Journal articles: 'Biochemical Pathways'

1

Breuer, Eun-Kyoung Yim, Mandi M. Murph, and Rolf J. Craven. "Biochemical Pathways in Cancer." Biochemistry Research International 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/268504.

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Sanford, Chris, Matthew L. K. Yip, Carl White, and John Parkinson. "Cell++—simulating biochemical pathways." Bioinformatics 22, no. 23 (October 11, 2006): 2918–25. http://dx.doi.org/10.1093/bioinformatics/btl497.

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Schunk, Axel. "Datenbank der „Biochemical Pathways”︁." Nachrichten aus der Chemie 52, no. 11 (November 2004): 1155–57. http://dx.doi.org/10.1002/nadc.20040521113.

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Burrows, R. B., G. R. Warnes, and R. C. Hanumara. "Statistical modelling of biochemical pathways." IET Systems Biology 1, no. 6 (November 1, 2007): 353–60. http://dx.doi.org/10.1049/iet-syb:20060074.

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Pardini, Giovanni, Paolo Milazzo, and Andrea Maggiolo-Schettini. "Component identification in biochemical pathways." Theoretical Computer Science 587 (July 2015): 104–24. http://dx.doi.org/10.1016/j.tcs.2015.03.013.

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Smith, C. L., A. D. Bolton, H. M. Abdolmalkey, and R. Shafa. "Biochemical pathways linked to schizophrenia." European Psychiatry 23 (April 2008): S177. http://dx.doi.org/10.1016/j.eurpsy.2008.01.992.

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BRAUSE, R. "ADAPTIVE MODELING OF BIOCHEMICAL PATHWAYS." International Journal on Artificial Intelligence Tools 13, no. 04 (December 2004): 851–62. http://dx.doi.org/10.1142/s0218213004001855.

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In bioinformatics, biochemical pathways can be modeled by many differential equations. It is still an open problem how to fit the huge amount of parameters of the equations to the available data. Here, the approach of systematically learning the parameters is necessary. In this paper, for the small, important example of inflammation modeling a network is constructed and different learning algorithms are proposed. It turned out that due to the nonlinear dynamics evolutionary approaches are necessary to fit the parameters for sparse, given data.

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Holme, P., M. Huss, and H. Jeong. "Subnetwork hierarchies of biochemical pathways." Bioinformatics 19, no. 4 (March 1, 2003): 532–38. http://dx.doi.org/10.1093/bioinformatics/btg033.

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Tominaga, Kazuto, Yoshikazu Suzuki, Keiji Kobayashi, Tooru Watanabe, Kazumasa Koizumi, and Koji Kishi. "Modeling Biochemical Pathways Using an Artificial Chemistry." Artificial Life 15, no. 1 (January 2009): 115–29. http://dx.doi.org/10.1162/artl.2009.15.1.15108.

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Artificial chemistries are candidates for methodologies that model and design biochemical systems. If artificial chemistries can deal with such systems in beneficial ways, they may facilitate activities in the new area of biomolecular engineering. In order to explore such possibilities, we illustrate four models of biochemical pathways described in our artificial chemistry based on string pattern matching and recombination. The modeled pathways are the replication of DNA, transcription from DNA to mRNA, translation from mRNA to protein, and the oxidation of fatty acids. The descriptions show that the present approach has good modularity and scalability that will be useful for modeling a huge network of pathways. Moreover, we give a procedure to perform reasoning in the artificial chemistry, which checks whether a specified collection of molecules can be generated in a given model, and we demonstrate that it works on a model that describes a natural biochemical pathway.

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Liu, Qinghua, and Zain Paroo. "Biochemical Principles of Small RNA Pathways." Annual Review of Biochemistry 79, no. 1 (June 7, 2010): 295–319. http://dx.doi.org/10.1146/annurev.biochem.052208.151733.

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11

Robinson, Richard. "The Fourth Dimension of Biochemical Pathways." PLoS Biology 6, no. 6 (June 17, 2008): e151. http://dx.doi.org/10.1371/journal.pbio.0060151.

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Kaneshiro, E. S. "Biochemical research elucidating metabolic pathways inPneumocystis." Parasite 17, no. 4 (December 2010): 285–91. http://dx.doi.org/10.1051/parasite/2010174285.

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Fairlamb, A. H. "Novel biochemical pathways in parasitic protozoa." Parasitology 99, S1 (January 1989): S93—S112. http://dx.doi.org/10.1017/s003118200008344x.

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SUMMARYThroughout evolution, enzymes and their metabolites have been highly conserved. Parasites are no exception to this and differ most markedly by the absence of metabolic pathways that are present in the mammalian host. In general, parasites are metabolically lazy and rely on the metabolism of the host both for a supply of prefabricated components such as purines, fatty acids, sterols and amino acids and for the removal of end-products. Nonetheless, parasites are metabolically highly sophisticated in that (1) they retain the genetic capacity to induce many pathways, when needed, and (2) they have developed complex mechanisms for their survival in the host. Certain unique features of the metabolism of trypanosomes, leishmania, malaria and anaerobic protozoa will be discussed. This will include (1) glycolysis and electron transport with reference to the unique organelles: the glycosome and the hydrogenosome, (2) purine salvage, pyrimidine biosynthesis and folic acid metabolism and (3) polyamine and thiol metabolism with special reference to the role of the unique metabolite of trypanosomes and leishmanias, trypanothione.

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Karp, P. D., and M. L. Mavrovouniotis. "Representing, analyzing, and synthesizing biochemical pathways." IEEE Expert 9, no. 2 (April 1994): 11–21. http://dx.doi.org/10.1109/64.294129.

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Bates, Philip D., Sten Stymne, and John Ohlrogge. "Biochemical pathways in seed oil synthesis." Current Opinion in Plant Biology 16, no. 3 (June 2013): 358–64. http://dx.doi.org/10.1016/j.pbi.2013.02.015.

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16

Hartwell, Leland. "A robust view of biochemical pathways." Nature 387, no. 6636 (June 1997): 855–57. http://dx.doi.org/10.1038/43072.

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Reitz, Martin, Oliver Sacher, Aleksey Tarkhov, Dietrich Trümbach, and Johann Gasteiger. "Enabling the exploration of biochemical pathways." Org. Biomol. Chem. 2, no. 22 (2004): 3226–37. http://dx.doi.org/10.1039/b410949j.

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18

Piškur, Jure, Klaus D. Schnackerz, Gorm Andersen, and Olof Björnberg. "Comparative genomics reveals novel biochemical pathways." Trends in Genetics 23, no. 8 (August 2007): 369–72. http://dx.doi.org/10.1016/j.tig.2007.05.007.

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19

Jensen, Roy A. "Evolution of biochemical pathways in prokaryotes." Origins of Life and Evolution of the Biosphere 16, no. 3-4 (September 1986): 245–46. http://dx.doi.org/10.1007/bf02422005.

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Mavrovouniotis, Michael L., George Stephanopoulos, and Gregory Stephanopoulos. "Computer-aided synthesis of biochemical pathways." Biotechnology and Bioengineering 36, no. 11 (December 20, 1990): 1119–32. http://dx.doi.org/10.1002/bit.260361107.

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21

Maurino, Veronica G. "Using energy-efficient synthetic biochemical pathways to bypass photorespiration." Biochemical Society Transactions 47, no. 6 (November 22, 2019): 1805–13. http://dx.doi.org/10.1042/bst20190322.

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Current crop yields will not be enough to sustain today's diets for a growing global population. As plant photosynthetic efficiency has not reached its theoretical maximum, optimizing photosynthesis is a promising strategy to enhance plant productivity. The low productivity of C3 plants is caused in part by the substantial energetic investments necessary to maintain a high flux through the photorespiratory pathway. Accordingly, lowering the energetic costs of photorespiration to enhance the productivity of C3 crops has been a goal of synthetic plant biology for decades. The use of synthetic bypasses to photorespiration in different plants showed an improvement of photosynthetic performance and growth under laboratory and field conditions, even though in silico predictions suggest that the tested synthetic pathways should confer a minimal or even negative energetic advantage over the wild type photorespiratory pathway. Current strategies increasingly utilize theoretical modeling and new molecular techniques to develop synthetic biochemical pathways that bypass photorespiration, representing a highly promising approach to enhance future plant productivity.

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22

Chen, Tian Sheng, Soon Sim Tan, Ronne Wee Yeh Yeo, Bao Ju Teh, Ruihua Luo, GuoDong Li, and Sai Kiang Lim. "Delineating Biological Pathways Unique to Embryonic Stem Cell-Derived Insulin-Producing Cell Lines from Their Noninsulin-Producing Progenitor Cell Lines." Endocrinology 151, no. 8 (May 25, 2010): 3600–3610. http://dx.doi.org/10.1210/en.2009-1418.

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To identify unique biochemical pathways in embryonic stem cell-derived insulin-producing cells as potential therapeutic targets to prevent or delay β-cell dysfunction or death in diabetic patients, comparative genome-wide gene expression studies of recently derived mouse insulin-producing cell lines and their progenitor cell lines were performed using microarray technology. Differentially expressed genes were functionally clustered to identify important biochemical pathways in these insulin-producing cell lines. Biochemical or cellular assays were then performed to assess the relevance of these pathways to the biology of these cells. A total of 185 genes were highly expressed in the insulin-producing cell lines, and computational analysis predicted the pentose phosphate pathway (PPP), clathrin-mediated endocytosis, and the peroxisome proliferator-activated receptor (PPAR) signaling pathway as important pathways in these cell lines. Insulin-producing ERoSHK cells were more resistant to hydrogen peroxide (H2O2)-induced oxidative stress. Inhibition of PPP by dehydroepiandrosterone and 6-aminonicotinamide abrogated this H2O2 resistance with a concomitant decrease in PPP activity as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Clathrin-mediated endocytosis, which is essential in maintaining membrane homeostasis in secreting cells, was up-regulated by glucose in ERoSHK but not in their progenitor ERoSH cells. Its inhibition by chlorpromazine at high glucose concentration was toxic to the cells. Troglitazone, a PPARG agonist, up-regulated expression of Ins1 and Ins2 but not Glut2. Gene expression analysis has identified the PPP, clathrin-mediated endocytosis, and the PPAR signaling pathway as the major delineating pathways in these insulin-producing cell lines, and their biological relevance was confirmed by biochemical and cellular assays.

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23

Schopf, J. William. "Precambrian Biochemical Evolution." Short Courses in Paleontology 1 (1988): 89–97. http://dx.doi.org/10.1017/s2475263000000696.

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It has become rather widely accepted in recent years that (1) during the geologic past, the Earth's atmosphere evolved from an initial “oxygen deficient” to a later “oxygen-rich” state; that (2) this change was a result chiefly of the cumulative effects of O2-producing “green plant-type” (including cyanobacterial) photosynthesis; and that (3) the transition occurred during the Precambrian, with stable oxygenic conditions having probably become established during the Early Proterozoic (viz., 2.5 to 1.7 Ga). Lines of evidence in support of these suppositions have been drawn from paleobiology, geology, mineralogy, isotopic and organic geochemistry, and comparative planetology – data well familiar to many paleontologists (for detailed discussion including a reference list of some 1,700 entries, see articles in Schopf, 1983). In addition, however, and although it is perhaps not widely recognized, it is of interest to note that the occurrence of such a transition seems also reflected by the nature and structure of the metabolic and biosynthetic pathways of extant living systems. To a paleontologist, this observation should not be surprising. Just as comparative studies of the embryology and structural adult anatomy of extant organisms can provide reliable evidence of phylogenetic relationships, comparative studies of biochemistry –in this case, of evolutionarily conservative, widespread, biochemical pathways – can similarly provide evidence of evolutionary derivation. And just as the structural morphology of currently living systems is a product of, having been influenced by, environments inhabited by evolutionary precursors (e.g., the limb structure of both aquatic and flying mammals reflecting derivation from lineages earlier adapted to the land environment), metabolic and biosynthetic pathways, especially required pathways involved in processes or producing products fundamental to survival, can be expected to provide evidence of past environmental conditions.

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Hong, Li, Veerendra Munugalavadla, and Reuben Kapur. "c-Kit-Mediated Overlapping and Unique Functional and Biochemical Outcomes via Diverse Signaling Pathways." Molecular and Cellular Biology 24, no. 3 (February 1, 2004): 1401–10. http://dx.doi.org/10.1128/mcb.24.3.1401-1410.2004.

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ABSTRACT A critical issue in understanding receptor tyrosine kinase signaling is the individual contribution of diverse signaling pathways in regulating cellular growth, survival, and migration. We generated a functionally and biochemically inert c-Kit receptor that lacked the binding sites for seven early signaling pathways. Restoring the Src family kinase (SFK) binding sites in the mutated c-Kit receptor restored cellular survival and migration but only partially rescued proliferation and was associated with the rescue of the Ras/mitogen-activated protein kinase, Rac/JNK kinase, and phosphatidylinositol 3-kinase (PI-3 kinase)/Akt pathways. In contrast, restoring the PI-3 kinase binding site in the mutated receptor did not affect cellular proliferation but resulted in a modest correction in cell survival and migration, despite a complete rescue in the activation of the PI-3 kinase/Akt pathway. Surprisingly, restoring the binding sites for Grb2, Grb7, or phospholipase C-γ had no effect on cellular growth or survival, migration, or activation of any of the downstream signaling pathways. These results argue that SFKs play a unique role in the control of multiple cellular functions and in the activation of distinct biochemical pathways via c-Kit.

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Markina, N. M., A. A. Kotlobay, and A. S. Tsarkova. "Heterologous Metabolic Pathways: Strategies for Optimal Expression in Eukaryotic Hosts." Acta Naturae 12, no. 2 (August 7, 2020): 28–39. http://dx.doi.org/10.32607/actanaturae.10966.

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Heterologous pathways are linked series of biochemical reactions occurring in a host organism after the introduction of foreign genes. Incorporation of metabolic pathways into host organisms is a major strategy used to increase the production of valuable secondary metabolites. Unfortunately, simple introduction of the pathway genes into the heterologous host in most cases does not result in successful heterologous expression. Extensive modification of heterologous genes and the corresponding enzymes on many different levels is required to achieve high target metabolite production rates. This review summarizes the essential techniques used tocreate heterologous biochemical pathways, with a focus on the key challenges arising in the process and the major strategies for overcoming them.

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Markina, N. M., A. A. Kotlobay, and A. S. Tsarkova. "Heterologous Metabolic Pathways: Strategies for Optimal Expression in Eukaryotic Hosts." Acta Naturae 12, no. 2 (August 7, 2020): 28–39. http://dx.doi.org/10.32607/actanaturae.11153.

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Heterologous pathways are linked series of biochemical reactions occurring in a host organism after the introduction of foreign genes. Incorporation of metabolic pathways into host organisms is a major strategy used to increase the production of valuable secondary metabolites. Unfortunately, simple introduction of the pathway genes into the heterologous host in most cases does not result in successful heterologous expression. Extensive modification of heterologous genes and the corresponding enzymes on many different levels is required to achieve high target metabolite production rates. This review summarizes the essential techniques used tocreate heterologous biochemical pathways, with a focus on the key challenges arising in the process and the major strategies for overcoming them.

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Sorribas, Albert, and Michael A. Savageau. "Strategies for representing metabolic pathways within biochemical systems theory: Reversible pathways." Mathematical Biosciences 94, no. 2 (June 1989): 239–69. http://dx.doi.org/10.1016/0025-5564(89)90066-7.

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Hayat, Faisal, Manoj Sonavane, Mikhail V. Makarov, Samuel A. J. Trammell, Pamela McPherson, Natalie R. Gassman, and Marie E. Migaud. "The Biochemical Pathways of Nicotinamide-Derived Pyridones." International Journal of Molecular Sciences 22, no. 3 (January 24, 2021): 1145. http://dx.doi.org/10.3390/ijms22031145.

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As catabolites of nicotinamide possess physiological relevance, pyridones are often included in metabolomics measurements and associated with pathological outcomes in acute kidney injury (AKI). Pyridones are oxidation products of nicotinamide, its methylated form, and its ribosylated form. While they are viewed as markers of over-oxidation, they are often wrongly reported or mislabeled. To address this, we provide a comprehensive characterization of these catabolites of vitamin B3, justify their nomenclature, and differentiate between the biochemical pathways that lead to their generation. Furthermore, we identify an enzymatic and a chemical process that accounts for the formation of the ribosylated form of these pyridones, known to be cytotoxic. Finally, we demonstrate that the ribosylated form of one of the pyridones, the 4-pyridone-3-carboxamide riboside (4PYR), causes HepG3 cells to die by autophagy; a process that occurs at concentrations that are comparable to physiological concentrations of this species in the plasma in AKI patients.

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Rajagopal, Manjunath C., and Sanjiv Sinha. "Cellular Thermometry Considerations for Probing Biochemical Pathways." Cell Biochemistry and Biophysics 79, no. 2 (April 2, 2021): 359–73. http://dx.doi.org/10.1007/s12013-021-00979-w.

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Nakayama, Kentaro, Naomi Nakayama, Hiroshi Katagiri, and Kohji Miyazaki. "Mechanisms of Ovarian Cancer Metastasis: Biochemical Pathways." International Journal of Molecular Sciences 13, no. 12 (September 18, 2012): 11705–17. http://dx.doi.org/10.3390/ijms130911705.

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31

Orr, Alan R. ""Visualization" of Biochemical Pathways with Enzyme Markers." American Biology Teacher 48, no. 8 (November 1, 1986): 485–86. http://dx.doi.org/10.2307/4448389.

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32

Samburskaya, O. V., S. Yu Kalinchenko, and N. V. Batkaeva. "BIOCHEMICAL PATHWAYS OF METABOLIC DISORDERS IN PSORIASIS." Juvenis Scientia 7, no. 6 (2021): 6–16. http://dx.doi.org/10.32415/jscientia_2021_7_6_6-16.

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The development of metabolic disorders occurs in psoriasis: insulin resistance, systemic inflammation, atherosclerosis, oxidative stress and obesity. The paper presents pathological biochemical pathways of metabolic disorders development which is caused by common cytokine profile chara-cteristic for psoriasis and obesity and they are tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and interleukin-8 (IL-8). The following links play a role in the development of insulin resistance: insulin receptor (IRS-1) and insulin receptor substrate (SIR-1), glucose transporter protein (GLUT-4), also there is a decrease in the phosphatidylinositol 3-kinase pathway (PI3AKT) activity, and an increase in the mitogen activating protein kinase (MAPK) activity. Factors influencing the development of inflammation are discussed: IL-6, C-reactive protein, tissue plasminogen activator inhibitor (PAI-1), monocyte chemoattractant protein 1 (MCP-1), proinflammatory adipokines; processes of vascular inflammation development, atherosclerosis development and oxidative stress. This article discusses endocrine disruption of adipocytes in obesity and the influence of adipokines and inflammatory mediators synthesized by fat cells on psoriatic disease. Advanced glycation end products (AGEs), hyperhomocysteinemia (HHcy) due to vitamin B12 and folic acid deficiency, and a 5,10-methylfolate reductase (MTHFR) mutation are also important in the clinical manifestations of psoriasis. The possibility of assessing metabolic disorders and dysfunction of various organs by changes in the levels of metabolites in the blood and skin of patients with psoriasis is discussed.

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33

Gaol. "Knowledge Discovery in Biochemical Pathways Using Minepathways." Journal of Computer Science 6, no. 11 (November 1, 2010): 1276–82. http://dx.doi.org/10.3844/jcssp.2010.1276.1282.

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34

Brause, R. "ADAPTIVE MODELING OF BIOCHEMICAL PATHWAYS FOR SEPSIS." Shock 21, Supplement (March 2004): 146. http://dx.doi.org/10.1097/00024382-200403001-00583.

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35

Budihardjo, Imawati, Holt Oliver, Michael Lutter, Xu Luo, and Xiaodong Wang. "Biochemical Pathways of Caspase Activation During Apoptosis." Annual Review of Cell and Developmental Biology 15, no. 1 (November 1999): 269–90. http://dx.doi.org/10.1146/annurev.cellbio.15.1.269.

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HARBORNE, JEFFREY B. "Constraints on the evolution of biochemical pathways." Biological Journal of the Linnean Society 39, no. 2 (February 1990): 135–51. http://dx.doi.org/10.1111/j.1095-8312.1990.tb00508.x.

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37

Hill, David P., Peter D’Eustachio, Tanya Z. Berardini, Christopher J. Mungall, Nikolai Renedo, and Judith A. Blake. "Modeling biochemical pathways in the gene ontology." Database 2016 (2016): baw126. http://dx.doi.org/10.1093/database/baw126.

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Qi, Yijun, Ahmet M. Denli, and Gregory J. Hannon. "Biochemical Specialization within Arabidopsis RNA Silencing Pathways." Molecular Cell 19, no. 3 (August 2005): 421–28. http://dx.doi.org/10.1016/j.molcel.2005.06.014.

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Curti, M., P. Degano, C. Priami, and C. T. Baldari. "Modelling biochemical pathways through enhanced π-calculus." Theoretical Computer Science 325, no. 1 (September 2004): 111–40. http://dx.doi.org/10.1016/j.tcs.2004.03.066.

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Hansen, Jørgen, and Morten C. Kielland-Brandt. "Modification of biochemical pathways in industrial yeasts." Journal of Biotechnology 49, no. 1-3 (August 1996): 1–12. http://dx.doi.org/10.1016/0168-1656(96)01523-4.

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Minch, E., M. de Rinaldis, and S. Weiss. "pathSCOUTTM: exploration and analysis of biochemical pathways." Bioinformatics 19, no. 3 (February 12, 2003): 431–32. http://dx.doi.org/10.1093/bioinformatics/btf880.

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Gasteiger, Johann. "Explorations into Chemical Reactions and Biochemical Pathways." Molecular Informatics 35, no. 11-12 (May 11, 2016): 588–92. http://dx.doi.org/10.1002/minf.201600038.

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Strohl, William R. "Biochemical Engineering of Natural Product Biosynthesis Pathways." Metabolic Engineering 3, no. 1 (January 2001): 4–14. http://dx.doi.org/10.1006/mben.2000.0172.

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Srividhya, Jeyaraman, Edmund J. Crampin, Patrick E. McSharry, and Santiago Schnell. "Reconstructing biochemical pathways from time course data." PROTEOMICS 7, no. 6 (March 2007): 828–38. http://dx.doi.org/10.1002/pmic.200600428.

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DANDEKAR, Thomas, Stefan SCHUSTER, Berend SNEL, Martijn HUYNEN, and Peer BORK. "Pathway alignment: application to the comparative analysis of glycolytic enzymes." Biochemical Journal 343, no. 1 (September 24, 1999): 115–24. http://dx.doi.org/10.1042/bj3430115.

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Comparative analysis of metabolic pathways in different genomes yields important information on their evolution, on pharmacological targets and on biotechnological applications. In this study on glycolysis, three alternative ways of comparing biochemical pathways are combined: (1) analysis and comparison of biochemical data, (2) pathway analysis based on the concept of elementary modes, and (3) a comparative genome analysis of 17 completely sequenced genomes. The analysis reveals a surprising plasticity of the glycolytic pathway. Isoenzymes in different species are identified and compared; deviations from the textbook standard are detailed. Several potential pharmacological targets and by-passes (such as the Entner-Doudoroff pathway) to glycolysis are examined and compared in the different species. Archaean, bacterial and parasite specific adaptations are identified and described.

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Gurusamy, Raman, and Sakthivel Natarajan. "Current Status on Biochemistry and Molecular Biology of Microbial Degradation of Nicotine." Scientific World Journal 2013 (2013): 1–15. http://dx.doi.org/10.1155/2013/125385.

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Bioremediation is one of the most promising methods to clean up polluted environments using highly efficient potent microbes. Microbes with specific enzymes and biochemical pathways are capable of degrading the tobacco alkaloids including highly toxic heterocyclic compound, nicotine. After the metabolic conversion, these nicotinophilic microbes use nicotine as the sole carbon, nitrogen, and energy source for their growth. Various nicotine degradation pathways such as demethylation pathway in fungi, pyridine pathway in Gram-positive bacteria, pyrrolidine pathway, and variant of pyridine and pyrrolidine pathways in Gram-negative bacteria have been reported. In this review, we discussed the nicotine-degrading pathways of microbes and their enzymes and biotechnological applications of nicotine intermediate metabolites.

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Rakhmonjonovna, Kapizova Dilafruz Rakhmonjonovna. "COMMON PATHWAYS OF PROTEIN AND AMINO ACID METABOLISM IN THE BODY." International Journal of Medical Sciences And Clinical Research 03, no. 06 (June 1, 2023): 49–52. http://dx.doi.org/10.37547/ijmscr/volume03issue06-09.

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Protein exchange is crucial for the life of the whole organism, each of its tissues and organs, some cells and subcellular components. Biochemical activity of the cell and all metabolic reactions occurring in it are related to the exchange of proteins.

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48

Ahmed, H., B. Tjaden, R. Hensel, and B. Siebers. "Embden–Meyerhof–Parnas and Entner–Doudoroff pathways in Thermoproteus tenax: metabolic parallelism or specific adaptation?" Biochemical Society Transactions 32, no. 2 (April 1, 2004): 303–4. http://dx.doi.org/10.1042/bst0320303.

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Genome data as well as biochemical studies have indicated that – as a peculiarity within hyperthermophilic Archaea – Thermoproteus tenax uses three different pathways for glucose metabolism, a variant of the reversible EMP (Embden–Meyerhof–Parnas) pathway and two different modifications of the ED (Entner–Doudoroff) pathway, a non-phosphorylative and a semi-phosphorylative version. An overview of the three different pathways is presented and the physiological function of the variants is discussed.

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49

Pogson, Grant H. "Constraints on the genetic process of biochemical adaptation." Canadian Journal of Zoology 66, no. 5 (May 1, 1988): 1139–45. http://dx.doi.org/10.1139/z88-166.

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The identification of selective constraints impeding the adaptive evolution of macromolecules and metabolic systems is compared between the two most prevalent approaches to the study of biochemical adaptation. Constraints discerned from the interspecific comparative method address the features of enzymes that are conserved across evolutionary lineages; constraints determined from the evolutionary genetic approach involve factors that interfere with the ability of natural selection to direct the adaptive process. Difficulties associated with the constraints identified by the comparative method are examined. These are shown to arise from the lack of an adequate definition of molecular adaptedness and from the confounding effects of factors that may act to constrain the process of biochemical adaptation. Constraints on this genetic process of biochemical adaptation are discussed at three levels of biological organization: populations, multienzyme pathways, and individual enzymes embedded within these pathways. A model is presented that allows for adaptive change in any pathway enzyme irrespective of its role in determining system flux.

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Yilmaz, Ali, Zafer Ugur, Ilyas Ustun, Sumeyya Akyol, Ray O. Bahado-Singh, Michael Maddens, Jan O. Aasly, and Stewart F. Graham. "Metabolic Profiling of CSF from People Suffering from Sporadic and LRRK2 Parkinson’s Disease: A Pilot Study." Cells 9, no. 11 (October 31, 2020): 2394. http://dx.doi.org/10.3390/cells9112394.

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CSF from unique groups of Parkinson’s disease (PD) patients was biochemically profiled to identify previously unreported metabolic pathways linked to PD pathogenesis, and novel biochemical biomarkers of the disease were characterized. Utilizing both 1H NMR and DI-LC-MS/MS we quantitatively profiled CSF from patients with sporadic PD (n = 20) and those who are genetically predisposed (LRRK2) to the disease (n = 20), and compared those results with age and gender-matched controls (n = 20). Further, we systematically evaluated the utility of several machine learning techniques for the diagnosis of PD. 1H NMR and mass spectrometry-based metabolomics, in combination with bioinformatic analyses, provided useful information highlighting previously unreported biochemical pathways and CSF-based biomarkers associated with both sporadic PD (sPD) and LRRK2 PD. Results of this metabolomics study further support our group’s previous findings identifying bile acid metabolism as one of the major aberrant biochemical pathways in PD patients. This study demonstrates that a combination of two complimentary techniques can provide a much more holistic view of the CSF metabolome, and by association, the brain metabolome. Future studies for the prediction of those at risk of developing PD should investigate the clinical utility of these CSF-based biomarkers in more accessible biomatrices. Further, it is essential that we determine whether the biochemical pathways highlighted here are recapitulated in the brains of PD patients with the aim of identifying potential therapeutic targets.

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Journal articles on the topic 'Biochemical Pathways'

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