Relevant bibliographies by topics / Protein metabolism

Academic literature on the topic 'Protein metabolism'

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Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Protein metabolism"

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Bakhtiyorovich, Eshburiev Sobir, and Kasimov SaifiddinJakhongir Ugli. "DIAGNOSIS OF PROTEIN METABOLISM DISORDERS IN FISH." American Journal Of Agriculture And Horticulture Innovations 03, no. 05 (May 1, 2023): 04–12. http://dx.doi.org/10.37547/ajahi/volume03issue05-02.

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This article describes the most important diagnostic tests in determining protein metabolism disorders of Fish and their importance. When diagnosing disorders of protein metabolism in fish, it is necessary to carry out an analysis of feeding them according to age (nutritional norms), characteristic clinical signs (loss of appetite, development of coxexia, lag behind growth and development), pathologoanatomic changes (accumulation of fat around internal azos, darkening of body color, coxexia, blood clots in the intestines), morphobiochemical changes in the blood (hemoglobin, erythrocyte count, average of hematocrit, leukocyte count, neutrophil with Rod nucleus, basophils, monocytes, lymphocytes, analysis of the average total protein, total calcium, inorganic phosphorus and retinol) is considered important.
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TAKAHASHI, Shin-Ichirou. "Hormone and protein metabolism. Insulin and protein metabolism." Journal of the agricultural chemical society of Japan 61, no. 10 (1987): 1300–1304. http://dx.doi.org/10.1271/nogeikagaku1924.61.1300.

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KATO, Shigeaki. "Hormone and protein metabolism. Glucocorticoid and protein metabolism." Journal of the agricultural chemical society of Japan 61, no. 10 (1987): 1309–11. http://dx.doi.org/10.1271/nogeikagaku1924.61.1309.

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TAKENAKA, Akio. "Hormone and protein metabolism. Glucagon and protein metabolism." Journal of the agricultural chemical society of Japan 61, no. 10 (1987): 1312–14. http://dx.doi.org/10.1271/nogeikagaku1924.61.1312.

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YAGASAKI, Kazumi. "Hormone and protein metabolism. Prostaglandin and protein metabolism." Journal of the agricultural chemical society of Japan 61, no. 10 (1987): 1315–18. http://dx.doi.org/10.1271/nogeikagaku1924.61.1315.

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Anderson, Kristin A., and Matthew D. Hirschey. "Mitochondrial protein acetylation regulates metabolism." Essays in Biochemistry 52 (May 25, 2012): 23–35. http://dx.doi.org/10.1042/bse0520023.

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Changes in cellular nutrient availability or energy status induce global changes in mitochondrial protein acetylation. Over one-third of all proteins in the mitochondria are acetylated, of which the majority are involved in some aspect of energy metabolism. Mitochondrial protein acetylation is regulated by SIRT3 (sirtuin 3), a member of the sirtuin family of NAD+-dependent protein deacetylases that has recently been identified as a key modulator of energy homoeostasis. In the absence of SIRT3, mitochondrial proteins become hyperacetylated, have altered function, and contribute to mitochondrial dysfunction. This chapter presents a review of the functional impact of mitochondrial protein acetylation, and its regulation by SIRT3.
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Emery, Peter. "Basic metabolism: protein." Surgery (Oxford) 27, no. 5 (May 2009): 185–89. http://dx.doi.org/10.1016/j.mpsur.2009.04.005.

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Emery, Peter W. "Basic metabolism: protein." Surgery (Oxford) 30, no. 5 (May 2012): 209–13. http://dx.doi.org/10.1016/j.mpsur.2012.02.008.

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Emery, Peter W. "Basic metabolism: protein." Surgery (Oxford) 33, no. 4 (April 2015): 143–47. http://dx.doi.org/10.1016/j.mpsur.2015.01.008.

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KATO, Hisanori. "Hormone and protein metabolism. Insulin-like growth factor and protein metabolism." Journal of the agricultural chemical society of Japan 61, no. 10 (1987): 1305–8. http://dx.doi.org/10.1271/nogeikagaku1924.61.1305.

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Dissertations / Theses on the topic "Protein metabolism"

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Chonlatee, Cheewasedtham. "Protein metabolism in fish." Thesis, University of Aberdeen, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327299.

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Barle, Hans. "Liver protein metabolism in man /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3151-8/.

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Cooper, Brendan Gerard. "Protein metabolism in human pregnancy." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315040.

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Munoz, Kathryn Anne. "Protein metabolism in unweighting atrophy." Diss., The University of Arizona, 1993. http://hdl.handle.net/10150/186136.

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The weightless environment results in atrophy of the anti-gravity muscles. Hindlimb suspension is a model for weightlessness induced atrophy. This study evaluated the effects of hindlimb suspension, microgravity and exercise training followed by suspension on skeletal muscle. Soleus mass, myofibrillar and sarcoplasmic protein content were measured in one to four day hindlimb suspended animals. Protein synthesis was measured by intramuscular injection of ³H phenylalanine with correction for the difference between tRNA and intracellular specific activities. Myofibrillar protein loss was minimal after two days of unweighting but significant after three days. Although sarcoplasmic protein content showed no change, synthesis of both protein pools declined in parallel. Myofibrillar degradation increased during the first three days of unweighting, partially accounting for protein loss. The decline in degradation during day four explained the slower rate of protein loss at this time. Sarcoplasmic protein degradation increased slightly during the first two days of unweighting then declined sharply, thus explaining the sparing of sarcoplasmic proteins. Animals exposed to weightlessness showed soleus atrophy similar to suspended animals. The plantaris and gastrocnemius had reduced growth while the extensor digitorum longus and tibialis anterior grew normally in flight and suspended animals. Insulin stimulated glucose uptake was enhanced in soleus, but not extensor digitorum longus of flight and suspended animals. In situ insulin and IGF-1 stimulated 2-deoxyglucose uptake was greater after six days of suspension. Voluntary wheel training increased soleus mass, protein content and in vivo protein synthesis which plateaued by three weeks. Suspended or trained-suspended animals showed reductions in soleus mass, protein content and synthesis compared to trained animals. However, trained-suspended animals showed higher values for protein content and synthesis compared to suspended animals. In conclusion, these studies show that unweighting atrophy is characterized by decreased synthesis and increased degradation of myofibrillar proteins, and a sparing of sarcoplasmic proteins due to slower degradation. Tail-cast hindlimb suspension may be used as a ground based model to mimic the effects of weightlessness on muscle proteins. Wheel training causes muscle hypertrophy; and although training prior to suspension provides some protection against protein loss, it does not prevent atrophy.
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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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Temprano, López Ana. "The lipin protein family in human adipocytes: lipid metabolism and obesity." Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/398025.

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Les lipins són una família conservada evolutivament de fosfatases de fosfatidat (PAP1) dependents de Mg2+, que generen diacilglicerol per a la síntesi de fosfolípids i triacilglicerol. En mamífers, la família consta de lipina-1, lipina-2 i lipina-3. Mentre en ratolins la mutació del gen Lpin1 causa lipodistròfia, les mutacions deletèries en el gen LPIN1 en humans no afecten la distribució del greix. No obstant, persones amb diabetis tipus 2 mostren nivells reduïts de l'expressió de LPIN1 i de l'activitat PAP1. Aquesta tesi estudia el paper de les lipins en el teixit adipós humà, la adipogènesi i la lipòlisi. Descobrim que la expressió de gens i proteïnes lipin és alterada en el teixit adipós de les persones amb diabetis tipus 2. Silenciant cada membre de la família lipin en la línia cel•lular humana de preadipòcits del síndrome Simpson-Golabi-Behmel (SGBS), mostrem que mentre que els tres membres tenen un paper en el primers estadis de l’adipogènesi, els preadipòcits silenciats de lipin es diferencien i acumulen lípids neutres, la qual cosa condueix a la hipòtesi de l'existència de vies alternatives per a la síntesi de triacilglicerol en adipòcits humans quan es reprimeix l'expressió de les lipin. Les lipin participen també en el reciclatge d'àcids grassos alliberats mitjançant la via lipolítica. Després de la inducció de la lipòlisi, les lipines són defosforilades i es desplacen a la membrana del reticle endoplasmàtic, on exerceixen la seva funció enzimàtica. Aquesta activació és induïda pels àcids grassos alliberats i s'inverteix amb la presència d’albúmina o triacsin C. La inducció d’adipòcits silenciats de cada lipina demostra el seu paper en el metabolisme dels lípids neutres. En resum, les lipin semblen no tenir un paper imprescindible en la adipogènesi humana però sí poden comprometre el reciclatge d'àcids grassos, important per a la homeòstasis lipídica.
Las lipinas son una familia de fosfatasas de fosfatidato (PAP1) dependientes de Mg2+ evolutivamente conservadas, que generan diacilglicerol para la síntesis de fosfolípidos y triacilglicerol. En mamíferos, la familia consiste en lipina-1, lipina-2, y lipina-3. Mientras en ratones la mutación del gen Lpin1 causa lipodistrofia, las mutaciones deletéreas en el gen LPIN1 en humanos no afectan a la distribución de grasa. Sin embargo, los individuos con diabetes tipo 2 manifiestan niveles reducidos de expresión de LPIN1 y de actividad PAP1. En esta tesis doctoral se estudia la función de las lipinas en el tejido adiposo humano, la adipogénesis y la lipólisis. Descubrimos que la expresión génica y proteica de las lipinas está alterada en el tejido adiposo de individuos con diabetes tipo 2. La depleción de cada miembro de las lipinas en la línea celular humana de preadipocitos del síndrome Simpson–Golabi–Behmel (SGBS), mostró que, a pesar de que los tres miembros tienen un papel en la adipogénesis temprana, los adipocitos deplecionados de lipinas se diferencian y acumulan lípidos neutros, llevándonos a la hipótesis de la existencia de vías alternativas para la síntesis de triacilglicerol en adipocitos humanos cuando la expresión de las lipinas es reprimida. Las lipinas también intervienen en el reciclaje de los ácidos grasos liberados por la vía lipolítica. Tras la inducción de la lipólisis, las lipinas son defosforiladas y se desplazan a la membrana del retículo endoplásmico, donde ejercen su función. Esta activación es inducida por los ácidos grasos liberados, y revertida con albúmina o triacsin C. La depleción de cada lipina en adipocitos SGBS y posterior inducción de la lipólisis, demuestra su papel en el metabolismo de lípidos neutros. En resumen, las lipinas parecen no tener un papel indispensable en la adipogénesis humana pero sí comprometer el reciclaje de ácidos grasos, importante para la homeostasis lipídica.
Lipins are evolutionarily conserved Mg2+-dependent phosphatidate phosphatases (PAP1) that generate diacylglycerol for phospholipid and triacylglycerol synthesis. In mammals the Lipin family consists of lipin-1, lipin-2 and lipin-3. Whereas mutations in the Lpin1 gene cause lipodystrophy in mouse models, LPIN1 deleterious mutations in humans do not affect fat distribution. However, reduced LPIN1 expression and PAP1 activity have been described in participants with type 2 diabetes. In this doctoral thesis we investigate the roles of all lipin family members in human adipose tissue, adipogenesis and lipolysis. We found that adipose tissue gene and protein expression of the lipin family is altered in type 2 diabetes. Depletion of every lipin family member in a human Simpson–Golabi–Behmel syndrome (SGBS) pre-adipocyte cell line showed that even though all members alter early stages of adipogenesis, lipin-silenced cells differentiate and accumulate neutral lipids, pointing to the hypothesis of alternative pathways for triacylglycerol synthesis under repression of lipin expression. Lipins also have a role in the recycling of the fatty acids released by the lipolytic pathway. They become dephosphorylated upon lipolytic induction, and translocate to their active site, the endoplasmic reticulum membrane. This activation is induced by fatty acids and reversed with albumin or triacsin C. Depletion of every lipin member and subsequently stimulation of lipolysis in SGBS adipocytes revealed a role for lipins in neutral lipid metabolism. Overall, our data support that lipins may not have an indispensable role in adipogenesis, but their depletion compromise fatty acid recycling and lipid homeostasis.
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Smith, Kate L. "Tumour associated proteolysis and protein metabolism." Thesis, Aston University, 1992. http://publications.aston.ac.uk/12604/.

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The effect of cancer cachexia on protein metabolism has been studied in mice transplanted with the MAC16 adenocarcinoma. The progressive cachexia induced by the MAC16 tumour was characterised by a reduction in carcass nitrogen between 16-30% weight loss and a reciprocal increase in tumour nitrogen content. Carcass nitrogen loss was accompanied by a concomitant decrease in gastrocnemius muscle weight and nitrogen content and also by a decrease in liver nitrogen content. The loss of gastrocnemius muscle throughout the progression of cachexia was attributable to a 60% decrease in the rate of protein synthesis and a 240% increase in the rate of protein degradation. The loss of skeletal muscle protein that may be mediated by an increased rate of protein degradation has been correlated with a circulatory catabolic factor present only in cachectic tumour-bearing animals, that degrades host muscle in vitro. The proteolysis-inducing factor was found to be heat stable, not a serine protease and was inhibited by indomethacin and eicosapentaenoic acid (EPA) in a dose-related manner. The proteolytic factor induced prostaglandin E2 formation in the gastrocnemius muscle of non tumour-bearing animals and this effect was inhibited by indomethacin and EPA. In vivo studies show EPA (2.0g/kg-1 by gavage) to effectively reverse the decrease in body weight in animals bearing the MAC16 tumour with a concomitant reduction in tumour growth. Muscle from animals treated with EPA showed a decrease (60%) in protein degradation without an effect on protein synthesis. The action of the factor was largely mimicked by triarachidonin and trilinoleia. The increased serum levels of arachidonic acid in cachectic tumour-bearing animals may thus be responsible for increased protein degradation through prostanoid metabolism.
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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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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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Bowerman, Peter A. "Exploring protein interactions and intracellular localization in regulating flavonoid metabolism." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/77174.

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The organization of biological processes via protein-protein interactions and the subcellular localization of enzymes is believed to be fundamental to many aspects of metabolism. Although this organization has been demonstrated in several systems, the mechanisms by which it is established and regulated are still not well understood. The flavonoid biosynthetic pathway offers a unique system in which to study several important aspects of metabolism. Here we describe a novel toolset of mutant alleles within the flavonoid biosynthetic pathway. In addition, we discuss the use of several of these alleles together with a number of emerging technologies to probe the role of subcellular localization of chalcone synthase, the first committed flavonoid biosynthetic enzyme, on metabolic flux, and to characterize a novel chalcone synthase-interacting protein. The over-expression of this interacting protein induces novel phenotypes that are likely associated with the production or distribution of auxin. Further, interaction analyses between recombinant flavonoid biosynthetic enzymes point to the possibility that post-translational modifications play an important role in promoting interactions.
Ph. D.
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Books on the topic "Protein metabolism"

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L, Ferraiolo Bobbe, Mohler Marjorie A, and Gloff Carol A, eds. Protein pharmacokinetics and metabolism. New York: Plenum, 1992.

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M, Umpleby A., and Russell-Jones D. L, eds. Protein metabolism. London: Baillière Tindall, 1996.

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Welle, Stephen. Human Protein Metabolism. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1458-8.

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

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Ferraiolo, Bobbe L., Marjorie A. Mohler, and Carol A. Gloff, eds. Protein Pharmacokinetics and Metabolism. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-2329-5.

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Hasselgren, Per-Olof. Protein metabolism in sepsis. Austin: R.G. Landes Co., 1993.

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

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Protein homeostasis. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2011.

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C, Waterlow J., and Waterlow J. C, eds. Protein turnover. Cambridge, MA: CABI Pub., 2006.

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Ki, Paik Woon, and Kim Sangduk, eds. Protein methylation. Boca Raton, Fla: CRC Press, 1990.

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Book chapters on the topic "Protein metabolism"

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Lefebvre, Cedric W., Jay P. Babich, James H. Grendell, James H. Grendell, John E. Heffner, Ronan Thibault, Claude Pichard, et al. "Protein Metabolism." In Encyclopedia of Intensive Care Medicine, 1862–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_746.

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Griminger, P., and C. G. Scanes. "Protein Metabolism." In Avian Physiology, 326–44. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4862-0_14.

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Miller, Benjamin F., and Matthew M. Robinson. "Metabolism, Protein." In Encyclopedia of Exercise Medicine in Health and Disease, 576–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_131.

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Kowaltowski, Alicia, and Fernando Abdulkader. "Protein Metabolism." In Where Does All That Food Go?, 67–78. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-50968-2_6.

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Poortmans, J. R. "Protein Metabolism." In Principles of Exercise Biochemistry, 227–78. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000074370.

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Norberg, Åke, Felix Liebau, and Jan Wernerman. "Protein Metabolism." In The Stress Response of Critical Illness: Metabolic and Hormonal Aspects, 95–106. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27687-8_9.

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Welle, Stephen. "The Importance of Protein Dynamics." In Human Protein Metabolism, 1–10. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1458-8_1.

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Welle, Stephen. "Basic Mechanisms of Protein Turnover." In Human Protein Metabolism, 11–28. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1458-8_2.

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Welle, Stephen. "Methods for Studying Protein Metabolism in Humans." In Human Protein Metabolism, 29–71. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1458-8_3.

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Welle, Stephen. "Normative Data from Infancy to Old Age." In Human Protein Metabolism, 72–90. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4612-1458-8_4.

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Conference papers on the topic "Protein metabolism"

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Yang, L., Q. Yang, Q. H. Liu, H. Zhang, S. H. Sun, and T. C. Zhuang. "Rice protein level affects cholesterol metabolism." In EM 2011). IEEE, 2011. http://dx.doi.org/10.1109/icieem.2011.6035585.

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SCHÜTTE, MORITZ, NIELS KLITGORD, DANIEL SEGRÈ, and OLIVER EBENHÖH. "CO-EVOLUTION OF METABOLISM AND PROTEIN SEQUENCES." In Proceedings of the 9th Annual International Workshop on Bioinformatics and Systems Biology (IBSB 2009). IMPERIAL COLLEGE PRESS, 2010. http://dx.doi.org/10.1142/9781848165786_0013.

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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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Bee, G., F. Tessier, P. Schlegel, and M. Rodehutscord. "Variation in protein deposition efficiency as assessed by Dual Energy X-ray Absorptiometry measurements in barrows fed a protein-restricted diet." 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_16.

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Htoo, J. K. "Utilization of protein-bound or crystalline amino acids for protein deposition, growth and carcass composition of growing pigs in relation to sustainable production." 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_2.

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Lærke, H. N., L. Stødkilde, M. Ambye-Jensen, S. K. Jensen, J. F. Sørensen, J. V. Nørgaard, and K. E. Bach Knudsen. "Extracts of green biomass as source of protein for pigs." 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_28.

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Florescu, I. C., U. Krogh, and J. V. Nørgaard. "Amino acid absorption kinetics in pigs fed different protein sources." 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_86.

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Dorokhina, Yu A., and G. F. Ryzhkova. "Morphological and biochemical parameters of blood in rabbits when using energymetabolic compositions." In SPbVetScience. FSBEI HE St. Petersburg SUVM, 2023. http://dx.doi.org/10.52419/3006-2022-7-18-23.

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Modern animal husbandry can no longer be imagined without special biologically active additives and a variety of protein, vitamin and mineral complexes. Among all additives, a special place is occupied by energy-metabolic compositions that give animals all the most necessary and important substances. The composition of the EC includes: yantaric acid is a universal intracellular metabolite, widely involved in metabolic reactions in the body; citric acid is the main intermediate product of the metabolic cycle of tricarboxylic acids, plays an important role in the system of biochemical reactions of cellular respiration of living organisms; iodinol – uniquea fecal medicinal substance, it determines high biological activity, regulates immunity and metabolism in the body; cyanocoalamin (vitamin B12) - prevents the appearance of anemia, enhances immunity, plays an important role in regulating the function of hematopoietic organs; glycerin has antiseptic and preservative properties.
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Alvarenga, F. A. P., I. J. Lean, T. I. R. C. Alvarenga, and P. McGilchrist. "Impact of dietary protein levels on adrenaline sensitivity of beef cattle." 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_116.

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van Helvoort, M. H. A., and J. J. Zonderland. "Protein and lipid mass per sex derived from carcass backfat thickness." 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_155.

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Reports on the topic "Protein metabolism"

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Ohlrogge, J. B. Role of acyl carrier protein isoforms in plant lipid metabolism: Progress report. Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/6210587.

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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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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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Reue, K., S. Rehnmark, R. D. Cohen, T. H. Leete, M. H. Doolittle, C. S. Giometti, K. Mishler, and B. G. Slavin. The fatty liver dystrophy (fld) mutation: Developmentally related alterations in hepatic triglyceride metabolism and protein expression. Office of Scientific and Technical Information (OSTI), July 1997. http://dx.doi.org/10.2172/505325.

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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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Tiedje, James M. Integrated Analysis of Protein Complexes and Regulatory Networks Involved in Anaerobic Energy Metabolism of Shewanella Oneidensis MR-1. Office of Scientific and Technical Information (OSTI), June 2005. http://dx.doi.org/10.2172/893447.

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Cohen, Jerry D., and Ephraim Epstein. Metabolism of Auxins during Fruit Development and Ripening. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7573064.bard.

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We had proposed to look at several aspects of auxin metabolism in fruit tissues: 1) IAA biosynthesis from tryptophan and IAA biosynthesis via the non-tryptophan pathway; 2) changes in the capacity to form conjugates and catabolites of auxin at different times during fruit development and; 3) the effects of modifying auxin metabolism in fruit tissues. The latter work focused primarily on the maize iaglu gene, with initial studies also using a bacterial gene for hydrolysis of IAA-aspartate. These metabolic and molecular studies were necessary to define potential benefits of auxin metabolism modification and will direct future efforts for crop improvement by genetic methods. An in vitro system was developed for the production of tomato fruit in culture starting from immature flowers in order to ascertain the effect of auxin modification on fruit ripening. IAA supplied to the fruit culture media prior to breaker stage resulted in an increase in the time period between breaker and red-ripe stages from 7 days without additional IAA to 12 days when 10-5 M IAA was added. These results suggest that significant changes in the ripening period could be obtained by alteration of auxin relationships in tomato fruit. We generated transgenic tomato plants that express either the maize iaglu gene or reduced levels of the gene that encodes the enzyme IAA-glucose synthetase. A modified shuttle vector pBI 121 expressing the maize iaglu gene in both sense and antisense orientations under a 35S promoter was used for the study. The sense plants showed total lack of root initiation and development. The antisense transgenic plants, on the other hand, had unusually well developed root systems at early stages in development. Analysis showed that the amount and activity of the endogenous 75 kDa IAGLU protein was reduced in these plants and consequently these plants had reduced levels of IAA-glucose and lower overall esterified IAA.
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Granot, David, and Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, January 2003. http://dx.doi.org/10.32747/2003.7585189.bard.

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Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .
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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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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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