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Journal articles on the topic 'ATP-competitive'

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Published: 1 April 2023

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1

Lebakken, Connie S., Laurie J. Reichling, Jason M. Ellefson, and Steven M. Riddle. "Detection of Allosteric Kinase Inhibitors by Displacement of Active Site Probes." Journal of Biomolecular Screening 17, no. 6 (2012): 813–21. http://dx.doi.org/10.1177/1087057112439889.

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Non–adenosine triphosphate (ATP) competitive, allosteric inhibitors provide a promising avenue to develop highly selective small-molecule kinase inhibitors. Although this class of compounds is growing, detection of such inhibitors can be challenging as standard kinase activity assays preferentially detect compounds that bind to active kinases in an ATP competitive manner. We have previously described a time-resolved fluorescence resonance energy transfer (TR-FRET)–based kinase binding assay using the competitive displacement of ATP competitive active site fluorescent probes (“tracers”). Althou

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2

Agius, Michael P., Kristin Ko, Taylor K. Johnson, Sameer Phadke, and Matthew B. Soellner. "Conformation-tunable ATP-competitive kinase inhibitors." Chemical Communications 58, no. 21 (2022): 3541–44. http://dx.doi.org/10.1039/d1cc06893h.

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3

Garuti, L., M. Roberti, and G. Bottegoni. "Non-ATP Competitive Protein Kinase Inhibitors." Current Medicinal Chemistry 17, no. 25 (2010): 2804–21. http://dx.doi.org/10.2174/092986710791859333.

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4

Lee, Byung-Il, Hyung-Jun Ahn, Ki-Cheol Han, Dae-Ro Ahn, and Dong-Yun Shin. "Pyrogallin, an ATP-Competitive Inhibitor of JAK3." Bulletin of the Korean Chemical Society 32, no. 3 (2011): 1077–79. http://dx.doi.org/10.5012/bkcs.2011.32.3.1077.

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5

Schenone, S., C. Brullo, F. Musumeci, M. Radi, and M. Botta. "ATP-Competitive Inhibitors of mTOR: An Update." Current Medicinal Chemistry 18, no. 20 (2011): 2995–3014. http://dx.doi.org/10.2174/092986711796391651.

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6

Lazaro, Glorianne, Eleftherios Kostaras, and Igor Vivanco. "Inhibitors in AKTion: ATP-competitive vs allosteric." Biochemical Society Transactions 48, no. 3 (2020): 933–43. http://dx.doi.org/10.1042/bst20190777.

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Aberrant activation of the PI3K pathway is one of the commonest oncogenic events in human cancer. AKT is a key mediator of PI3K oncogenic function, and thus has been intensely pursued as a therapeutic target. Multiple AKT inhibitors, broadly classified as either ATP-competitive or allosteric, are currently in various stages of clinical development. Herein, we review the evidence for AKT dependence in human tumours and focus on its therapeutic targeting by the two drug classes. We highlight the future prospects for the development and implementation of more effective context-specific AKT inhibi

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7

Parrish, Cynthia A., Nicholas D. Adams, Kurt R. Auger, et al. "Novel ATP-Competitive Kinesin Spindle Protein Inhibitors." Journal of Medicinal Chemistry 50, no. 20 (2007): 4939–52. http://dx.doi.org/10.1021/jm070435y.

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8

Ito, Masahiro, Misa Iwatani, Yusuke Kamada, et al. "Discovery of selective ATP-competitive eIF4A3 inhibitors." Bioorganic & Medicinal Chemistry 25, no. 7 (2017): 2200–2209. http://dx.doi.org/10.1016/j.bmc.2017.02.035.

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9

Zarębska, Ewa A., Krzysztof Kusy, Ewa M. Słomińska, Łukasz Kruszyna, and Jacek Zieliński. "Plasma Nucleotide Dynamics during Exercise and Recovery in Highly Trained Athletes and Recreationally Active Individuals." BioMed Research International 2018 (October 9, 2018): 1–11. http://dx.doi.org/10.1155/2018/4081802.

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Circulating plasma ATP is able to regulate local skeletal muscle blood flow and 02 delivery causing considerable vasodilatation during exercise. We hypothesized that sport specialization and specific long-term training stimuli have an impact on venous plasma [ATP] and other nucleotides concentration. Four athletic groups consisting of sprinters (n=11; age range 21–30 yr), endurance-trained athletes (n=16; age range 18–31 yr), futsal players (n=14; age range 18–30 yr), and recreationally active individuals (n=12; age range 22–33 yr) were studied. Venous blood samples were collected at rest, dur

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10

Lyle, S., D. H. Geller, K. Ng, J. Stanczak, J. Westley, and N. B. Schwartz. "Kinetic mechanism of adenosine 5′-phosphosulphate kinase from rat chondrosarcoma." Biochemical Journal 301, no. 2 (1994): 355–59. http://dx.doi.org/10.1042/bj3010355.

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Biosynthesis of the activated sulphate donor adenosine 3′-phosphate 5′-phosphosulphate (PAPS) involves the sequential action of two enzyme activities. ATP-sulphurylase catalyses the formation of APS (adenosine 5′-phosphosulphate) from ATP and free sulphate, and APS is then phosphorylated by APS kinase to produce PAPS. Initial-velocity patterns for rat chondrosarcoma APS kinase indicate a single-displacement formal mechanism with KmAPS 76 nM and KmATP = 24 microM. Inhibition studies using analogues of substrates and products were carried out to determine the reaction mechanism. An analogue of P

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11

Takahashi, Hideyuki, and Hideo Namiki. "Mechanism of membrane redistribution of protein kinase C by its ATP-competitive inhibitors." Biochemical Journal 405, no. 2 (2007): 331–40. http://dx.doi.org/10.1042/bj20070299.

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ATP-competitive inhibitors of PKC (protein kinase C) such as the bisindolylmaleimide GF 109203X, which interact with the ATP-binding site in the PKC molecule, have also been shown to affect several redistribution events of PKC. However, the reason why these inhibitors affect the redistribution is still controversial. In the present study, using immunoblot analysis and GFP (green fluorescent protein)-tagged PKC, we showed that, at commonly used concentrations, these ATP-competitive inhibitors alone induced redistribution of DAG (diacylglycerol)-sensitive PKCα, PKCβII, PKCδ and PKCϵ, but not aty

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12

Quartieri, Francesca, Marcella Nesi, Nilla R. Avanzi, et al. "Identification of unprecedented ATP-competitive choline kinase inhibitors." Bioorganic & Medicinal Chemistry Letters 51 (November 2021): 128310. http://dx.doi.org/10.1016/j.bmcl.2021.128310.

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13

Tang, Colin P., Owen Clark, John R. Ferrarone, et al. "GCN2 kinase activation by ATP-competitive kinase inhibitors." Nature Chemical Biology 18, no. 2 (2021): 207–15. http://dx.doi.org/10.1038/s41589-021-00947-8.

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14

Freeman-Cook, Kevin D., Christopher Autry, Gary Borzillo, et al. "Design of Selective, ATP-Competitive Inhibitors of Akt." Journal of Medicinal Chemistry 53, no. 12 (2010): 4615–22. http://dx.doi.org/10.1021/jm1003842.

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15

Tunnicliff, G., and T. L. Youngs. "Competitive Inhibition of Mouse Brain -Aminobutyrate Aminotransferase by ATP." Experimental Biology and Medicine 192, no. 1 (1989): 11–15. http://dx.doi.org/10.3181/00379727-192-42947.

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16

Papa, F. R. "Bypassing a Kinase Activity with an ATP-Competitive Drug." Science 302, no. 5650 (2003): 1533–37. http://dx.doi.org/10.1126/science.1090031.

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17

Huck, Bayard R., and Igor Mochalkin. "Recent progress towards clinically relevant ATP-competitive Akt inhibitors." Bioorganic & Medicinal Chemistry Letters 27, no. 13 (2017): 2838–48. http://dx.doi.org/10.1016/j.bmcl.2017.04.090.

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18

Quintás-Cardama, A. "Experimental non-ATP-competitive therapies for chronic myelogenous leukemia." Leukemia 22, no. 5 (2008): 932–40. http://dx.doi.org/10.1038/leu.2008.47.

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19

Barf, Tjeerd, Allard Kaptein, Sander de Wilde, et al. "Structure-based lead identification of ATP-competitive MK2 inhibitors." Bioorganic & Medicinal Chemistry Letters 21, no. 12 (2011): 3818–22. http://dx.doi.org/10.1016/j.bmcl.2011.04.018.

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20

Zhang, Dingwa, Deyong He, Xiaoliang Pan, and Lijun Liu. "Systematic profiling of ATP response to acquired drug-resistant EGFR family kinase mutations." Journal of the Serbian Chemical Society 85, no. 10 (2020): 1265–78. http://dx.doi.org/10.2298/jsc191124028z.

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Kinase-targeted cancer therapy (KTCT) with ATP-competitive inhibitors has been widely applied in clinics. However, a number of kinase missense mutations were observed to confer acquired drug resistance during therapy, largely limiting the clinical application of kinase inhibitors in KTCT. Instead of directly influencing inhibitor binding, kinase mutations can also cause generic resistance to ATP-competitive inhibitors by increasing ATP affinity. Herein, the intermolecular interaction of the ATP molecule with clinically observed drug-resistant EGFR family kinase mutations involved in human canc

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21

Pinzi, Luca. "On the development of B-Raf inhibitors acting through innovative mechanisms." F1000Research 11 (April 26, 2022): 237. http://dx.doi.org/10.12688/f1000research.108761.2.

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B-Raf is a protein kinase participating to the regulation of many biological processes in cells. Several studies have demonstrated that this protein is frequently upregulated in human cancers, especially when it bears activating mutations. In the last years, few ATP-competitive inhibitors of B-Raf have been marketed for the treatment of melanoma and are currently under clinical evaluation on a variety of other types of cancer. Although the introduction of drugs targeting B-Raf has provided significant advances in cancer treatment, responses to ATP-competitive inhibitors remain limited, mainly

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22

Pinzi, Luca. "On the development of B-Raf inhibitors acting through innovative mechanisms." F1000Research 11 (April 26, 2022): 237. http://dx.doi.org/10.12688/f1000research.108761.2.

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B-Raf is a protein kinase participating to the regulation of many biological processes in cells. Several studies have demonstrated that this protein is frequently upregulated in human cancers, especially when it bears activating mutations. In the last years, few ATP-competitive inhibitors of B-Raf have been marketed for the treatment of melanoma and are currently under clinical evaluation on a variety of other types of cancer. Although the introduction of drugs targeting B-Raf has provided significant advances in cancer treatment, responses to ATP-competitive inhibitors remain limited, mainly

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23

Pinzi, Luca. "On the development of B-Raf inhibitors acting through innovative mechanisms." F1000Research 11 (February 25, 2022): 237. http://dx.doi.org/10.12688/f1000research.108761.1.

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B-Raf is a protein kinase participating to the regulation of many biological processes in cells. Recent studies have demonstrated that this protein is frequently overactivated in human cancers, especially when it bears activating mutations. In recent years, few ATP-competitive inhibitors of B-Raf have been marketed for the treatment of melanoma and are currently under clinical evaluation on a variety of other types of cancer. Although the introduction of drugs targeting B-Raf has provided significant advances in cancer treatment, responses to such ATP-competitive inhibitors remain limited, mai

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24

Wilson, Brice A. P., Muhammad S. Alam, Tad Guszczynski, et al. "Discovery and Characterization of a Biologically Active Non–ATP-Competitive p38 MAP Kinase Inhibitor." Journal of Biomolecular Screening 21, no. 3 (2015): 277–89. http://dx.doi.org/10.1177/1087057115615518.

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Mitogen-activated protein kinase (MAPK) p38 is part of a broad and ubiquitously expressed family of MAPKs whose activity is responsible for mediating an intracellular response to extracellular stimuli through a phosphorylation cascade. p38 is central to this signaling node and is activated by upstream kinases while being responsible for activating downstream kinases and transcription factors via phosphorylation. Dysregulated p38 activity is associated with numerous autoimmune disorders and has been implicated in the progression of several types of cancer. A number of p38 inhibitors have been t

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25

Khandekar, Sanjay S., Bingbing Feng, Tracey Yi, Susan Chen, Nicholas Laping, and Neal Bramson. "A Liquid Chromatography/Mass Spectrometry-Based Method for the Selection of ATP Competitive Kinase Inhibitors." Journal of Biomolecular Screening 10, no. 5 (2005): 447–55. http://dx.doi.org/10.1177/1087057105274846.

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The currently approved kinase inhibitors for therapeutic uses and a number of kinase inhibitors that are undergoing clinical trials are directed toward the adenosine triphosphate (ATP) binding site of protein kinases. The 5β-fluorosulfonylbenzoyl 5'-adenosine (FSBA) is an ATP-affinity reagent that covalently modifies a conserved lysine present in the nucleotide-binding site of most kinases. The authors have developed a liquid chromatography/mass spectrometry-basedmethod tomonitor binding ofATP competitive protein kinase inhibitors using FSBAas a nonselective activity-based probe for protein ki

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26

Chung, Vincent, Ling Wang, Margaret S. Fletcher, et al. "First-time in-human study of VMD-928, an allosteric and irreversible TrkA selective inhibitor, in patients with solid tumors or lymphoma." Journal of Clinical Oncology 37, no. 15_suppl (2019): TPS3146. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.tps3146.

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TPS3146 Background: Tropomysin receptor kinase A (TrkA) is a protein encoded by the NTRK1 gene. NTRK fusions involving the kinase domain are oncogenic for multiple tumor types and larotrectinib was recently approved for advanced solid tumors harboring NTRK gene fusions. Larotrectinib, an ATP-competitive, reversible pan-TrkA/B/C inhibitor, has shown impressive response rates in patients harboring these fusions; however, resistance can develop due to acquired ATP-site mutations. This has been previously identified in other oncogenic driver kinases such as ALK and EGFR treated with ATP-competitiv

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27

Schenone, S., C. Brullo, and M. Botta. "Small Molecules ATP-Competitive Inhibitors of FLT3: A Chemical Overview." Current Medicinal Chemistry 15, no. 29 (2008): 3113–32. http://dx.doi.org/10.2174/092986708786848613.

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28

Ma, Bin, Doug Marcotte, Murugan Paramasivam, et al. "ATP-Competitive MLKL Binders Have No Functional Impact on Necroptosis." PLOS ONE 11, no. 11 (2016): e0165983. http://dx.doi.org/10.1371/journal.pone.0165983.

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29

Karni, Rotem, Sarit Mizrachi, Ella Reiss-Sklan, Aviv Gazit, Oded Livnah, and Alexander Levitzki. "The pp60c-Src inhibitor PP1 is non-competitive against ATP." FEBS Letters 537, no. 1-3 (2003): 47–52. http://dx.doi.org/10.1016/s0014-5793(03)00069-3.

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30

Shen, Guobing, Miaoqing Liu, Jianjun Lu, and Tao Meng. "Practical synthesis of Vistusertib (AZD2014), an ATP competitive mTOR inhibitor." Tetrahedron Letters 60, no. 52 (2019): 151333. http://dx.doi.org/10.1016/j.tetlet.2019.151333.

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31

Wu, Ke, Jingzhi Pang, Dong Song, et al. "Selectivity Mechanism of ATP-Competitive Inhibitors for PKB and PKA." Chemical Biology & Drug Design 86, no. 1 (2014): 9–18. http://dx.doi.org/10.1111/cbdd.12472.

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32

Freeman-Cook, Kevin D., Christopher Autry, Gary Borzillo, et al. "Corrections to Design of Selective, ATP-Competitive Inhibitors of Akt." Journal of Medicinal Chemistry 53, no. 15 (2010): 5895. http://dx.doi.org/10.1021/jm100769x.

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33

Garc�a-Echeverr�a, Carlos, Peter Traxler, and Dean B. Evans. "ATP site-directed competitive and irreversible inhibitors of protein kinases." Medicinal Research Reviews 20, no. 1 (2000): 28–57. http://dx.doi.org/10.1002/(sici)1098-1128(200001)20:1<28::aid-med2>3.0.co;2-2.

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34

Wang, Ruixiu, and James E. Thompson. "Detection of ATP Competitive Protein Kinase Inhibition by Western Blotting." Analytical Biochemistry 299, no. 1 (2001): 110–12. http://dx.doi.org/10.1006/abio.2001.5410.

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35

Kirkland, Lindsay O., and Campbell McInnes. "Non-ATP competitive protein kinase inhibitors as anti-tumor therapeutics." Biochemical Pharmacology 77, no. 10 (2009): 1561–71. http://dx.doi.org/10.1016/j.bcp.2008.12.022.

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36

Rosborough, Brian, Dàlia Raïch-Regué, Benjamin Matta та ін. "Rapamycin-resistant mTORC1 restrains dendritic cell B7-H1 expression that requires IL-1β to enhance regulatory T cell induction (P1349)". Journal of Immunology 190, № 1_Supplement (2013): 63.27. http://dx.doi.org/10.4049/jimmunol.190.supp.63.27.

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Abstract Introduction: The mammalian Target of Rapamycin (mTOR) is a central regulator of dendritic cell (DC) function that performs the catalytic activity of mTOR complex (mTORC)1 and 2. mTORC2 functions independently from mTORC1 and is resistant to inhibition by rapamycin (RAPA); however, mTORC1 has both RAPA-sensitive and -resistant outputs. Our goal was to ascertain the role of RAPA-resistant mTOR in DC. Methods: WT C57BL/6 or B7-H1-/- bone marrow-derived DC were generated with the addition of RAPA or ATP-competitive mTOR inhibitor, which blocks all mTOR signaling. DC lacking rictor, an mT

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37

Roulin, Didier, Nicolas Demartines, and Olivier Dormond. "ATP-competitive inhibitors of mTOR: new perspectives in the treatment of renal cell carcinoma." Biochemical Society Transactions 39, no. 2 (2011): 492–94. http://dx.doi.org/10.1042/bst0390492.

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Targeting mTOR (mammalian target of rapamycin) is an effective approach in the treatment of advanced RCC (renal cell carcinoma). Rapamycin-like drugs (rapalogues) have shown clinical activities and have been approved for the treatment of RCC. Recently, with the development of ATP-competitive inhibitors of mTOR, therapies targeting mTOR have entered a new era. Here, we discuss the biological relevance of blocking mTOR in RCC and review the mechanisms of action of rapalogues in RCC. We also advance some perspectives on the use of ATP-competitive inhibitors of mTOR in RCC.

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38

Li, Chunqiong, Xuewen Zhang, Na Zhang, et al. "Identification and Biological Evaluation of CK2 Allosteric Fragments through Structure-Based Virtual Screening." Molecules 25, no. 1 (2020): 237. http://dx.doi.org/10.3390/molecules25010237.

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Casein kinase II (CK2) is considered as an attractive cancer therapeutic target, and recent efforts have been made to develop its ATP-competitive inhibitors. However, achieving selectivity with respect to related kinases remains challenging due to the highly conserved ATP-binding pocket of kinases. Allosteric inhibitors, by targeting the much more diversified allosteric site relative to the highly conserved ATP-binding pocket, might be a promising strategy with the enhanced selectivity and reduced toxicity than ATP-competitive inhibitors. The previous studies have highlighted the traditional s

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39

O’Connor, Suzanne, Yann-Vaï Le Bihan, Isaac M. Westwood, et al. "Discovery and Characterization of a Cryptic Secondary Binding Site in the Molecular Chaperone HSP70." Molecules 27, no. 3 (2022): 817. http://dx.doi.org/10.3390/molecules27030817.

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Heat Shock Protein 70s (HSP70s) are key molecular chaperones that are overexpressed in many cancers and often associated with metastasis and poor prognosis. It has proven difficult to develop ATP-competitive, drug-like small molecule inhibitors of HSP70s due to the flexible and hydrophilic nature of the HSP70 ATP-binding site and its high affinity for endogenous nucleotides. The aim of this study was to explore the potential for the inhibition of HSP70 through alternative binding sites using fragment-based approaches. A surface plasmon resonance (SPR) fragment screen designed to detect seconda

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40

Xu, Jimin, Jing Ai, Sheng Liu, et al. "Design and synthesis of 3,3′-biscoumarin-based c-Met inhibitors." Org. Biomol. Chem. 12, no. 22 (2014): 3721–34. http://dx.doi.org/10.1039/c4ob00364k.

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41

Napoleon, John V., Sarbjit Singh, Sandeep Rana, et al. "Small molecule binding to inhibitor of nuclear factor kappa-B kinase subunit beta in an ATP non-competitive manner." Chemical Communications 57, no. 38 (2021): 4678–81. http://dx.doi.org/10.1039/d1cc01245b.

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42

Shapiro, Adam B., Helen Plant, Jarrod Walsh, et al. "Discovery of ATP-Competitive Inhibitors of tRNAIle Lysidine Synthetase (TilS) by High-Throughput Screening." Journal of Biomolecular Screening 19, no. 8 (2014): 1137–46. http://dx.doi.org/10.1177/1087057114534981.

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A novel, ultrahigh-throughput, fluorescence anisotropy–based assay was developed and used to screen a 1.4-million-sample library for compounds that compete with adenosine triphosphate (ATP) for binding to Escherichia coli tRNAIle lysidine synthetase (TilS), an essential, conserved, ATP-dependent, tRNA-modifying enzyme of bacterial pathogens. TilS modifies a cytidine base in the anticodon loop of Ile2 tRNA by attaching lysine, thereby altering codon recognition of the CAU anticodon from AUG (methionine) to AUA (isoleucine). A scintillation proximity assay for the incorporation of lysine into Il

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43

Katari, Naresh Kumar, Rambabu Gundla, Phani Kumar Reddy, et al. "Molecular Docking Studies of Glabrene and Human Epidermal Growth Factor Receptor Kinase." INNOSC Theranostics and Pharmacological Sciences 4, no. 1 (2022): 38–49. http://dx.doi.org/10.36922/itps.v4i1.56.

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Background: Human epidermal growth factor receptor 2 (Her2) gene located in human chromosome17, encodes Her2 tyrosine kinase protein, and is overexpressed in breast cancer cells. Her2 is activated on phosphorylation of tyrosine by adenosine triphosphate (ATP). Nonetheless, Her2 excessively partakes in the development and prognosis of specific types of aggressive breast cancers. Therefore, Her2 inhibition therapy is primary target for the treatment of aggressive breast cancer. At present, lapatinib is one of the Food and Drug Administration approved Her2 inhibitors used in cancer therapy. In mo

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44

Cuthbertson, Peter, Amal Elhage, Dena Al-Rifai, et al. "6-Furopyridine Hexamethylene Amiloride Is a Non-Selective P2X7 Receptor Antagonist." Biomolecules 12, no. 9 (2022): 1309. http://dx.doi.org/10.3390/biom12091309.

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P2X7 is an extracellular adenosine 5′-triphopshate (ATP)-gated cation channel present on leukocytes, where its activation induces pro-inflammatory cytokine release and ectodomain shedding of cell surface molecules. Human P2X7 can be partially inhibited by amiloride and its derivatives at micromolar concentrations. This study aimed to screen a library of compounds derived from amiloride or its derivative 5-(N,N-hexamethylene) amiloride (HMA) to identify a potential P2X7 antagonist. 6-Furopyridine HMA (6-FPHMA) was identified as a novel P2X7 antagonist and was characterized further. 6-FPHMA impa

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45

McArdell, J. E. C., C. J. Bruton, and T. Atkinson. "The isolation of a peptide from the catalytic domain of Bacillus stearothermophilus tryptophyl-tRNA synthetase. The interaction of Brown MX-5BR with tyrosyl-tRNA synthetase." Biochemical Journal 243, no. 3 (1987): 701–7. http://dx.doi.org/10.1042/bj2430701.

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Tryptophyl-tRNA synthetase is irreversibly inactivated by Procion Brown MX-5BR with an apparent dissociation constant (KD) of 8.8 microM and maximum rate of inactivation k3 0.192 s-1. The specificity of the interaction is supported by two previously reported observations. Firstly, Brown MX-5BR inactivation of tryptophyl-tRNA synthetase is inhibited by substrates, and secondly, the animated derivative of Brown MX-5BR is a competitive inhibitor of tryptophyl-tRNA synthetase with a Ki of 2 X 10(-4) M with respect to both tryptophan and ATP. Tryptic digestion of the dye-affinity-labelled enzyme an

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46

Park, Seojeong, Soo-Yeon Hwang, Jaeho Shin, Hyunji Jo, Younghwa Na, and Youngjoo Kwon. "A chromenone analog as an ATP-competitive, DNA non-intercalative topoisomerase II catalytic inhibitor with preferences toward the alpha isoform." Chemical Communications 55, no. 85 (2019): 12857–60. http://dx.doi.org/10.1039/c9cc05524j.

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47

Deans, N. L., R. D. Allison, and D. L. Purich. "Steady-state kinetic mechanism of bovine brain tubulin: tyrosine ligase." Biochemical Journal 286, no. 1 (1992): 243–51. http://dx.doi.org/10.1042/bj2860243.

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The ATP-dependent resynthesis of tubulin from tyrosine and untyrosinated tubulin was examined to establish the most probable steady-state kinetic mechanism of the tubulin: tyrosine ligase (ADP-forming). Three pair-wise sets of initial rate experiments, involving variation of two substrates pair-wise with the third substrate held at a high (but non-saturating) level, yielded convergent-line data, a behaviour that is diagnostic for sequential mechanisms. Michaelis constants were 14 microM, 1.9 microM and 17 microM for ATP, untyrosinated tubulin and L-tyrosine respectively, and the maximal veloci

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48

Cozza, Giorgio, Andrea Bortolato, Ernesto Menta, Ennio Cavalletti, Silvano Spinelli, and Stefano Moro. "ATP Non-Competitive Ser/Thr Kinase Inhibitors as Potential Anticancer Agents." Anti-Cancer Agents in Medicinal Chemistry 9, no. 7 (2009): 778–86. http://dx.doi.org/10.2174/187152009789056930.

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49

Pitman, Melissa R., Jason A. Powell, Carl Coolen, et al. "A selective ATP-competitive sphingosine kinase inhibitor demonstrates anti-cancer properties." Oncotarget 6, no. 9 (2015): 7065–83. http://dx.doi.org/10.18632/oncotarget.3178.

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50

Hornakova, T., L. Springuel, J. Devreux, et al. "Oncogenic JAK1 and JAK2-activating mutations resistant to ATP-competitive inhibitors." Haematologica 96, no. 6 (2011): 845–53. http://dx.doi.org/10.3324/haematol.2010.036350.

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