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1

Monchi, Mehran. "Citrate pathophysiology and metabolism." Transfusion and Apheresis Science 56, no. 1 (2017): 28–30. http://dx.doi.org/10.1016/j.transci.2016.12.013.

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2

Korithoski, Bryan, Kirsten Krastel, and Dennis G. Cvitkovitch. "Transport and Metabolism of Citrate by Streptococcus mutans." Journal of Bacteriology 187, no. 13 (2005): 4451–56. http://dx.doi.org/10.1128/jb.187.13.4451-4456.2005.

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ABSTRACT Streptococcus mutans, a normal inhabitant of dental plaque, is considered a primary etiological agent of dental caries. Two virulence determinants of S. mutans are its acidogenicity and aciduricity (the ability to produce acid and the ability to survive and grow at low pH, respectively). Citric acid is ubiquitous in nature; it is a component of fruit juices, bones, and teeth. In lactic acid bacteria citrate transport has been linked to increased survival in acidic conditions. We identified putative citrate transport and metabolism genes in S. mutans, which led us to investigate citrat
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3

Chen, Fangfang, Hanna Friederike Willenbockel, and Thekla Cordes. "Mapping the Metabolic Niche of Citrate Metabolism and SLC13A5." Metabolites 13, no. 3 (2023): 331. http://dx.doi.org/10.3390/metabo13030331.

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The small molecule citrate is a key molecule that is synthesized de novo and involved in diverse biochemical pathways influencing cell metabolism and function. Citrate is highly abundant in the circulation, and cells take up extracellular citrate via the sodium-dependent plasma membrane transporter NaCT encoded by the SLC13A5 gene. Citrate is critical to maintaining metabolic homeostasis and impaired NaCT activity is implicated in metabolic disorders. Though citrate is one of the best known and most studied metabolites in humans, little is known about the consequences of altered citrate uptake
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4

Mortera, Pablo, Agata Pudlik, Christian Magni, Sergio Alarcón, and Juke S. Lolkema. "Ca2+-Citrate Uptake and Metabolism in Lactobacillus casei ATCC 334." Applied and Environmental Microbiology 79, no. 15 (2013): 4603–12. http://dx.doi.org/10.1128/aem.00925-13.

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ABSTRACTThe putative citrate metabolic pathway inLactobacillus caseiATCC 334 consists of the transporter CitH, a proton symporter of the citrate-divalent metal ion family of transporters CitMHS, citrate lyase, and the membrane-bound oxaloacetate decarboxylase complex OAD-ABDH. Resting cells ofLactobacillus caseiATCC 334 metabolized citrate in complex with Ca2+and not as free citrate or the Mg2+-citrate complex, thereby identifying Ca2+-citrate as the substrate of the transporter CitH. The pathway was induced in the presence of Ca2+and citrate during growth and repressed by the presence of gluc
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5

Sarantinopoulos, Panagiotis, George Kalantzopoulos, and Effie Tsakalidou. "Citrate Metabolism by Enterococcus faecalis FAIR-E 229." Applied and Environmental Microbiology 67, no. 12 (2001): 5482–87. http://dx.doi.org/10.1128/aem.67.12.5482-5487.2001.

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ABSTRACT Citrate metabolism by Enterococcus faecalis FAIR-E 229 was studied in various growth media containing citrate either in the presence of glucose or lactose or as the sole carbon source. In skim milk (130 mM lactose, 8 mM citrate), cometabolism of citrate and lactose was observed from the first stages of the growth phase. Lactose was stoichiometrically converted into lactate, while citrate was converted into acetate, formate, and ethanol. When de Man-Rogosa-Sharpe (MRS) broth containing lactose (28 mM) instead of glucose was used,E. faecalis FAIR-E 229 catabolized only the carbohydrate.
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6

Cartledge, S., D. J. Candy, and R. J. Hawker. "Citrate metabolism by human platelets." Transfusion Medicine 7, no. 3 (1997): 211–15. http://dx.doi.org/10.1046/j.1365-3148.1997.d01-28.x.

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7

Kanbe, Chiyuki, and Kinji Uchida. "Citrate Metabolism by Pediococcus halophilus." Applied and Environmental Microbiology 53, no. 6 (1987): 1257–62. http://dx.doi.org/10.1128/aem.53.6.1257-1262.1987.

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8

Antranikian, Garabed, and Friedrich Giffhorn. "Citrate metabolism in anaerobic bacteria." FEMS Microbiology Letters 46, no. 2 (1987): 175–98. http://dx.doi.org/10.1111/j.1574-6968.1987.tb02458.x.

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9

Magni, Christian, Diego de Mendoza, Wil N. Konings, and Juke S. Lolkema. "Mechanism of Citrate Metabolism inLactococcus lactis: Resistance against Lactate Toxicity at Low pH." Journal of Bacteriology 181, no. 5 (1999): 1451–57. http://dx.doi.org/10.1128/jb.181.5.1451-1457.1999.

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ABSTRACT Measurement of the flux through the citrate fermentation pathway in resting cells of Lactococcus lactis CRL264 grown in a pH-controlled fermentor at different pH values showed that the pathway was constitutively expressed, but its activity was significantly enhanced at low pH. The flux through the citrate-degrading pathway correlated with the magnitude of the membrane potential and pH gradient that were generated when citrate was added to the cells. The citrate degradation rate and proton motive force were significantly higher when glucose was metabolized at the same time, a phenomeno
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10

Pudlik, Agata M., and Juke S. Lolkema. "Rerouting Citrate Metabolism in Lactococcus lactis to Citrate-Driven Transamination." Applied and Environmental Microbiology 78, no. 18 (2012): 6665–73. http://dx.doi.org/10.1128/aem.01811-12.

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ABSTRACTOxaloacetate is an intermediate of the citrate fermentation pathway that accumulates in the cytoplasm ofLactococcus lactisILCitM(pFL3) at a high concentration due to the inactivation of oxaloacetate decarboxylase. An excess of toxic oxaloacetate is excreted into the medium in exchange for citrate by the citrate transporter CitP (A. M. Pudlik and J. S. Lolkema, J. Bacteriol. 193:4049–4056, 2011). In this study, transamination of amino acids with oxaloacetate as the keto donor is described as an additional mechanism to relieve toxic stress. Redirection of the citrate metabolic pathway in
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11

Vaningelgem, Frederik, Veerle Ghijsels, Effie Tsakalidou, and Luc De Vuyst. "Cometabolism of Citrate and Glucose by Enterococcus faecium FAIR-E 198 in the Absence of Cellular Growth." Applied and Environmental Microbiology 72, no. 1 (2006): 319–26. http://dx.doi.org/10.1128/aem.72.1.319-326.2006.

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ABSTRACT Citrate metabolism by Enterococcus faecium FAIR-E 198, an isolate from Greek Feta cheese, was studied in modified MRS (mMRS) medium under different pH conditions and glucose and citrate concentrations. In the absence of glucose, this strain was able to metabolize citrate in a pH range from constant pH 5.0 to 7.0. At a constant pH 8.0, no citrate was metabolized, although growth took place. The main end products of citrate metabolism were acetate, formate, acetoin, and carbon dioxide, whereas ethanol and diacetyl were present in smaller amounts. In the presence of glucose, citrate was
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12

NAKAMURA, Yumiko, Yasuhide TONOGAI, Sumiko TSUJI, and Yoshio ITO. "Metabolism of Citric Acid, Potassium Citrate, Sodium Citrate and Calcium Citrate in the Rat." Food Hygiene and Safety Science (Shokuhin Eiseigaku Zasshi) 28, no. 4 (1987): 251–60. http://dx.doi.org/10.3358/shokueishi.28.251.

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13

Li, Heng, Nancy E. Ramia, Frédéric Borges, Anne-Marie Revol-Junelles, Finn Kvist Vogensen, and Jørgen J. Leisner. "Identification of Potential Citrate Metabolism Pathways in Carnobacterium maltaromaticum." Microorganisms 9, no. 10 (2021): 2169. http://dx.doi.org/10.3390/microorganisms9102169.

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In the present study, we describe the identification of potential citrate metabolism pathways for the lactic acid bacterium (LAB) Carnobacterium maltaromaticum. A phenotypic assay indicated that four of six C. maltaromaticum strains showed weak (Cm 6-1 and ATCC 35586) or even delayed (Cm 3-1 and Cm 5-1) citrate utilization activity. The remaining two strains, Cm 4-1 and Cm 1-2 gave negative results. Additional analysis showed no or very limited utilization of citrate in media containing 1% glucose and 22 or 30 mM citrate and inoculated with Cm 6-1 or ATCC 35586. Two potential pathways of citra
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14

Lu, Chuang, Wenhui Yang, Huaxi Zhang, et al. "ATP Citrate Lyase ClACLB-1 Facilitates Citrate Cleavage in Lemon." Plants 14, no. 1 (2024): 53. https://doi.org/10.3390/plants14010053.

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Citric acid is an important organic acid with wide applications and diverse biological functionality. As the predominant organic acid in lemons, citric acid plays a crucial role in determining the flavor of citrus, especially in lemons. ATP citrate lyase (ACL, EC4.1.3.8) is the keg gene in citric acid metabolism. Several research studies on ACL only focused on high-sugar- and low-acid-content citrus varieties; however, the ACL mechanism in lemons with high acid and low sugar levels remains undetermined. In this study, a key candidate gene, ClACLB-1, for citrate cleavage was identified from the
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15

Hooks, Mark A., J. William Allwood, Joanna K. D. Harrison, et al. "Selective induction and subcellular distribution of ACONITASE 3 reveal the importance of cytosolic citrate metabolism during lipid mobilization in Arabidopsis." Biochemical Journal 463, no. 2 (2014): 309–17. http://dx.doi.org/10.1042/bj20140430.

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The cytosolic location of AtACO3 and its importance in citrate metabolism support the operation of the classic glyoxylate cycle and not direct mitochondrial metabolism of citrate during lipid mobilization in seedlings of oilseed plants, such as Arabidopsis.
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16

Drexler, Konstantin, Katharina M. Schmidt, Katrin Jordan, et al. "Cancer-associated cells release citrate to support tumour metastatic progression." Life Science Alliance 4, no. 6 (2021): e202000903. http://dx.doi.org/10.26508/lsa.202000903.

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Citrate is important for lipid synthesis and epigenetic regulation in addition to ATP production. We have previously reported that cancer cells import extracellular citrate via the pmCiC transporter to support their metabolism. Here, we show for the first time that citrate is supplied to cancer by cancer-associated stroma (CAS) and also that citrate synthesis and release is one of the latter’s major metabolic tasks. Citrate release from CAS is controlled by cancer cells through cross-cellular communication. The availability of citrate from CAS regulated the cytokine profile, metabolism and fea
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17

Melnick, Joel Z., Patricia A. Preisig, Robert J. Alpern, and Michel Baum. "Renal citrate metabolism and urinary citrate excretion in the infant rat." Kidney International 57, no. 3 (2000): 891–97. http://dx.doi.org/10.1046/j.1523-1755.2000.057003891.x.

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18

Yasukawa, Shu, Masato Takamatsu, Shoichi Ebisuno, Shigeyoshi Morimoto, Toshihiko Yoshida, and Tadashi Ohkawa. "STUDIES ON CITRATE METABOLISM IN UROLITHIASIS." Japanese Journal of Urology 76, no. 12 (1985): 1848–54. http://dx.doi.org/10.5980/jpnjurol1928.76.12_1848.

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19

Yasukawa, Shu, Masaki Uehara, Shigeyoshi Morimoto, et al. "STUDIES OF CITRATE METABOLISM IN UROLITHIASIS." Japanese Journal of Urology 78, no. 4 (1987): 626–33. http://dx.doi.org/10.5980/jpnjurol1928.78.4_626.

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20

Icard, Philippe, Ludovic Fournel, Marco Alifano, and Hubert Lincet. "Extracellular Citrate and Cancer Metabolism—Letter." Cancer Research 78, no. 17 (2018): 5176. http://dx.doi.org/10.1158/0008-5472.can-18-1666.

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21

Mycielska, Maria E., and Edward K. Geissler. "Extracellular Citrate and Cancer Metabolism—Response." Cancer Research 78, no. 17 (2018): 5177. http://dx.doi.org/10.1158/0008-5472.can-18-1899.

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22

Popova, Tatyana N., and Miguel Â. A. Pinheiro de Carvalho. "Citrate and isocitrate in plant metabolism." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1364, no. 3 (1998): 307–25. http://dx.doi.org/10.1016/s0005-2728(98)00008-5.

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23

Hugenholtz, Jeroen. "Citrate metabolism in lactic acid bacteria." FEMS Microbiology Reviews 12, no. 1-3 (1993): 165–78. http://dx.doi.org/10.1111/j.1574-6976.1993.tb00017.x.

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24

Rea, Mary C., and Timothy M. Cogan. "Glucose prevents citrate metabolism by enterococci." International Journal of Food Microbiology 88, no. 2-3 (2003): 201–6. http://dx.doi.org/10.1016/s0168-1605(03)00181-8.

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25

Jaramillo-Martinez, Valeria, Sathish Sivaprakasam, Vadivel Ganapathy, and Ina L. Urbatsch. "Drosophila INDY and Mammalian INDY: Major Differences in Transport Mechanism and Structural Features despite Mostly Similar Biological Functions." Metabolites 11, no. 10 (2021): 669. http://dx.doi.org/10.3390/metabo11100669.

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INDY (I’m Not Dead Yet) is a plasma membrane transporter for citrate, first identified in Drosophila. Partial deficiency of INDY extends lifespan in this organism in a manner similar to that of caloric restriction. The mammalian counterpart (NaCT/SLC13A5) also transports citrate. In mice, it is the total, not partial, absence of the transporter that leads to a metabolic phenotype similar to that caloric restriction; however, there is evidence for subtle neurological dysfunction. Loss-of-function mutations in SLC13A5 (solute carrier gene family 13, member A5) occur in humans, causing a recessiv
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26

Sánchez, Claudia, Ana Rute Neves, João Cavalheiro, et al. "Contribution of Citrate Metabolism to the Growth of Lactococcus lactis CRL264 at Low pH." Applied and Environmental Microbiology 74, no. 4 (2007): 1136–44. http://dx.doi.org/10.1128/aem.01061-07.

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ABSTRACT Lactococcus lactis subsp. lactis biovar diacetylactis CRL264 is a natural strain isolated from cheese (F. Sesma, D. Gardiol, A. P. de Ruiz Holgado, and D. de Mendoza, Appl. Environ. Microbiol. 56:2099-2103, 1990). The effect of citrate on the growth parameters at a very acidic pH value was studied with this strain and with derivatives whose citrate uptake capacity was genetically manipulated. The culture pH was maintained at 4.5 to prevent alkalinization of the medium, a well-known effect of citrate metabolism. In the presence of citrate, the maximum specific growth rate and the speci
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27

Martin, Mauricio G., Christian Magni, Diego de Mendoza, and Paloma López. "CitI, a Transcription Factor Involved in Regulation of Citrate Metabolism in Lactic Acid Bacteria." Journal of Bacteriology 187, no. 15 (2005): 5146–55. http://dx.doi.org/10.1128/jb.187.15.5146-5155.2005.

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ABSTRACT A large variety of lactic acid bacteria (LAB) can utilize citrate under fermentative conditions. Although much information concerning the metabolic pathways leading to citrate utilization by LAB has been gathered, the mechanisms regulating these pathways are obscure. In Weissella paramesenteroides (formerly called Leuconostoc paramesenteroides), transcription of the citMDEFCGRP citrate operon and the upstream divergent gene citI is induced by the presence of citrate in the medium. Although genetic experiments have suggested that CitI is a transcriptional activator whose activity can b
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28

Patil, Shivaputra A., June A. Mayor, and Ronald S. Kaplan. "Citrate transporter inhibitors: possible new anticancer agents." Future Medicinal Chemistry 14, no. 9 (2022): 665–79. http://dx.doi.org/10.4155/fmc-2021-0341.

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The culmination of 80+ years of cancer research implicates the aberrant metabolism in tumor cells as a root cause of pathogenesis. Citrate is an essential molecule in intermediary metabolism, and its amplified availability to critical pathways in cancer cells via citrate transporters confers a high rate of cancer cell growth and proliferation. Inhibiting the plasma membrane and mitochondrial citrate transporters – whether individually, in combination, or partnered with complementary metabolic targets – in order to combat cancer may prove to be a consequential chemotherapeutic strategy. This re
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29

Strijbis, Karin, and Ben Distel. "Intracellular Acetyl Unit Transport in Fungal Carbon Metabolism." Eukaryotic Cell 9, no. 12 (2010): 1809–15. http://dx.doi.org/10.1128/ec.00172-10.

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ABSTRACT Acetyl coenzyme A (acetyl-CoA) is a central metabolite in carbon and energy metabolism. Because of its amphiphilic nature and bulkiness, acetyl-CoA cannot readily traverse biological membranes. In fungi, two systems for acetyl unit transport have been identified: a shuttle dependent on the carrier carnitine and a (peroxisomal) citrate synthase-dependent pathway. In the carnitine-dependent pathway, carnitine acetyltransferases exchange the CoA group of acetyl-CoA for carnitine, thereby forming acetyl-carnitine, which can be transported between subcellular compartments. Citrate synthase
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30

Isken, F., T. Schulz, M. Möhlig, A. Pfeiffer, and M. Ristow. "Chemical Inhibition of Citrate Metabolism Alters Glucose Metabolism in Mice." Hormone and Metabolic Research 38, no. 8 (2006): 543–45. http://dx.doi.org/10.1055/s-2006-949528.

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31

Cabral, María E., María C. Abeijón Mukdsi, Roxana B. Medina de Figueroa, and Silvia N. González. "Citrate metabolism by Enterococcus faecium and Enterococcus durans isolated from goat’s and ewe’s milk: influence of glucose and lactose." Canadian Journal of Microbiology 53, no. 5 (2007): 607–15. http://dx.doi.org/10.1139/w07-011.

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Citrate metabolism by Enterococcus faecium ET C9 and Enterococcus durans Ov 421 was studied as sole energy source and in presence of glucose or lactose. Both strains utilized citrate as the sole energy source. Enterococcus faecium ET C9 showed diauxic growth in the presence of a limiting concentration of glucose. Neither strain used citrate until glucose was fully metabolized. The strains showed co-metabolism of citrate and lactose. Lactate, acetate, formate, and flavour compounds (diacetyl, acetoin, and 2,3-butanediol) were detected in both strains. The highest production of flavour compounds
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32

Leandro, João G. B., Jair M. Espindola-Netto, Maria Carolina F. Vianna, et al. "Exogenous citrate impairs glucose tolerance and promotes visceral adipose tissue inflammation in mice." British Journal of Nutrition 115, no. 6 (2016): 967–73. http://dx.doi.org/10.1017/s0007114516000027.

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AbstractOverweight and obesity have become epidemic worldwide and are linked to sedentary lifestyle and the consumption of processed foods and drinks. Citrate is a metabolite that plays central roles in carbohydrate and lipid metabolism. In addition, citrate is the additive most commonly used by the food industry, and therefore is highly consumed. Extracellular citrate can freely enter the cells via the constitutively expressed plasma membrane citrate transporter. Within the cytosol, citrate is readily metabolised by ATP-citrate lyase into acetyl-CoA – the metabolic precursor of endogenously p
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33

Vezzoli, Giuseppe, Giulia Magni, Monica Avino, and Teresa Arcidiacono. "Ruolo del citrato nel metabolismo osseo." Giornale di Clinica Nefrologica e Dialisi 32, no. 1 (2020): 15–20. http://dx.doi.org/10.33393/gcnd.2020.991.

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Citrate is an organic compound involved in tricarboxylic acid cycle, regulation of acid-base balance, lipid metabolism and bone formation. The 90% of body citrate is deposited in bone tissue and is released with calcium ions during bone resorption; therefore, bone resorption contributes to maintain normal plasma levels of citrate together with kidney excretion. The parallel release of citrate and calcium from bones decreases the possibility of calcium-phosphate precipitation in soft tissues, as citrate can bind calcium ions in organic fluids. Citrate may also take part to the bone formation as
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34

Bandell, M., M. E. Lhotte, C. Marty-Teysset, et al. "Mechanism of the Citrate Transporters in Carbohydrate and Citrate Cometabolism in Lactococcus andLeuconostoc Species." Applied and Environmental Microbiology 64, no. 5 (1998): 1594–600. http://dx.doi.org/10.1128/aem.64.5.1594-1600.1998.

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ABSTRACT Citrate metabolism in the lactic acid bacterium Leuconostoc mesenteroides generates an electrochemical proton gradient across the membrane by a secondary mechanism (C. Marty-Teysset, C. Posthuma, J. S. Lolkema, P. Schmitt, C. Divies, and W. N. Konings, J. Bacteriol. 178:2178–2185, 1996). Reports on the energetics of citrate metabolism in the related organism Lactococcus lactis are contradictory, and this study was performed to clarify this issue. Cloning of the membrane potential-generating citrate transporter (CitP) of Leuconostoc mesenteroides revealed an amino acid sequence that is
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35

Chen, Feifei, Qingmin Zhao, Ziqiong Yang, et al. "Citrate serves as a signal molecule to modulate carbon metabolism and iron homeostasis in Staphylococcus aureus." PLOS Pathogens 20, no. 7 (2024): e1012425. http://dx.doi.org/10.1371/journal.ppat.1012425.

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Pathogenic bacteria’s metabolic adaptation for survival and proliferation within hosts is a crucial aspect of bacterial pathogenesis. Here, we demonstrate that citrate, the first intermediate of the tricarboxylic acid (TCA) cycle, plays a key role as a regulator of gene expression in Staphylococcus aureus. We show that citrate activates the transcriptional regulator CcpE and thus modulates the expression of numerous genes involved in key cellular pathways such as central carbon metabolism, iron uptake and the synthesis and export of virulence factors. Citrate can also suppress the transcriptio
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36

Wiegand, Anna, Gioia Fischer, Harald Seeger, et al. "Impact of potassium citrate on urinary risk profile, glucose and lipid metabolism of kidney stone formers in Switzerland." Clinical Kidney Journal 13, no. 6 (2019): 1037–48. http://dx.doi.org/10.1093/ckj/sfz098.

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Abstract Background Hypocitraturia and hypercalciuria are the most prevalent risk factors in kidney stone formers (KSFs). Citrate supplementation has been introduced for metaphylaxis in KSFs. However, beyond its effects on urinary parameters and stone recurrence, only a few studies have investigated the impact of citrate on other metabolic pathways such as glucose or lipid metabolism. Methods We performed an observational study using data from the Swiss Kidney Stone Cohort. Patients were subdivided into two groups based on treatment with potassium citrate or not. The outcomes were changes of u
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Susilaningsih, Dwi, Asahedi Umoro, Fredrick Onyango Ochieng, et al. "ISOLASI GEN SITRAT SINTASE BAKTERI Pseudomonas aerugenosa PS2 DARI RIZOSFER POHON KRUING (Dipterocarpus sp.) UNTUK MODEL KONSTRUKSI METABOLISME SEL MIKROALGA BERKARBOHIDRAT RENDAH." BERITA BIOLOGI 18, no. 2 (2019): 247–53. http://dx.doi.org/10.14203/beritabiologi.v18i2.2967.

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Pseudomonas has the potential ability for production of citrate synthase synthesis. Pseudomonas aeruginosa could synthesize the enzyme of citrate synthase which is most likely compatible with microalgae cell. Pseudomonas aerugenosa can be found in the rhizosphere of Kruing (Dipterocarpus sp., Dipterocarpaceae). This bacteria is commonly used in agriculture purposes because it is able to synthesize organic acid such as citric acid. These organic acids are synthesized from a reaction between oxaloacetate and acetyl CoA, catalyzed by citrate synthase (CS) in the tricarboxylic acid cycle (TCA). Rh
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38

Kennes, C., H. C. Dubourguler, G. Albagnac, and E. J. Nyns. "Citrate metabolism byLactobacillus plantarumisolated from orange juice." Journal of Applied Bacteriology 70, no. 5 (1991): 380–84. http://dx.doi.org/10.1111/j.1365-2672.1991.tb02952.x.

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39

Igamberdiev, Abir U. "Citrate valve integrates mitochondria into photosynthetic metabolism." Mitochondrion 52 (May 2020): 218–30. http://dx.doi.org/10.1016/j.mito.2020.04.003.

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40

Mycielska, Maria E., Ameet Patel, Nahit Rizaner, et al. "Citrate transport and metabolism in mammalian cells." BioEssays 31, no. 1 (2009): 10–20. http://dx.doi.org/10.1002/bies.080137.

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41

Pashchenko, A. G., I. I. Kovalchuk, and R. S. Fedoruk. "Mineral composition of the organism tissues and honeycombs of melliferous bees under the conditions of feeding them soybean flour and citrates of Cobalt and Nickel." Scientific Messenger of LNU of Veterinary Medicine and Biotechnology 21, no. 93 (2019): 60–64. http://dx.doi.org/10.32718/nvlvet9311.

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The inadequacy of mineral nutrition leads to inhibition of physiological and metabolic reactions in the body of honeybees. It is known that Cobalt chloride is used to activate oviposition of the queen bee. It was established that Cobalt and Nickel citrate, obtained by the method of nanotechnology, corrects the mineral metabolism and affects the metabolism of bees. It is known that Cobalt plays an important role in the work of enzymes; synthesis of vitamin B12, promotes assimilation of vitamins A, E, C; increases protein metabolism, participates in hematopoiesis. Nickel also has a pronounced ef
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42

Huang, Qingyu, Jie Zhang, Lianzhong Luo, et al. "Metabolomics reveals disturbed metabolic pathways in human lung epithelial cells exposed to airborne fine particulate matter." Toxicology Research 4, no. 4 (2015): 939–47. http://dx.doi.org/10.1039/c5tx00003c.

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43

DEBORDE, CATHERINE, DOMINIQUE B. ROLIN, ARNAUD BONDON, JACQUES D. DE CERTAINES, and PATRICK BOYAVAL. "In vivo nuclear magnetic resonance study of citrate metabolism in Propionibacterium freudenreichii subsp. shermanii." Journal of Dairy Research 65, no. 3 (1998): 503–14. http://dx.doi.org/10.1017/s0022029998002878.

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Citrate metabolism by resting cells of Propionibacterium freudenreichii subsp. shermanii was investigated. In vivo13C nuclear magnetic resonance spectroscopy was used to study the pathway of citrate breakdown and to probe its utilization, non-invasively, in living cell suspensions. [2,4-13C]citrate was metabolized by resting cells to glutamate labelled in positions 2 and 4. In the presence of lactate or pyruvate, its rate of consumption was faster, but it was still converted to glutamate. No catabolic pathway other than the first third of a turn of the tricarboxylic acid cycle was used by Prop
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Parkinson, E. Kenneth, Jerzy Adamski, Grit Zahn, et al. "Extracellular citrate and metabolic adaptations of cancer cells." Cancer and Metastasis Reviews 40, no. 4 (2021): 1073–91. http://dx.doi.org/10.1007/s10555-021-10007-1.

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Abstract It is well established that cancer cells acquire energy via the Warburg effect and oxidative phosphorylation. Citrate is considered to play a crucial role in cancer metabolism by virtue of its production in the reverse Krebs cycle from glutamine. Here, we review the evidence that extracellular citrate is one of the key metabolites of the metabolic pathways present in cancer cells. We review the different mechanisms by which pathways involved in keeping redox balance respond to the need of intracellular citrate synthesis under different extracellular metabolic conditions. In this conte
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Li, Longlong, Mengling Peng, Chongyang Ge, Lei Yu, and Haitian Ma. "(-)-Hydroxycitric Acid Reduced Lipid Droplets Accumulation Via Decreasing Acetyl-Coa Supply and Accelerating Energy Metabolism in Cultured Primary Chicken Hepatocytes." Cellular Physiology and Biochemistry 43, no. 2 (2017): 812–31. http://dx.doi.org/10.1159/000481564.

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Background/Aims: (-)-Hydroxycitric acid (HCA) had been shown to suppress fat accumulation in animals and humans, while the underlying biochemical mechanism is not fully understood, especially little information is available on whether (-)-HCA regulates energy metabolism and consequently affects fat deposition. Methods: Hepatocytes were cultured for 24 h and then exposed to (-)-HCA (0, 1, 10, 50 µM), enzyme protein content was determined by ELISA; lipid metabolism gene mRNA levels were detected by RT-PCR. Results: (-)-HCA significantly decreased the number and total area of lipid droplets. ATP-
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Bond, Daniel R., Tünde Mester, Camilla L. Nesbø, Andrea V. Izquierdo-Lopez, Frank L. Collart, and Derek R. Lovley. "Characterization of Citrate Synthase from Geobacter sulfurreducens and Evidence for a Family of Citrate Synthases Similar to Those of Eukaryotes throughout the Geobacteraceae." Applied and Environmental Microbiology 71, no. 7 (2005): 3858–65. http://dx.doi.org/10.1128/aem.71.7.3858-3865.2005.

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ABSTRACT Members of the family Geobacteraceae are commonly the predominant Fe(III)-reducing microorganisms in sedimentary environments, as well as on the surface of energy-harvesting electrodes, and are able to effectively couple the oxidation of acetate to the reduction of external electron acceptors. Citrate synthase activity of these organisms is of interest due to its key role in acetate metabolism. Prior sequencing of the genome of Geobacter sulfurreducens revealed a putative citrate synthase sequence related to the citrate synthases of eukaryotes. All citrate synthase activity in G. sulf
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Iacobazzi, Vito, and Vittoria Infantino. "Citrate – new functions for an old metabolite." Biological Chemistry 395, no. 4 (2014): 387–99. http://dx.doi.org/10.1515/hsz-2013-0271.

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Abstract Citrate is an important substrate in cellular energy metabolism. It is produced in the mitochondria and used in the Krebs cycle or released into cytoplasm through a specific mitochondrial carrier, CIC. In the cytosol, citrate and its derivatives, acetyl-CoA and oxaloacetate, are used in normal and pathological processes. Beyond the classical role as metabolic regulator, recent studies have highlighted that citrate is involved in inflammation, cancer, insulin secretion, histone acetylation, neurological disorders, and non-alcoholic fatty liver disease. Monitoring changes in the citrate
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Icard, Philippe, Antoine Coquerel, Zherui Wu, et al. "Understanding the Central Role of Citrate in the Metabolism of Cancer Cells and Tumors: An Update." International Journal of Molecular Sciences 22, no. 12 (2021): 6587. http://dx.doi.org/10.3390/ijms22126587.

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Citrate plays a central role in cancer cells’ metabolism and regulation. Derived from mitochondrial synthesis and/or carboxylation of α-ketoglutarate, it is cleaved by ATP-citrate lyase into acetyl-CoA and oxaloacetate. The rapid turnover of these molecules in proliferative cancer cells maintains a low-level of citrate, precluding its retro-inhibition on glycolytic enzymes. In cancer cells relying on glycolysis, this regulation helps sustain the Warburg effect. In those relying on an oxidative metabolism, fatty acid β-oxidation sustains a high production of citrate, which is still rapidly conv
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Miglionico, Rocchina, Ilenia Matera, Giovanna Maria Ventola, et al. "Gene Expression Reprogramming by Citrate Supplementation Reduces HepG2 Cell Migration and Invasion." International Journal of Molecular Sciences 25, no. 12 (2024): 6509. http://dx.doi.org/10.3390/ijms25126509.

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Citrate, which is obtained from oxaloacetate and acetyl-CoA by citrate synthase in mitochondria, plays a key role in both normal and cancer cell metabolism. In this work, we investigated the effect of 10 mM extracellular citrate supplementation on HepG2 cells. Gene expression reprogramming was evaluated by whole transcriptome analysis using gene set enrichment analysis (GSEA). The transcriptomic data were validated through analyzing changes in the mRNA levels of selected genes by qRT-PCR. Citrate-treated cells exhibited the statistically significant dysregulation of 3551 genes; 851 genes were
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Karp, Heini J., Maarit E. Ketola, and Christel J. E. Lamberg-Allardt. "Acute effects of calcium carbonate, calcium citrate and potassium citrate on markers of calcium and bone metabolism in young women." British Journal of Nutrition 102, no. 9 (2009): 1341–47. http://dx.doi.org/10.1017/s0007114509990195.

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Both K and Ca supplementation may have beneficial effects on bone through separate mechanisms. K in the form of citrate or bicarbonate affects bone by neutralising the acid load caused by a high protein intake or a low intake of alkalising foods, i.e. fruits and vegetables. Ca is known to decrease serum parathyroid hormone (S-PTH) concentration and bone resorption. We compared the effects of calcium carbonate, calcium citrate and potassium citrate on markers of Ca and bone metabolism in young women. Twelve healthy women aged 22–30 years were randomised into four controlled 24 h study sessions,
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