Array ( [0] => {{cs1 config|name-list-style=vanc}} [1] => {{citation style|details=Multiple page-numbers in a single ref that is used multiple times: unclear which supports which. Some ISBN might be for wrong edition of the book. Need page-numbers for refs to whole broad-coverage textbooks. |date=August 2017}} [2] => {{chembox [3] => | Verifiedfields = changed [4] => | Watchedfields = changed [5] => | verifiedrevid = 477240040 [6] => | Name = Acetyl-CoA [7] => | ImageFile = Acetyl-CoA-2D_colored.svg [8] => | ImageSize = 320 [9] => | ImageFile2 = Acetyl-CoA-3D-balls.png [10] => | ImageSize2 = 320 [11] => | ImageFile3 = Acetyl-CoA-3D-vdW.png [12] => | ImageSize3 = 320 [13] => | PIN = ''O''1-{(3''R'')-4-[(3-{[2-(Acetylsulfanyl)ethyl]amino}-3-oxopropyl)amino]-3-hydroxy-2,2-dimethyl-4-oxobutyl} ''O''3-{[(2''R'',3''S'',4''R'',5''R'')-5-(6-amino-9''H''-purin-9-yl)-4-hydroxy-3-(phosphonooxy)oxolan-2-yl]methyl} dihydrogen diphosphate [14] => | OtherNames = [15] => | Section1 = {{Chembox Identifiers [16] => | IUPHAR_ligand = 3038 [17] => | InChIKey = ZSLZBFCDCINBPY-ZSJPKINUBJ [18] => | InChI = 1/C23H38N7O17P3S/c1-12(31)51-7-6-25-14(32)4-5-26-21(35)18(34)23(2,3)9-44-50(41,42)47-49(39,40)43-8-13-17(46-48(36,37)38)16(33)22(45-13)30-11-29-15-19(24)27-10-28-20(15)30/h10-11,13,16-18,22,33-34H,4-9H2,1-3H3,(H,25,32)(H,26,35)(H,39,40)(H,41,42)(H2,24,27,28)(H2,36,37,38)/t13-,16-,17-,18+,22-/m1/s1 [19] => | SMILES1 = CC(=O)SCCNC(=O)CCNC(=O)[C@@H](C(C)(C)COP(=O)(O)OP(=O)(O)OC[C@@H]1[C@H]([C@H]([C@@H](O1)n2cnc3c2ncnc3N)O)OP(=O)(O)O)O [20] => | StdInChI_Ref = {{stdinchicite|correct|chemspider}} [21] => | StdInChI = 1S/C23H38N7O17P3S/c1-12(31)51-7-6-25-14(32)4-5-26-21(35)18(34)23(2,3)9-44-50(41,42)47-49(39,40)43-8-13-17(46-48(36,37)38)16(33)22(45-13)30-11-29-15-19(24)27-10-28-20(15)30/h10-11,13,16-18,22,33-34H,4-9H2,1-3H3,(H,25,32)(H,26,35)(H,39,40)(H,41,42)(H2,24,27,28)(H2,36,37,38)/t13-,16-,17-,18+,22-/m1/s1 [22] => | StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} [23] => | StdInChIKey = ZSLZBFCDCINBPY-ZSJPKINUSA-N [24] => | CASNo = 72-89-9 [25] => | CASNo_Ref = {{cascite|correct|CAS}} [26] => | CASNo_Comment = (free acid) [27] => | UNII_Ref = {{fdacite|correct|FDA}} [28] => | UNII = 76Q83YLO3O [29] => | ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} [30] => | ChemSpiderID=392413 [31] => | PubChem = 444493 [32] => | KEGG_Ref = {{keggcite|changed|kegg}} [33] => | KEGG = C00024 [34] => | ChEBI_Ref = {{ebicite|correct|EBI}} [35] => | ChEBI = 15351 [36] => | SMILES = O=C(SCCNC(=O)CCNC(=O)[C@H](O)C(C)(C)COP(=O)(O)OP(=O)(O)OC[C@H]3O[C@@H](n2cnc1c(ncnc12)N)[C@H](O)[C@@H]3OP(=O)(O)O)C [37] => | MeSHName = Acetyl+Coenzyme+A [38] => }} [39] => | Section2 = {{Chembox Properties [40] => | C=23 | H=38 | N=7 | O=17 | P=3 | S=1 [41] => | Appearance = [42] => | Density = [43] => | MeltingPt = [44] => | BoilingPt = [45] => | LambdaMax = 260 nm; 232 nm{{cite book |last1=Dawson |first1=Rex M. C. |last2=Elliott |first2=Daphne C. |last3=Elliott |first3=William H. |last4=Jones |first4=Kenneth M. |title=Data for Biochemical Research |date=2002 |publisher=Clarendon Press |isbn=978-0-19-855299-4 |edition=3rd|page=117}} [46] => | Absorbance = [[Molar attenuation coefficient|ε260]] = 16.4 mM−1 cm−1 (adenosine)
[[Molar attenuation coefficient|ε232]] = 8.7 mM−1 cm−1 (thioester)
Δ[[Molar attenuation coefficient|ε232]] on thioester hydrolysis = −4.5 mM−1 cm−1 [47] => }} [48] => | Section3 = {{Chembox Hazards [49] => | MainHazards = [50] => | FlashPt = [51] => | AutoignitionPt = [52] => }} [53] => | Section4 = [54] => | Section5 = [55] => | Section6 = [56] => }} [57] => '''Acetyl-CoA''' ('''acetyl coenzyme A''') is a molecule that participates in many [[biochemical reaction]]s in protein, carbohydrate and lipid [[metabolism]].{{cite web|url=http://chemistry.elmhurst.edu/vchembook/623acetylCoAfate.html|title=Acetyl CoA Crossroads|website=chemistry.elmhurst.edu|access-date=2016-11-08|archive-date=2016-11-15|archive-url=https://web.archive.org/web/20161115202146/http://chemistry.elmhurst.edu/vchembook/623acetylCoAfate.html|url-status=dead}} Its main function is to deliver the [[acetyl]] group to the [[citric acid cycle]] (Krebs cycle) to be [[oxidation|oxidized]] for energy production. [58] => [59] => [[Coenzyme A]] (CoASH or CoA) consists of a [[cysteamine|β-mercaptoethylamine group]] linked to [[pantothenic acid]] (vitamin B5) through an [[amide linkage]]{{cite web|url=http://library.med.utah.edu/NetBiochem/FattyAcids/2_4.html|title=Fatty Acids -- Structure of Acetyl CoA|website=library.med.utah.edu|access-date=2017-06-02}} and 3'-phosphorylated ADP. The acetyl group (indicated in blue in the structural diagram on the right) of acetyl-CoA is linked to the [[sulfhydryl]] substituent of the β-mercaptoethylamine group. This [[thioester]] linkage is a "high energy" bond, which is particularly reactive. [[Hydrolysis]] of the thioester bond is [[exergonic]] (−31.5 kJ/mol). [60] => [61] => CoA is acetylated to acetyl-CoA by the breakdown of [[carbohydrates]] through [[glycolysis]] and by the breakdown of [[fatty acids]] through [[Beta oxidation|β-oxidation]]. Acetyl-CoA then enters the citric acid cycle, where the acetyl group is oxidized to carbon dioxide and water, and the energy released is captured in the form of 11 [[Adenosine triphosphate|ATP]] and one [[Guanosine triphosphate|GTP]] per acetyl group. [62] => [63] => [[Konrad Bloch]] and [[Feodor Lynen]] were awarded the 1964 [[Nobel Prize in Physiology or Medicine]] for their discoveries linking acetyl-CoA and fatty acid metabolism. [[Fritz Lipmann]] won the Nobel Prize in 1953 for his discovery of the cofactor [[coenzyme A]].{{cite web |title=All Nobel Prizes in Physiology or Medicine |url=https://www.nobelprize.org/prizes/lists/all-nobel-laureates-in-physiology-or-medicine/ |website=The Nobel Prize}} [64] => [65] => == Role == [66] => Acetyl-CoA is a [[metabolic intermediate]] that is involved in many metabolic pathways in an organism. It is produced during the breakdown of [[glucose]], [[fatty acids]], and [[Amino acid|amino acids]], and is used in the synthesis of many other [[biomolecules]], including [[cholesterol]], [[fatty acid]]s, and [[ketone bodies]]. Acetyl-CoA is also a key molecule in the [[citric acid cycle]], which is a series of chemical reactions that occur in the [[Mitochondrion|mitochondria]] of cells and is responsible for generating energy in the form of [[Adenosine triphosphate|ATP]].{{cite journal |vauthors=Zhang S, Yang W, Chen H, Liu B, Lin B, Tao Y |title=Metabolic engineering for efficient supply of acetyl-CoA from different carbon sources in Escherichia coli |journal=Microb Cell Fact |volume=18 |issue=1 |pages=130 |date=August 2019 |pmid=31387584 |doi=10.1186/s12934-019-1177-y |pmc=6685171 |url= |doi-access=free }}{{cite web | url=https://bio.libretexts.org/Bookshelves/Microbiology/Microbiology_%28Boundless%29/05%3A_Microbial_Metabolism/5.12%3A_Biosynthesis/5.12G%3A_The_Acetyl-CoA_Pathway | title=5.12G: The Acetyl-CoA Pathway | date=9 May 2017 }} [67] => [68] => In addition, acetyl-CoA is a precursor for the biosynthesis of various acetyl-chemicals, acting as an intermediate to transfer an acetyl group during the biosynthesis of those acetyl-chemicals. Acetyl-CoA is also involved in the regulation of various cellular mechanisms by providing acetyl groups to target amino acid residues for post-translational [[acetylation]] reactions of proteins.{{cite web | title=Central Metabolic Intermediate | website=MedchemExpress.com | url=https://www.medchemexpress.com/acetyl-coenzyme-a.html | access-date=15 February 2024}} [69] => [70] => == Biosynthesis == [71] => The acetylation of CoA is determined by the carbon sources.{{cite journal|last1=Hynes|first1=Michael J.|last2=Murray|first2=Sandra L.|date=2010-07-01|title=ATP-Citrate Lyase Is Required for Production of Cytosolic Acetyl Coenzyme A and Development in Aspergillus nidulans|journal=Eukaryotic Cell|language=en|volume=9|issue=7|pages=1039–1048|doi=10.1128/EC.00080-10|issn=1535-9778|pmc=2901662|pmid=20495057}}{{cite journal|last1=Wellen|first1=Kathryn E.|last2=Thompson|first2=Craig B.|date=2012-04-01|title=A two-way street: reciprocal regulation of metabolism and signalling|journal=Nature Reviews Molecular Cell Biology|language=en|volume=13|issue=4|pages=270–276|doi=10.1038/nrm3305|issn=1471-0072|pmid=22395772|s2cid=244613}} [72] => [73] => === Extramitochondrial === [74] => * At high [[glucose]] levels, [[glycolysis]] takes place rapidly, thus increasing the amount of [[citrate]] produced from the [[citric acid cycle]]. This citrate is then exported to other [[organelle]]s outside the mitochondria to be broken into acetyl-CoA and [[oxaloacetate]] by the [[enzyme]] [[ATP citrate lyase]] (ACL). This principal reaction is coupled with the [[hydrolysis]] of ATP.{{cite book|url=https://books.google.com/books?id=d1nu4vcml8sC&q=reaction+of+ATP+citrate+lyase+produces+acetyl+coA&pg=PA253|title=Functional Metabolism: Regulation and Adaptation|last=Storey|first=Kenneth B.|date=2005-02-25|publisher=John Wiley & Sons|isbn=9780471675570|language=en}}{{cite web|url=https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=47|title=ACLY ATP citrate lyase [Homo sapiens (human)] - Gene - NCBI|website=www.ncbi.nlm.nih.gov|access-date=2016-11-06}} [75] => * At low glucose levels: [76] => ** CoA is acetylated using [[acetate]] by [[acetyl-CoA synthetase]] (ACS), also coupled with [[adenosine triphosphate|ATP]] hydrolysis.{{cite journal|last=Ragsdale|first=S. W.|title=Life with carbon monoxide|journal=CRC Critical Reviews in Biochemistry and Molecular Biology|date=2004|volume=39|issue=3|pages=165–195|doi=10.1080/10409230490496577|pmid=15596550|s2cid=16194968}} [77] => ** [[Ethanol]] also serves as a carbon source for acetylation of CoA utilizing the enzyme [[alcohol dehydrogenase]].{{cite book|url=https://books.google.com/books?id=xN0YYypnZVkC&q=reaction+of+Acetyl+CoA+synthase+produce+Acetyl+CoA&pg=PA275|title=Textbook of Biochemistry for Dental/Nursing/Pharmacy Students|last=Chatterjea|date=2004-01-01|publisher=Jaypee Brothers Publishers|isbn=9788180612046|language=en}}{{Dead link|date=February 2024 |bot=InternetArchiveBot |fix-attempted=yes }} [78] => ** Degradation of branched-chain [[ketogenic]] [[amino acid]]s such as [[valine]], [[leucine]], and [[isoleucine]] occurs. These amino acids are converted to α-ketoacids by [[transamination]] and eventually to [[isovaleryl-CoA]] through oxidative decarboxylation by an α-ketoacid dehydrogenase complex. Isovaleryl-CoA undergoes [[dehydrogenation]], [[carboxylation]] and hydration to form another CoA-derivative intermediate before it is cleaved into acetyl-CoA and [[acetoacetate]].{{cite book|url=https://archive.org/details/biochemistrychap00jere|title=Biochemistry|last1=Berg|first1=Jeremy M.|last2=Tymoczko|first2=John L.|last3=Stryer|first3=Lubert|year=2002|publisher=W. H. Freeman|isbn=978-0716730514|edition=5th}}{{page needed|date=August 2017}} [79] => [80] => === Intramitochondrial === [81] => [[File:Pyruvate dehydrogenase complex reaction.svg|left|thumb|[[Pyruvate dehydrogenase]] complex reaction]] [82] => * At high glucose levels, acetyl-CoA is produced through [[glycolysis]].{{cite book|url=https://books.google.com/books?id=y8JQAwAAQBAJ&q=acetyl+coA+pathway&pg=PA149|title=Guide to Biochemistry|last=Blackstock|first=James C.|date=2014-06-28|publisher=Butterworth-Heinemann|isbn=9781483183671|language=en}} [[Pyruvate]] undergoes oxidative decarboxylation in which it loses its [[carboxyl]] group (as [[carbon dioxide]]) to form acetyl-CoA, giving off 33.5 kJ/mol of energy. The oxidative conversion of pyruvate into acetyl-CoA is referred to as the '''pyruvate dehydrogenase reaction'''. It is catalyzed by the [[pyruvate dehydrogenase complex]]. Other conversions between pyruvate and acetyl-CoA are possible. For example, [[pyruvate formate lyase]] [[disproportionates]] pyruvate into acetyl-CoA and [[formic acid]]. [83] => [[File:Metabolism4.jpg|right|thumb|282px|[[beta-oxidation|β-Oxidation]] of [[fatty acid]]s]] [84] => * At low glucose levels, the production of acetyl-CoA is linked to [[beta oxidation|β-oxidation]] of [[fatty acid]]s. Fatty acids are first converted to acyl-CoA. Acyl-CoA is then degraded in a four-step cycle of [[oxidation]], [[Hydration reaction|hydration]], [[oxidation]] and [[thiolysis]] catalyzed by four respective enzymes, namely [[acyl-CoA dehydrogenase]], [[enoyl-CoA hydratase]], [[3-hydroxyacyl-CoA dehydrogenase]], and [[thiolase]]. The cycle produces a new fatty acid chain with two fewer carbons and acetyl-CoA as a byproduct.{{cite journal|last1=Houten|first1=Sander Michel|last2=Wanders|first2=Ronald J. A.|date=2010-03-02|title=A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation|journal=Journal of Inherited Metabolic Disease|language=en|volume=33|issue=5|pages=469–477|doi=10.1007/s10545-010-9061-2|issn=0141-8955|pmc=2950079|pmid=20195903}} [85] => [86] => ==Functions== [87] => [88] => === Intermediates in various pathways === [89] => * In [[cellular respiration]] [90] => * [[Citric acid cycle]]: [91] => ** Through a series of chemical reactions, stored energy is released through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins into [[adenosine triphosphate]] (ATP) and [[carbon dioxide]]. [92] => * [[Fatty acid metabolism]] [93] => ** Acetyl-CoA is produced by the breakdown of both [[carbohydrate]]s (by [[glycolysis]]) and [[lipids]] (by [[Beta oxidation|β-oxidation]]). It then enters the citric acid cycle in the mitochondrion by combining with [[Oxaloacetic acid|oxaloacetate]] to form [[citric acid|citrate]].{{cite book |last1= Stryer |first1= Lubert | title=Biochemistry. | edition= Fourth |location= New York |publisher= W.H. Freeman and Company|date= 1995 |pages= 510–515, 559–565, 581–613, 614–623, 775–778 |isbn= 978-0-7167-2009-6 }}{{cite web|url=http://pharmaxchange.info/press/2013/10/oxidation-of-fatty-acids/|title=Oxidation of fatty acids|date=2013-10-11}} [94] => ** Two acetyl-CoA molecules condense to form [[acetoacetyl-CoA]], which gives rise to the formation of [[Acetoacetic acid|acetoacetate]] and [[beta-Hydroxybutyric acid|β-hydroxybutyrate]]. Acetoacetate, β-hydroxybutyrate, and their spontaneous breakdown product [[acetone]]{{cite web|url=http://watcut.uwaterloo.ca/webnotes/Metabolism/fatKetoneBodyMetabolism.html|title=Ketone body metabolism|publisher=University of Waterloo}} are frequently, but confusingly, known as [[ketone bodies]] (as they are not "bodies" at all, but water-soluble chemical substances). The ketone bodies are released by the [[liver]] into the blood. All cells with mitochondria can take ketone bodies up from the blood and reconvert them into acetyl-CoA, which can then be used as fuel in their citric acid cycles, as no other tissue can divert its oxaloacetate into the [[gluconeogenesis|gluconeogenic pathway]] in the way that the liver does. Unlike free fatty acids, ketone bodies can cross the [[blood–brain barrier]] and are therefore available as fuel for the cells of the [[central nervous system]], acting as a substitute for glucose, on which these cells normally survive. The occurrence of high levels of ketone bodies in the blood during [[starvation]], a [[low-carbohydrate diet]], prolonged heavy exercise, and uncontrolled [[Type 1 diabetes|type-1 diabetes mellitus]] is known as [[ketosis]], and in its extreme form in out-of-control type-1 diabetes mellitus, as [[ketoacidosis]]. [95] => ** On the other hand, when the [[insulin]] concentration in the blood is high, and that of [[glucagon]] is low (i.e. after meals), the acetyl-CoA produced by glycolysis condenses as normal with oxaloacetate to form citrate in the mitochondrion. However, instead of continuing through the citric acid cycle to be converted to carbon dioxide and water, the citrate is removed from the mitochondrion into the [[cytoplasm]]. There it is cleaved by [[ATP citrate lyase]] into acetyl-CoA and oxaloacetate. The oxaloacetate is returned to the mitochondrion as malate (and then converted back into oxaloacetate to transfer more acetyl-CoA out of the mitochondrion).{{cite journal | doi = 10.1159/000100426 | title = SREBP-1c Transcription Factor and Lipid Homeostasis: Clinical Perspective | journal = Hormone Research | year = 2007 | first = P. | last = Ferre |author2=F. Foufelle | volume = 68 | issue = 2 | pages = 72–82| pmid = 17344645 | quote = this process is outlined graphically in page 73| doi-access = free }} This cytosolic acetyl-CoA can then be used to synthesize fatty acids through carboxylation by [[acetyl-CoA carboxylase]] into [[Malonyl-CoA|malonyl CoA]], the first committed step in the synthesis of fatty acids.{{cite book |last=Voet |first=Donald |author2=Judith G. Voet |author3=Charlotte W. Pratt |title=Fundamentals of Biochemistry, 2nd Edition |publisher=John Wiley and Sons, Inc. |year=2006 |pages=[https://archive.org/details/fundamentalsofbi00voet_0/page/547 547, 556] |isbn=978-0-471-21495-3 |url=https://archive.org/details/fundamentalsofbi00voet_0/page/547 }} This conversion occurs primarily in the liver, [[adipose tissue]] and lactating [[mammary gland]]s, where the fatty acids are combined with [[glycerol]] to form [[triglyceride]]s, the major fuel reservoir of most animals. Fatty acids are also components of the [[phospholipid]]s that make up the bulk of the [[lipid bilayer]]s of all [[cellular membrane]]s. [96] => ** In plants, ''de novo'' fatty acid synthesis occurs in the [[plastid]]s. Many [[seed]]s accumulate large reservoirs of seed oils to support [[germination]] and early growth of the seedling before it is a net [[photosynthesis|photosynthetic]] organism. [97] => ** The [[cytosol]]ic acetyl-CoA can also condense with [[acetoacetyl-CoA]] to form 3-hydroxy-3-methylglutaryl-CoA ([[HMG-CoA]]) which is the rate-limiting step controlling the [[Mevalonate pathway|synthesis of cholesterol]]. [[Cholesterol]] can be used as is, as a structural component of cellular membranes, or it can be used to synthesize [[Steroid#Steroidogenesis|steroid hormones]], [[Bile acids|bile salts]], and [[vitamin D]]. [98] => ** Acetyl-CoA can be [[carboxylated]] in the cytosol by [[acetyl-CoA carboxylase]], giving rise to [[malonyl-CoA]], a substrate required for synthesis of [[flavonoid]]s and related [[polyketide]]s, for elongation of fatty acids to produce [[wax]]es, [[cuticle]], and seed oils in members of the [[Brassica]] family, and for [[malonate|malonation]] of proteins and other phytochemicals.{{cite journal|year=2005|title=Reverse Genetic Characterization of Cytosolic Acetyl-CoA Generation by ATP-Citrate Lyase in Arabidopsis|journal=The Plant Cell Online|volume=17|issue=1|pages=182–203|doi=10.1105/tpc.104.026211|pmid=15608338|last1=Fatland|first1=B. L.|pmc=544498}} In plants, these include [[sesquiterpene]]s, [[brassinosteroid]]s (hormones), and membrane [[sterol]]s. [99] => * [[Steroid synthesis]]: [100] => ** Acetyl-CoA participates in the [[mevalonate pathway]] by partaking in the synthesis of hydroxymethyl glutaryl-CoA. [101] => * [[Acetylcholine]] synthesis: [102] => ** Acetyl-CoA is also an important component in the biogenic synthesis of the [[neurotransmitter]] [[acetylcholine]]. [[Choline]], in combination with acetyl-CoA, is catalyzed by the enzyme [[choline acetyltransferase]] to produce acetylcholine and [[coenzyme A]] as a byproduct. [103] => * [[Melatonin]] synthesis [104] => * Acetylation [105] => ** Acetyl-CoA is also the source of the acetyl group incorporated onto certain [[lysine]] residues of [[histone]] and nonhistone proteins in the [[posttranslational modification]] [[acetylation]]. This acetylation is catalyzed by [[acetyltransferases]]. This acetylation affects [[cell growth]], [[mitosis]], and [[apoptosis]].{{cite journal|last1=Yi|first1=C. H.|last2=Vakifahmetoglu-Norberg|first2=H.|last3=Yuan|first3=J.|date=2011-01-01|title=Integration of Apoptosis and Metabolism|journal=Cold Spring Harbor Symposia on Quantitative Biology|language=en|volume=76|pages=375–387|doi=10.1101/sqb.2011.76.010777|issn=0091-7451|pmid=22089928|doi-access=free}} [106] => *Allosteric regulator [107] => ** Acetyl-CoA serves as an [[allosteric regulation|allosteric regulator]] of [[pyruvate dehydrogenase kinase]] (PDK). It regulates through the ratio of acetyl-CoA versus CoA. Increased concentration of acetyl-CoA activates PDK.{{cite journal|last1=Pettit|first1=Flora H.|last2=Pelley|first2=John W.|last3=Reed|first3=Lester J.|date=1975-07-22|title=Regulation of pyruvate dehydrogenase kinase and phosphatase by acetyl-CoA/CoA and NADH/NAD ratios|journal=Biochemical and Biophysical Research Communications|volume=65|issue=2|pages=575–582|doi=10.1016/S0006-291X(75)80185-9|pmid=167775}} [108] => ** Acetyl-CoA is also an allosteric activator of [[pyruvate carboxylase]].{{cite journal|last1=Jitrapakdee|first1=Sarawut|last2=Maurice|first2=Martin St.|author3-link=Ivan Rayment|last3=Rayment|first3=Ivan|last4=Cleland|first4=W. Wallace|last5=Wallace|first5=John C.|last6=Attwood|first6=Paul V.|date=2008-08-01|title=Structure, Mechanism and Regulation of Pyruvate Carboxylase|journal=The Biochemical Journal|volume=413|issue=3|pages=369–387|doi=10.1042/BJ20080709|issn=0264-6021|pmc=2859305|pmid=18613815}} [109] => [110] => ==Interactive pathway map== [111] => ''Click on genes, proteins and metabolites below to visit [[Portal:Gene Wiki|Gene Wiki]] pages and related Wikipedia articles. The pathway can be downloaded and edited at [http://www.wikipathways.org WikiPathways].'' [112] => {| style="margin-left: auto; margin-right: auto; border: none;" [113] => | width="390px"|{{TCACycle_WP78|highlight=Acetyl-CoA|header=}} [114] => | width="390px"|{{StatinPathway_WP430|highlight=Acetyl-coa|header=}} [115] => |} [116] => [117] => ==See also== [118] => * [[Malonyl-CoA decarboxylase]] [119] => [120] => ==References== [121] => {{reflist}} [122] => [123] => ==External links== [124] => * {{MeshName|Acetyl+Coenzyme+A}} [125] => [126] => {{Fatty-acid metabolism intermediates}} [127] => {{Cholesterol metabolism intermediates}} [128] => {{Glycolysis}} [129] => {{Citric acid cycle}} [130] => {{Amino acid metabolism intermediates}} [131] => {{Acetylcholine receptor modulators}} [132] => {{Authority control}} [133] => [134] => {{DEFAULTSORT:Acetyl-Coa}} [135] => [[Category:Cholinergics]] [136] => [[Category:Metabolism]] [137] => [[Category:Thioesters of coenzyme A]] [138] => [[Category:Glycolysis]] [139] => [[Category:Metabolic intermediates]] [] => )
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Acetyl-CoA

Acetyl-CoA is a molecule that plays a crucial role in various biological processes, particularly in cellular energy production. It is a high-energy compound that serves as both an important intermediate and a carrier of carbon atoms in the metabolic pathways of all living organisms.

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It is a high-energy compound that serves as both an important intermediate and a carrier of carbon atoms in the metabolic pathways of all living organisms. The Wikipedia page on Acetyl-CoA provides a comprehensive overview of this essential molecule. It begins by explaining its chemical structure and how it is formed through the breakdown of glucose or fatty acids during cellular respiration. The page then delves into the various metabolic pathways in which Acetyl-CoA participates, such as the Krebs cycle, fatty acid synthesis, and ketogenesis. The article also explores the diverse functions of Acetyl-CoA beyond energy metabolism. For instance, it highlights its role in the production of neurotransmitters, sterols, and certain amino acids. Moreover, the page discusses the significance of Acetyl-CoA in epigenetics, where it acts as a substrate for histone acetylation – a process that can impact gene expression. Furthermore, the Wikipedia entry covers important physiological aspects related to Acetyl-CoA, including its involvement in lipid metabolism, cholesterol synthesis, and biotin-dependent carboxylation reactions. It also briefly touches upon the clinical relevance of Acetyl-CoA and its potential implications in certain diseases, such as cancer and neurological disorders. Overall, the Wikipedia page provides a comprehensive look into Acetyl-CoA, elucidating its central role in cellular metabolism and highlighting its broad range of functions in various biological processes.

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