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    ENOX2 ecto-NOX disulfide-thiol exchanger 2 [ Homo sapiens (human) ]

    Gene ID: 10495, updated on 3-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    ENOX2 inhibition enhances infiltration of effector memory T-cell and mediates response to chemotherapy in immune-quiescent nasopharyngeal carcinoma.

    ENOX2 inhibition enhances infiltration of effector memory T-cell and mediates response to chemotherapy in immune-quiescent nasopharyngeal carcinoma.
    Kam NW, Laczka O, Li X, Wilkinson J, Hung D, Lai SPH, Wu KC, Tsao SW, Dai W, Che CM, Lee VH, Kwong DL., Free PMC Article

    02/2/2024
    ENOX2 NADH Oxidase: A BCR-ABL1-Dependent Cell Surface and Secreted Redox Protein in Chronic Myeloid Leukemia.

    ENOX2 NADH Oxidase: A BCR-ABL1-Dependent Cell Surface and Secreted Redox Protein in Chronic Myeloid Leukemia.
    Baykal-Köse S, Voldoire M, Desterke C, Sorel N, Cayssials E, Johnson-Ansah H, Guerci-Bresler A, Bennaceur-Griscelli A, Chomel JC, Turhan AG., Free PMC Article

    05/30/2023
    The tumor-associated NADH oxidase (tNOX)-mediated modulation of the NAD+ concentration and SIRT1 are involved in oxaliplatin-induced apoptosis.

    Tumor-associated NADH oxidase (tNOX)-NAD+-sirtuin 1 axis contributes to oxaliplatin-induced apoptosis of gastric cancer cells.
    Chen HY, Cheng HL, Lee YH, Yuan TM, Chen SW, Lin YY, Chueh PJ., Free PMC Article

    09/2/2017
    These findings not only shed light on the molecular mechanism of the anticancer properties of capsaicin, but also the transcription regulation of tNOX expression that may potentially explain how POU3F2 is associated with tumorigenesis.

    Capsaicin Inhibited Aggressive Phenotypes through Downregulation of Tumor-Associated NADH Oxidase (tNOX) by POU Domain Transcription Factor POU3F2.
    Chen HY, Lee YH, Chen HY, Yeh CA, Chueh PJ, Lin YM., Free PMC Article

    04/15/2017
    The findings support a role for arNOX as a major source of oxidative damage leading to cross-linking of skin proteins.

    Age-related NADH oxidase (arNOX)-catalyzed oxidative damage to skin proteins.
    Meadows C, Morré DJ, Morré DM, Draelos ZD, Kern D.

    05/16/2015
    The results suggest that phosphorylation of serine-504 by PKCdelta modulates the biological function of tNOX.

    Phosphorylation of serine-504 of tNOX (ENOX2) modulates cell proliferation and migration in cancer cells.
    Zeng ZM, Chuang SM, Chang TC, Hong CW, Chou JC, Yang JJ, Chueh PJ.

    09/15/2012
    this result suggests that hnRNP F directs formation of the exon 4 minus variant of ENOX2.

    hnRNP F directs formation of an exon 4 minus variant of tumor-associated NADH oxidase (ENOX2).
    Tang X, Kane VD, Morré DM, Morré DJ.

    02/25/2012
    increased NADH levels resulting from ENOX2 inhibition result in decreased prosurvival sphingosine-1-phosphate and increased proapoptotic ceramide, both of which may be important to initiation of the ENOX2 inhibitor-induced apoptotic cascade.

    Metabolite modulation of HeLa cell response to ENOX2 inhibitors EGCG and phenoxodiol.
    Wu LY, De Luca T, Watanabe T, Morré DM, Morré DJ.

    09/10/2011
    ENOX2 is a dimeric protein containing 4 coppers/dimer capable of carrying out concerted four electron transfers from NADH or ubiquinol to molecular oxygen as required to form water.

    Essential role of copper in the activity and regular periodicity of a recombinant, tumor-associated, cell surface, growth-related and time-keeping hydroquinone (NADH) oxidase with protein disulfide-thiol interchange activity (ENOX2).
    Tang X, Chueh PJ, Jiang Z, Layman S, Martin B, Kim C, Morré DM, Morré DJ.

    03/12/2011
    arNOX activity correlates with age and reaches a maximum at about age 65 in males and 55 in females.

    arNOX: generator of reactive oxygen species in the skin and sera of aging individuals subject to external modulation.
    Morré DM, Meadows C, Morré DJ.

    08/16/2010
    Enhanced arNOX activity correlates with age and with oxidative changes contributing to skin aging.

    Age-related ENOX protein (arNOX) activity correlated with oxidative skin damage in the elderly.
    Morré DM, Meadows C, Hostetler B, Weston N, Kern D, Draelos Z, Morré DJ.

    01/21/2010
    These results indicate that tNOX is suppressed during apoptosis and demonstrate that tNOX down-regulation sensitizes cells to stress-induced growth reduction, suggesting that tNOX is required for transformed cell growth.

    Stress-induced down-regulation of tumor-associated NADH oxidase during apoptosis in transformed cells.
    Mao LC, Wang HM, Lin YY, Chang TK, Hsin YH, Chueh PJ.

    01/21/2010
    A relationship of tNOX to unregulated growth of cancer cells was provided by data where growth of HeLa cells was inhibited by transfection with the exon 5 antisense oligonucleotides

    Antisense experiments demonstrate an exon 4 minus splice variant mRNA as the basis for expression of tNOX, a cancer-specific cell surface protein.
    Tang X, Morré DJ, Morré DM.

    01/21/2010
    results indicate that shRNA targeting of tNOX inhibits the growth of cervical cancer cells, and reduces cell migration via a decrease in the membrane association of Rac.

    RNA interference targeting tNOX attenuates cell migration via a mechanism that involves membrane association of Rac.
    Liu SC, Yang JJ, Shao KN, Chueh PJ.

    01/21/2010
    tNOX is both necessary and sufficient for the cellular anticancer activities attributed to both EGCg and capsaicin. *tNOX enzyme

    tNOX is both necessary and sufficient as a cellular target for the anticancer actions of capsaicin and the green tea catechin (-)-epigallocatechin-3-gallate.
    Chueh PJ, Wu LY, Morré DM, Morré DJ.

    01/21/2010
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