Editing Metabolic pathway

{{Short description|Linked series of chemical reactions occurring within a cell}}
{{Biochemistry sidebar}}
In [[biochemistry]], a '''metabolic pathway''' is a linked series of [[chemical reaction]]s occurring within a [[cell (biology)|cell]].  The [[reactant]]s, products, and [[Metabolic intermediate|intermediates]] of an [[enzymatic reaction]] are known as [[metabolites]], which are modified by a sequence of chemical reactions [[catalyze]]d by [[enzyme]]s.<ref name="Nelson">{{cite book| vauthors = Nelson DL, Cox MM |title=Lehninger principles of biochemistry|date=2008|publisher=W.H. Freeman|location=New York|isbn=978-0-7167-7108-1|edition=5th|url=https://archive.org/details/lehningerprincip00lehn_1}}</ref>{{rp|26}} In most cases of a metabolic pathway, the [[product (chemistry)|product]] of one enzyme acts as the [[substrate (chemistry)|substrate]] for the next. However, side products are considered waste and removed from the cell.<ref>{{Cite book|title=Biochemistry and molecular biology| vauthors = Alison S, Papachristodoulou DK, Despo K, Elliott WH, Elliott DC |isbn=978-0-19-960949-9 |edition=Fifth|location=Oxford|oclc=862091499|year = 2014}}</ref>

Different metabolic pathways function in the position within a [[Eukaryotic Cell|eukaryotic cell]] and the significance of the pathway in the given compartment of the cell.<ref>{{cite book|title=An Introduction to Metabolic Pathways by S. DAGLEY|date=March 1971|publisher=Sigma Xi, The Scientific Research Society|edition=Vol. 59, No. 2|page=266| vauthors = Nicholson DE }}</ref> For instance, the [[electron transport chain]] and [[oxidative phosphorylation]] all take place in the [[mitochondrial membrane]].<ref name="Harvey">{{cite book| vauthors = Harvey RA |title=Biochemistry|date=2011|publisher=Wolters Kluwer|location=Baltimore, MD |isbn=978-1-60831-412-6|edition=5th}}</ref>{{rp|73, 74 & 109}} In contrast, [[glycolysis]], [[pentose phosphate pathway]], and [[Fatty acid synthesis|fatty acid biosynthesis]] all occur in the [[cytosol]] of a cell.<ref name="Voet, Voet, Pratt">{{cite book| vauthors = Voet D, Voet JD, Pratt CW |title=Fundamentals of Biochemistry: Life at the Molecular Level|date=2013|publisher=Wiley|location=Hoboken, NJ|isbn=978-0470-54784-7|edition=4th|title-link=Fundamentals of Biochemistry: Life at the Molecular Level}}</ref>{{rp|441–442}}

There are two types of metabolic pathways that are characterized by their ability to either synthesize molecules with the utilization of energy ([[Anabolism|anabolic pathway]]), or break down complex molecules and release energy in the process ([[Catabolism|catabolic pathway]]).<ref name="Campbell">{{cite book | vauthors = Reece JB, Campbell NA |title=Campbell Biology |date=2011 |publisher=Benjamin Cummings / Pearson |location=Boston |isbn=978-0-321-55823-7 |edition=9th |pages=[https://archive.org/details/campbellbiologyj00reec/page/143 143] }}</ref>

The two pathways complement each other in that the energy released from one is used up by the other. The degradative process of a catabolic pathway provides the energy required to conduct the [[biosynthesis]] of an anabolic pathway.<ref name="Campbell"/> In addition to the two distinct metabolic pathways is the [[amphibolic]] pathway, which can be either catabolic or anabolic based on the need for or the availability of energy.<ref>{{cite book| vauthors = Berg JM, Tymoczko JL, Stryer L, Gatto GJ |title=Biochemistry|date=2012|publisher=W.H. Freeman|location=New York|isbn=978-1-4292-2936-4 |page=429|edition=7th}}</ref>

Pathways are required for the maintenance of [[homeostasis]] within an [[organism]] and the [[Flux (metabolism)|flux]] of metabolites through a pathway is regulated depending on the needs of the cell and the availability of the substrate. The end product of a pathway may be used immediately, initiate another metabolic pathway or be stored for later use. The [[metabolism]] of a cell consists of an elaborate [[metabolic network|network]] of interconnected pathways that enable the synthesis and breakdown of molecules (anabolism and catabolism).

==Overview==
[[File:Net reactions for glycolysis of glucose, oxidative decarboxylation of pyruvate, and Krebs cycle..png|alt=Glycolysis, Oxidative Decarboxylation of Pyruvate, and Tricarboxylic Acid (TCA) Cycle|thumb|Net reactions of common metabolic pathways|650x650px]]

Each metabolic pathway consists of a series of biochemical reactions that are connected by their intermediates: the products of one reaction are the [[Substrate (biochemistry)|substrates]] for subsequent reactions, and so on. Metabolic pathways are often considered to flow in one direction. Although all chemical reactions are technically reversible, conditions in the cell are often such that it is [[thermodynamics|thermodynamically]] more favorable for [[flux]] to proceed in one direction of a reaction.<ref>{{Cite journal| vauthors = Cornish-Bowden A, Cárdenas M |author-link1=Athel Cornish-Bowden|date=2000|title=Irreversible reactions in metabolic simulations: how reversible is irreversible?|url=http://academic.sun.ac.za/natural/biochem/btk/book/cornish-bowden.pdf|journal=Animating the Cellular Map|pages=65–71}}</ref> For example, one pathway may be responsible for the synthesis of a particular amino acid, but the breakdown of that amino acid may occur via a separate and distinct pathway. One example of an exception to this "rule" is the metabolism of [[glucose]]. [[Glycolysis]] results in the breakdown of glucose, but several reactions in the glycolysis pathway are reversible and participate in the re-synthesis of glucose ([[gluconeogenesis]]).{{cn|date=March 2023}}
* [[Glycolysis]] was the first metabolic pathway discovered:
# As [[glucose]] enters a cell, it is immediately [[phosphorylated]] by [[Adenosine triphosphate|ATP]] to [[glucose 6-phosphate]] in the irreversible first step.
# In times of excess [[lipid]] or [[protein]] energy sources, certain reactions in the [[glycolysis]] pathway may run in reverse to produce [[glucose 6-phosphate]], which is then used for storage as [[glycogen]] or [[starch]].
* Metabolic pathways are often [[Control theory|regulated]] by [[feedback inhibition]].
* Some metabolic pathways flow in a 'cycle' wherein each component of the cycle is a substrate for the subsequent reaction in the cycle, such as in the [[Krebs Cycle]] (see below).
* [[Anabolism|Anabolic]] and [[catabolic]] pathways in [[eukaryotes]] often occur independently of each other, separated either physically by compartmentalization within [[organelles]] or separated biochemically by the requirement of different enzymes and co-factors.

==Major metabolic pathways==
{{for|additional infographics of major metabolic pathways|#External links}}
{{metabolic metro}}
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===Catabolic pathway (catabolism)===
A '''[[catabolic pathway]]''' is a series of reactions that bring about a net release of energy in the form of a high energy phosphate bond formed with the energy carriers adenosine diphosphate (ADP) and guanosine diphosphate (GDP) to produce adenosine triphosphate (ATP) and guanosine triphosphate (GTP), respectively.<ref name="Harvey"/>{{rp|91–93}} The net reaction is, therefore, thermodynamically favorable, for it results in a lower free energy for the final products.<ref name="Clarke">{{cite book| vauthors = Berg JM, Tymoczko JL, Stryer L |title=Biochemistry|date=2002|publisher=W. H. Freeman|location=New York, NY |isbn=978-0-7167-3051-4 |edition=5th |url=https://archive.org/details/biochemistrychap00jere}}</ref>{{rp|578–579}} A catabolic pathway is an exergonic system that produces chemical energy in the form of ATP, GTP, NADH, NADPH, FADH2, etc. from energy containing sources such as carbohydrates, fats, and proteins. The end products are often carbon dioxide, water, and ammonia. Coupled with an endergonic reaction of anabolism, the cell can synthesize new macromolecules using the original precursors of the anabolic pathway.<ref>{{cite book| vauthors = Raven PH, Evert RF, Eichhorn SE |title=Biology of plants|date=2011|publisher=Freeman|location=New York, NY|isbn=978-1-4292-1961-7|pages=100–106|edition=8th }}</ref> An example of a coupled reaction is the phosphorylation of [[Fructose 6-phosphate|fructose-6-phosphate]] to form the intermediate [[Fructose 1,6-bisphosphate|fructose-1,6-bisphosphate]] by the enzyme [[phosphofructokinase]] accompanied by the hydrolysis of ATP in the pathway of [[glycolysis]]. The resulting chemical reaction within the metabolic pathway is highly thermodynamically favorable and, as a result, irreversible in the cell.

<chem>Fructose-6-Phosphate + ATP -> Fructose-1,6-Bisphosphate + ADP</chem>

====Cellular respiration====
{{Main|Cellular respiration}}

A core set of energy-producing [[catabolic]] pathways occur within all living organisms in some form. These pathways transfer the energy released by breakdown of [[nutrient]]s into [[Adenosine triphosphate|ATP]] and other small molecules used for energy (e.g. [[Guanosine triphosphate|GTP]], [[NADPH]], [[FADH2|FADH<sub>2</sub>]]). All cells can perform [[anaerobic respiration]] by [[glycolysis]]. Additionally, most organisms can perform more efficient [[aerobic respiration]] through the [[citric acid cycle]] and [[oxidative phosphorylation]]. Additionally [[plant]]s, [[algae]] and [[cyanobacteria]] are able to use sunlight to [[anabolic]]ally synthesize compounds from non-living matter by [[photosynthesis]].
[[File:Gluconeogenese Schema 2.png|thumb|Gluconeogenesis mechanism|557x557px]]

===Anabolic pathway (anabolism)===
In contrast to catabolic pathways, '''[[anabolic pathways]]''' require an energy input to construct macromolecules such as polypeptides, nucleic acids, proteins, polysaccharides, and lipids. The isolated reaction of anabolism is unfavorable in a cell due to a positive [[Gibbs free energy]] (+Δ''G''). Thus, an input of chemical energy through a coupling with an [[exergonic reaction]] is necessary.<ref name="Nelson"/>{{rp|25–27}} The coupled reaction of the catabolic pathway affects the thermodynamics of the reaction by lowering the overall [[activation energy]] of an anabolic pathway and allowing the reaction to take place.<ref name="Nelson"/>{{rp|25}} Otherwise, an [[endergonic reaction]] is non-spontaneous.

An anabolic pathway is a biosynthetic pathway, meaning that it combines smaller molecules to form larger and more complex ones.<ref name="Clarke"/>{{rp|570}} An example is the reversed pathway of glycolysis, otherwise known as [[gluconeogenesis]], which occurs in the liver and sometimes in the kidney to maintain proper glucose concentration in the blood and supply the brain and muscle tissues with adequate amount of glucose. Although gluconeogenesis is similar to the reverse pathway of glycolysis, it contains four distinct enzymes([[pyruvate carboxylase]], [[phosphoenolpyruvate carboxykinase]], [[fructose 1,6-bisphosphatase]], [[glucose 6-phosphatase]]) from glycolysis that allow the pathway to occur spontaneously.<ref>{{cite book| vauthors = Berg JM, Tymoczko JL, Stryer L, Gatto GJ |title=Biochemistry|date=2012|publisher=W.H. Freeman|location=New York|isbn=978-1-4292-2936-4 |pages=480–482|edition=7th}}</ref>

===Amphibolic pathway (Amphibolism)===
[[File:Amphibolic Properties of the Citric Acid Cycle.gif|Amphibolic properties of the citric acid cycle|thumb|506x506px]]

An '''[[amphibolic|amphibolic pathway]]''' is one that can be either catabolic or anabolic based on the availability of or the need for energy.<ref name="Clarke"/>{{rp|570}} The currency of energy in a biological cell is [[adenosine triphosphate]] (ATP), which stores its energy in the [[High-energy phosphate|phosphoanhydride bonds]]. The energy is utilized to conduct biosynthesis, facilitate movement, and regulate active transport inside of the cell.<ref name="Clarke"/>{{rp|571}} Examples of amphibolic pathways are the citric acid cycle and the glyoxylate cycle. These sets of chemical reactions contain both energy producing and utilizing pathways.<ref name="Voet, Voet, Pratt"/>{{rp|572}} To the right is an illustration of the amphibolic properties of the TCA cycle.

The [[glyoxylate cycle|glyoxylate shunt pathway]] is an alternative to the [[Citric acid cycle|tricarboxylic acid (TCA) cycle]], for it redirects the pathway of TCA to prevent full oxidation of carbon compounds, and to preserve high energy carbon sources as future energy sources. This pathway occurs only in plants and bacteria and transpires in the absence of glucose molecules.<ref>{{cite book| veditors = Pray L, Relman DA, Choffnes ER <!--rapporteurs, Forum on Microbial Threat, Board on Global Health, Institute of Medicine of the National Academies-->|title=The science and applications of synthetic and systems biology workshop summary|date=2011|publisher=National Academies Press|location=Washington, D.C.|isbn=978-0-309-21939-6|page=135}}</ref>

==Regulation==

The flux of the entire pathway is regulated by the rate-determining steps.<ref name="Nelson"/>{{rp|577–578}} These are the slowest steps in a network of reactions. The rate-limiting step occurs near the beginning of the pathway and is regulated by feedback inhibition, which ultimately controls the overall rate of the pathway.<ref>{{cite book| veditors = Kruger NJ | vauthors = Hill SA, Ratcliffe RG |title=Regulation of primary metabolic pathways in plants : [proceedings of an international conference held on 9 - 11 January 1997 at St Hugh's College, Oxford under the auspices of the Phytochemical Society of Europe] |date=1999|publisher=Kluwer|location=Dordrecht [u.a.]|isbn=978-0-7923-5494-9 |pages=258}}</ref> The metabolic pathway in the cell is regulated by covalent or non-covalent modifications. A covalent modification involves an addition or removal of a chemical bond, whereas a non-covalent modification (also known as allosteric regulation) is the binding of the regulator to the enzyme via [[hydrogen bond]]s, electrostatic interactions, and [[Van der Waals force]]s.<ref>{{cite book| vauthors = White D |title=The physiology and biochemistry of prokaryotes|date=1995|publisher=Oxford Univ. Press|location=New York [u.a.]|isbn=978-0-19-508439-9 |pages=133}}</ref>

The rate of turnover in a metabolic pathway, also known as the [[Flux (metabolism)|metabolic flux]], is regulated based on the stoichiometric reaction model, the utilization rate of metabolites, and the translocation pace of molecules across the [[lipid bilayer]].<ref name="Weckwerth">{{cite book|title=Metabolomics methods and protocols|date=2006|publisher=Humana Press|isbn=978-1-59745-244-1 |location=Totowa, N.J.|pages=177| veditors = Weckwerth W }}</ref> The regulation methods are based on experiments involving [[Carbon-13|13C-labeling]], which is then analyzed by [[Nuclear magnetic resonance spectroscopy|nuclear magnetic resonance (NMR)]] or [[Gas chromatography–mass spectrometry|gas chromatography–mass spectrometry (GC–MS)]]–derived mass compositions. The aforementioned techniques synthesize a statistical interpretation of mass distribution in [[proteinogenic amino acid]]s to the catalytic activities of enzymes in a cell.<ref name="Weckwerth"/>{{rp|178}}

==Clinical applications in targeting metabolic pathways==

===Targeting oxidative phosphorylation===
Metabolic pathways can be targeted for clinically therapeutic uses. Within the mitochondrial metabolic network, for instance, there are various pathways that can be targeted by compounds to prevent cancer cell proliferation.<ref name="Frattaruolo">{{cite journal | vauthors = Frattaruolo L, Brindisi M, Curcio R, Marra F, Dolce V, Cappello AR | title = Targeting the Mitochondrial Metabolic Network: A Promising Strategy in Cancer Treatment | journal = International Journal of Molecular Sciences | volume = 21 | issue = 17 | pages = 2–11 | date = August 2020 | pmid = 32825551 | pmc = 7503725 | doi = 10.3390/ijms21176014 | doi-access = free }}</ref> One such pathway is [[oxidative phosphorylation]] (OXPHOS) within the [[electron transport chain]] (ETC). Various inhibitors can downregulate the electrochemical reactions that take place at Complex I, II, III, and IV, thereby preventing the formation of an electrochemical gradient and downregulating the movement of electrons through the ETC. The substrate-level phosphorylation that occurs at ATP synthase can also be directly inhibited, preventing the formation of ATP that is necessary to supply energy for cancer cell proliferation.<ref>{{cite journal | vauthors = Yadav N, Kumar S, Marlowe T, Chaudhary AK, Kumar R, Wang J, O'Malley J, Boland PM, Jayanthi S, Kumar TK, Yadava N, Chandra D | display-authors = 6 | title = Oxidative phosphorylation-dependent regulation of cancer cell apoptosis in response to anticancer agents | journal = Cell Death & Disease | volume = 6 | issue = 11 | pages = e1969 | date = November 2015 | pmid = 26539916 | pmc = 4670921 | doi = 10.1038/cddis.2015.305 }}</ref> Some of these inhibitors, such as [[lonidamine]] and [[atovaquone]],<ref name="Frattaruolo"/> which inhibit Complex II and Complex III, respectively, are currently undergoing clinical trials for [[Food and Drug Administration|FDA]] approval. Other non-FDA-approved inhibitors have still shown experimental success in vitro.

===Targeting Heme===

[[Heme]], an important prosthetic group present in Complexes I, II, and IV can also be targeted, since heme biosynthesis and uptake have been correlated with increased cancer progression.<ref>{{cite journal | vauthors = Hooda J, Cadinu D, Alam MM, Shah A, Cao TM, Sullivan LA, Brekken R, Zhang L | display-authors = 6 | title = Enhanced heme function and mitochondrial respiration promote the progression of lung cancer cells | journal = PLOS ONE | volume = 8 | issue = 5 | pages = e63402 | date = 2013 | pmid = 23704904 | pmc = 3660535 | doi = 10.1371/journal.pone.0063402 | doi-access = free | bibcode = 2013PLoSO...863402H }}</ref> Various molecules can inhibit heme via different mechanisms. For instance, [[succinylacetone]] has been shown to decrease heme concentrations by inhibiting δ-aminolevulinic acid in murine erythroleukemia cells.<ref>{{cite journal | vauthors = Ebert PS, Hess RA, Frykholm BC, Tschudy DP | title = Succinylacetone, a potent inhibitor of heme biosynthesis: effect on cell growth, heme content and delta-aminolevulinic acid dehydratase activity of malignant murine erythroleukemia cells | journal = Biochemical and Biophysical Research Communications | volume = 88 | issue = 4 | pages = 1382–1390 | date = June 1979 | pmid = 289386 | doi = 10.1016/0006-291x(79)91133-1 }}</ref> The primary structure of heme-sequestering peptides, such as HSP1 and HSP2, can be modified to downregulate heme concentrations and reduce proliferation of non-small lung cancer cells.<ref>{{cite journal | vauthors = Sohoni S, Ghosh P, Wang T, Kalainayakan SP, Vidal C, Dey S, Konduri PC, Zhang L | display-authors = 6 | title = Elevated Heme Synthesis and Uptake Underpin Intensified Oxidative Metabolism and Tumorigenic Functions in Non-Small Cell Lung Cancer Cells | journal = Cancer Research | volume = 79 | issue = 10 | pages = 2511–2525 | date = May 2019 | pmid = 30902795 | doi = 10.1158/0008-5472.CAN-18-2156 | s2cid = 85456667 }}</ref>

===Targeting the tricarboxylic acid cycle and glutaminolysis===
The [[tricarboxylic acid cycle]] (TCA) and [[glutaminolysis]] can also be targeted for cancer treatment, since they are essential for the survival and proliferation of cancer cells. [[Ivosidenib]] and [[enasidenib]], two FDA-approved cancer treatments, can arrest the TCA cycle of cancer cells by inhibiting isocitrate dehydrogenase-1 (IDH1) and isocitrate dehydrogenase-2 (IDH2), respectively.<ref name="Frattaruolo"/>  Ivosidenib is specific to acute myeloid leukemia (AML) and cholangiocarcinoma, whereas enasidenib is specific to just acute myeloid leukemia (AML).

In a clinical trial consisting of 185 adult patients with cholangiocarcinoma and an IDH-1 mutation, there was a statistically significant improvement (p<0.0001; HR: 0.37) in patients randomized to ivosidenib. Still, some of the adverse side effects in these patients included fatigue, nausea, diarrhea, decreased appetite, ascites, and anemia.<ref>{{cite web |title=FDA approves Ivosidenib for advanced or metastatic cholangiocarcinoma |url=https://www.fda.gov/drugs/resources-information-approved-drugs/fda-approves-ivosidenib-advanced-or-metastatic-cholangiocarcinoma |website=U.S. Food & Drug Administration|date=26 August 2021 }}</ref> In a clinical trial consisting of 199 adult patients with AML and an IDH2 mutation, 23% of patients experienced complete response (CR) or complete response with partial hematologic recovery (CRh) lasting a median of 8.2 months while on enasidenib. Of the 157 patients who required transfusion at the beginning of the trial, 34% no longer required transfusions during the 56-day time period on enasidenib. Of the 42% of patients who did not require transfusions at the beginning of the trial, 76% still did not require a transfusion by the end of the trial.  Side effects of enasidenib included nausea, diarrhea, elevated bilirubin and, most notably, differentiation syndrome.<ref>{{cite web |title=FDA granted regular approval to enasidenib for the treatment of relapsed or refractory AML |url=https://www.fda.gov/drugs/resources-information-approved-drugs/fda-granted-regular-approval-enasidenib-treatment-relapsed-or-refractory-aml |website=U.S. Food & Drug Administration|date=9 February 2019 }}</ref>

[[Glutaminase]] (GLS), the enzyme responsible for converting glutamine to glutamate via hydrolytic deamidation during the first reaction of glutaminolysis, can also be targeted. In recent years, many small molecules, such as azaserine, acivicin, and CB-839 have been shown to inhibit glutaminase, thus reducing cancer cell viability and inducing apoptosis in cancer cells.<ref>{{cite journal | vauthors = Matés JM, Di Paola FJ, Campos-Sandoval JA, Mazurek S, Márquez J | title = Therapeutic targeting of glutaminolysis as an essential strategy to combat cancer | journal = Seminars in Cell & Developmental Biology | volume = 98 | pages = 34–43 | date = February 2020 | pmid = 31100352 | doi = 10.1016/j.semcdb.2019.05.012 | s2cid = 157067127 | doi-access = free | hdl = 10630/32822 | hdl-access = free }}</ref> Due to its effective antitumor ability in several cancer types such as ovarian, breast and lung cancers, CB-839 is the only GLS inhibitor currently undergoing clinical studies for FDA-approval.

== Genetic engineering of metabolic pathways ==
Many metabolic pathways are of commercial interest. For instance, the production of many [[antibiotic]]s or other drugs requires complex pathways. The pathways to produce such compounds can be transplanted into microbes or other more suitable organism for production purposes. For example, the world's supply of the anti-cancer drug [[vinblastine]] is produced by relatively ineffient extraction and purification of the precursors [[vindoline]] and [[catharanthine]] from the plant ''[[Catharanthus roseus]]'', which are then chemically converted into vinblastine. The biosynthetic pathway to produce vinblastine, including 30 enzymatic steps, has been transferred into yeast cells which is a convenient system to grow in large amounts. With these genetic modifications yeast can use its own metabolites [[geranyl pyrophosphate]] and [[tryptophan]] to produce the precursors of catharanthine and vindoline. This process required 56 genetic edits, including expression of 34 heterologous genes from plants in yeast cells.<ref>{{cite journal | vauthors = Zhang J, Hansen LG, Gudich O, Viehrig K, Lassen LM, Schrübbers L, Adhikari KB, Rubaszka P, Carrasquer-Alvarez E, Chen L, D'Ambrosio V, Lehka B, Haidar AK, Nallapareddy S, Giannakou K, Laloux M, Arsovska D, Jørgensen MA, Chan LJ, Kristensen M, Christensen HB, Sudarsan S, Stander EA, Baidoo E, Petzold CJ, Wulff T, O'Connor SE, Courdavault V, Jensen MK, Keasling JD | display-authors = 6 | title = A microbial supply chain for production of the anti-cancer drug vinblastine | journal = Nature | volume = 609 | issue = 7926 | pages = 341–347 | date = September 2022 | pmid = 36045295 | pmc = 9452304 | doi = 10.1038/s41586-022-05157-3 | bibcode = 2022Natur.609..341Z }}</ref>

== See also ==
* [[KaPPA-View4]] (2010)
* [[Metabolism]]
* [[Metabolic control analysis]]
* [[Metabolic network]]
* [[Metabolic network modelling]]
* [[Metabolic engineering]]
* [[Biochemical systems equation]]
* [[Linear biochemical pathway]]
{{clear right}}

== References ==
{{Reflist|35em}}

== External links ==
{{Commons category|Metabolic pathways}}
* [http://biochemical-pathways.com/#/map/1 Full map of metabolic pathways]
* [http://www.astrojan.nhely.hu/protein/bohr1.htm Biochemical pathways, Gerhard Michal]
* [https://www.brenda-enzymes.org/pathway_index.php Overview Map from BRENDA]
* [https://www.biocyc.org/ BioCyc: Metabolic network models for thousands of sequenced organisms]
* [https://www.genome.jp/kegg/ KEGG: Kyoto Encyclopedia of Genes and Genomes]
* [https://reactome.org/ Reactome, a database of reactions, pathways and biological processes]
* [https://metacyc.org/ MetaCyc: A database of experimentally elucidated metabolic pathways (2,200+ pathways from more than 2,500 organisms)]
* [https://metabomaps.brenda-enzymes.org MetaboMAPS: A platform for pathway sharing and data visualization on metabolic pathways]
* [https://web.archive.org/web/20131016111652/http://pathloc.cbi.pku.edu.cn/ The Pathway Localization database (PathLocdb)]
* [https://web.archive.org/web/20160824171528/https://david.ncifcrf.gov/ DAVID: Visualize genes on pathway maps]
* [https://www.wikipathways.org/ Wikipathways: pathways for the people]
* [http://cpdb.molgen.mpg.de/ ConsensusPathDB]
* [http://www.metabolicpathways.teithe.gr/ ''metpath'': Integrated interactive metabolic chart]

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