitefly proteome from whole whiteflies and dissected organs after begomovirus acquisition. 3) Validate gene expression by q-RTPCR and sub-cellular localization of candidate ESTs identified in microarray and proteomic analyses. 4) Verify functionality of candidate ESTs using an RNAi approach, and to link these datasets to overall functional whitefly anatomical studies. During the first and second years biological experiments with TYLCV and SLCV acquisition and transmission were completed to verify the suitable parameters for sample collection for microarray experiments. The parameters were generally found to be similar to previously published results by our groups and others. Samples from whole whiteflies and midguts of the B, A and Q biotypes that acquired TYLCV and SLCV were collected in both the US and Israel and hybridized to B. tabaci microarray. The data we analyzed, candidate genes that respond to both viruses in the three tested biotypes were identified and their expression that included quantitative real-time PCR and co-localization was verified for HSP70 by the Israeli group. In addition, experiments were undertaken to employ in situ hybridization to localize several candidate genes (in progress) using an oligonucleotide probe to the primary endosymbiont as a positive control. A proteome and corresponding transcriptome to enable more effective protein identification of adult whiteflies was constructed by the US group. Further validation of the transmission route of begomoviruses, mainly SLCV and the involvement of the digestive and salivary systems was investigated (Cicero and Brown). Due to time and budget constraints the RNAi-mediated silencing objective to verify gene function was not accomplished as anticipated. HSP70, a strong candidate protein that showed over-expression after TYLCV and SLCV acquisition and retention by B. tabaci, and co-localization with TYLCV in the midgut, was further studies. Besides this protein, our joint research resulted in the identification of many intriguing candidate genes and proteins that will be followed up by additional experiments during our future research. To identify these proteins it was necessary to increase the number and breadth of whitefly ESTs substantially and so whitefly cDNAs from various libraries made during the project were sequenced (Sanger, 454). As a result, the proteome annotation (ID) was far more successful than in the initial attempt to identify proteins using Uniprot or translated insect ESTs from public databases. The extent of homology shared by insects in different orders was surprisingly low, underscoring the imperative need for genome and transcriptome sequencing of homopteran insects. Having increased the number of EST from the original usable 5500 generated several years ago to >600,000 (this project+NCBI data mining), we have identified about one fifth of the whitefly proteome using these new resources. Also we have created a database that links all identified whitefly proteins to the PAVEdb-ESTs in the database, resulting in a useful dataset to which additional ESTS will be added. We are optimistic about the prospect of linking the proteome ID results to the transcriptome database to enable our own and other labs the opportunity to functionally annotate not only genes and proteins involved in our area of interest (whitefly mediated transmission) but for the plethora of other functionalities that will emerge from mining and functionally annotating other key genes and gene families in whitefly metabolism, development, among others. This joint grant has resulted in the identification of numerous candidate proteins involved in begomovirus transmission by B. tabaci. A next major step will be to capitalize on validated genes/proteins to develop approaches to interfere with the virus transmission.
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Amir, Rachel, David J. Oliver, Gad Galili, and Jacline V. Shanks. The Role of Cysteine Partitioning into Glutathione and Methionine Synthesis During Normal and Stress Conditions. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7699850.bard.

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The objective of this research is to study the nature of the competition for cysteine (Cys), the first organic sulfur-containing compound, between its two main metabolites, glutathione (GSH) and methionine (Met). GSH plays a central role in protecting plants during various stresses, while Met, an essential amino acid, regulates essential processes and metabolites in plant cells through its metabolite S-adenosyl-Met. Our results, which are based on flux analysis and measurements of Met- metabolites, show that the flux towards Met synthesis is high during non-stress conditions, however the flux is significantly reduced under stress conditions, when there is high synthesis of GSH. Under oxidative stress the expression level of the regulatory enzyme of Met synthesis, cystathionine g-synthase (CGS) was reduced. By using three different systems, we have found that that GSH down regulates the expression level of CGS, thus reducing Met synthesis. We have found that this regulation occurs at the post-transcriptional level, and further studies have shown that it occurs at post-translationaly. To reveal how oxidative stress affects the flux towards Met and GSH, flux analysis was performed. We have found that the level of Met is significantly reduced, while the level of glutathione significantly increases during stress. Under stress conditions most of the glutathione is converted from GSH to GSSG (the oxidised form of glutathione). These results suggest that under normal growth conditions, Cys is channelled towards both pathways to support GSH accumulation and the synthesis of growth-essential Met metabolites. However, during oxidative stress, when a high level of GSH is required to protect the plants, the levels of GSH increase while those of CGS are reduced. This reduction leaves more Cys available for GSH synthesis under stress conditions. In addition we have also studied the effects of high GSH level on the transcriptome profile. The analysis revealed that GSH affects the expression level of many major genes coding to enzymes or proteins associated with photosynthesis, starch degradation, hormone metabolism (especially genes associated with jasmonate), biotic stress (especially genes associated with PR-proteins), cytochrome P450 genes, regulation of transcription and signaling (especially genes associated with receptor kinases and calcium). These results suggest that indeed GSH levels affect different pathways and metabolites in plants.
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Wang, X. F., and M. Schuldiner. Systems biology approaches to dissect virus-host interactions to develop crops with broad-spectrum virus resistance. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134163.bard.

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More than 60% of plant viruses are positive-strand RNA viruses that cause billion-dollar losses annually and pose a major threat to stable agricultural production, including cucumber mosaic virus (CMV) that infects numerous vegetables and ornamental trees. A highly conserved feature among these viruses is that they form viral replication complexes (VRCs) to multiply their genomes by hijacking host proteins and remodeling host intracellular membranes. As a conserved and indispensable process, VRC assembly also represents an excellent target for the development of antiviral strategies that can be used to control a wide-range of viruses. Using CMV and a model virus, brome mosaic virus (BMV), and relying on genomic tools and tailor-made large-scale resources specific for the project, our original objectives were to: 1) Identify host proteins that are required for viral replication complex assembly. 2) Dissect host requirements that determine viral host range. 3) Provide proof-of-concept evidence of a viral control strategy by blocking the viral replication complex-localized phospholipid synthesis. We expect to provide new ways and new concepts to control multiple viruses by targeting a conserved feature among positive-strand RNA viruses based on our results. Our work is going according to the expected timeline and we are progressing well on all aims. For Objective 1, among ~6,000 yeast genes, we have identified 96 hits that were possibly play critical roles in viral replication. These hits are involved in cellular pathways of 1) Phospholipid synthesis; 2) Membrane-shaping; 3) Sterol synthesis and transport; 4) Protein transport; 5) Protein modification, among many others. We are pursuing several genes involved in lipid metabolism and transport because cellular membranes are primarily composed of lipids and lipid compositional changes affect VRC formation and functions. For Objective 2, we have found that CPR5 proteins from monocotyledon plants promoted BMV replication while those from dicotyledon plants inhibited it, providing direct evidence that CPR5 protein determines the host range of BMV. We are currently examining the mechanisms by which dicot CPR5 genes inhibit BMV replication and expressing the dicot CPR5 genes in monocot plants to control BMV infection. For Objective 3, we have demonstrated that substitutions in a host gene involved in lipid synthesis, CHO2, prevented the VRC formation by directing BMV replication protein 1a (BMV 1a), which remodels the nuclear membrane to form VRCs, away from the nuclear membrane, and thus, no VRCs were formed. This has been reported in Journal of Biological Chemistry. Based on the results from Objective 3, we have extended our plan to demonstrate that an amphipathic alpha-helix in BMV 1a is necessary and sufficient to target BMV 1a to the nuclear membrane. We further found that the counterparts of the BMV 1a helix from a group of viruses in the alphavirus-like superfamily, such as CMV, hepatitis E virus, and Rubella virus, are sufficient to target VRCs to the designated membranes, revealing a conserved feature among the superfamily. A joint manuscript describing these exciting results and authored by the two labs will be submitted shortly. We have also successfully set up systems in tomato plants: 1) to efficiently knock down gene expression via virus-induced gene silencing so we could test effects of lacking a host gene(s) on CMV replication; 2) to overexpress any gene transiently from a mild virus (potato virus X) so we could test effects of the overexpressed gene(s) on CMV replication. In summary, we have made promising progress in all three Objectives. We have identified multiple new host proteins that are involved in VRC formation and may serve as good targets to develop antiviral strategies; have confirmed that CPR5 from dicot plants inhibited viral infection and are generating BMV-resistance rice and wheat crops by overexpressing dicot CPR5 genes; have demonstrated to block viral replication by preventing viral replication protein from targeting to the designated organelle membranes for the VRC formation and this concept can be further employed for virus control. We are grateful to BARD funding and are excited to carry on this project in collaboration.
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Harmon, David L., Israel Bruckental, Gerald B. Huntington, Yoav Aharoni, and Amichai Arieli. Influence of Small Intestinal Protein on Carbohydrate Assimilation in Beef and Dairy Cattle. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7570572.bard.

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The long term goal of the proposed research, "Influence of small intestinal protein on carbohydrate assimilation and metabolism in beef and dairy cattle" was to define the limits of small intestinal starch digestion and clarify regulatory mechanisms involved in starch assimilation in cattle. It was hypothesized that dietary protein plays a critical role in the regulation of intestinal digestion; however, studies clearly identifying this role were lacking. The first two experiments quantified starch digestion (disappearance from the small intestine) in response to known increments in duodenal protein supply and found that the quantity of DM, OM and starch disappearing from the small intestine increased linearly (P <.01) with protein infusion. A follow-up experiment also demonstrated that casein infusion linearly increased pancreatic a-amylase concentration and secretion rate. The final experiment provided critical data on metabolic fates of glucose derived from intestinal starch digestion. These data demonstrated that increasing postruminal starch supply does increase the metabolism of glucose by visceral tissues: however, this increase is minor (20%) compared with the increase in portal production (70%). These changes can have a dramatic impact on the glucose economy of the animal and result in large increases in the amount of glucose reaching peripheral tissues.
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