| Name | cytochrome c |
|---|---|
| Synonyms | CYC; CYCS; Cytochrome C; HCS; Cytochrome Cs |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16786197 | Li Z, Zong H, Kong X, Zhang S, Wang H, Sun Q, Gu J: Cell surface beta 1, 4-galactosyltransferase 1 promotes apoptosis by inhibiting epidermal growth factor receptor pathway. Mol Cell Biochem. 2006 Oct;291(1-2):69-76. Epub 2006 Jun 20. Our previous studies have shown that overexpression of beta1,4-galactosyltransferase1 (beta1,4GT1) leads to increased apoptosis induced by cycloheximide (CHX) in SMMC-7721 human hepatocarcinoma cells. As a result, the release of cytochrome c from mitochondria to cytosol was increased and caspase-3 was activated. |
1(0,0,0,1) | Details |
| 19372210 | Li TW, Zhang Q, Oh P, Xia M, Chen H, Bemanian S, Lastra N, Circ M, Moyer MP, Mato JM, Aw TY, Lu SC: and inhibit cellular FLICE inhibitory protein expression and induce apoptosis in colon cancer cells. Mol Pharmacol. 2009 Jul;76(1):192-200. Epub 2009 Apr 16. This required de novo RNA synthesis and was associated with activation of procaspase-8, Bid cleavage, and release of cytochrome c from the mitochondria. |
1(0,0,0,1) | Details |
| 20080135 | Acrani GO, Gomes R, Proenca-Modena JL, da Silva AF, Carminati PO, Silva ML, Santos RI, Arruda E: Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression. Virus Res. 2010 Apr;149(1):56-63. Epub 2010 Jan 18. Mitochondrial release of cytochrome C and activation of caspases 9 and 3 were also detected by western blot analysis. Results obtained in cells treated with chloroquine and cycloheximide indicated that viral uncoating and replication are required for apoptosis induction by OROV. |
1(0,0,0,1) | Details |
| 18331646 | Feng P, Li T, Guan Z, Franklin RB, Costello LC: The involvement of Bax in zinc-induced mitochondrial apoptogenesis in malignant prostate cells. Mol Cancer. 2008 Mar 10;7:25. The accumulation of cellular zinc has a direct effect on the mitochondria that results in the release of cytochrome c, which initiates the caspase cascade that leads to apoptosis. |
1(0,0,0,1) | Details |
| 16763728 | Shibayama-Imazu T, Sonoda I, Sakairi S, Aiuchi T, Ann WW, Nakajo S, Itabe H, Nakaya K: Production of and dissipation of mitochondrial transmembrane potential by trigger apoptosis in human ovarian cancer TYK-nu cells. Apoptosis. 2006 Sep;11(9):1535-43. Furthermore, both the production of and the induction of apoptosis by (2) were inhibited almost completely by cycloheximide, an inhibitor of protein synthesis, suggesting that the synthesis of enzymes for the production of might be required for these processes. Since reacts with radicals, such as within the hydrophobic environment of the mitochondrial membrane, we postulate that (2)-induced oxidative stress in mitochondria might damage mitochondrial membranes, with subsequent release of cytochrome c, the activation of procaspase 3 and, eventually, apoptosis. |
1(0,0,0,1) | Details |
| 16966373 | Gyrd-Hansen M, Farkas T, Fehrenbacher N, Bastholm L, Hoyer-Hansen M, Elling F, Wallach D, Flavell R, Kroemer G, Nylandsted J, Jaattela M: Apoptosome-independent activation of the lysosomal cell death pathway by caspase-9. Mol Cell Biol. 2006 Nov;26(21):7880-91. Epub 2006 Sep 11. The apoptosome, a heptameric complex of Apaf-1, cytochrome c, and caspase-9, has been considered indispensable for the activation of caspase-9 during apoptosis. |
1(0,0,0,1) | Details |
| 17194804 | Lee SY, Cherla RP, Tesh VL: Simultaneous induction of apoptotic and survival signaling pathways in macrophage-like THP-1 cells by Shiga toxin 1. Infect Immun. 2007 Mar;75(3):1291-302. Epub 2006 Dec 28. Finally, the protein synthesis inhibitors Stx1 and anisomycin triggered limited apoptosis and prolonged JNK and p38 MAPK activation, while macrophage-like cells treated with cycloheximide remained viable and showed transient activation of MAPKs. Despite the partial resistance of macrophage-like THP-1 cells to Stx1-mediated killing, treatment of these cells with Stx1 activated a broad array of caspases, disrupted the mitochondrial membrane potential (DeltaPsi (m)), and released cytochrome c into the cytoplasm. |
1(0,0,0,1) | Details |
| 16151639 | Brecht K, Simonen M, Heim J: Upregulation of alpha globin promotes apoptotic cell death in the hematopoietic cell line FL5.12. Apoptosis. 2005 Oct;10(5):1043-62. Caspase-8, -9 and -3 as well as the proapoptotic factor Bax and cytochrome c were activated. |
1(0,0,0,1) | Details |
| 19952118 | Ballot C, Kluza J, Martoriati A, Nyman U, Formstecher P, Joseph B, Bailly C, Marchetti P: Essential role of mitochondria in apoptosis of cancer cells induced by the marine alkaloid Lamellarin D. Mol Cancer Ther. 2009 Dec;8(12):3307-17. Epub . However, lamellarin D killed efficiently mutated p53 or p53 null cancer cells, and sensitivity to lamellarin D was abrogated neither by cycloheximide nor in enucleated cells. Lamellarin D-induced cytochrome c release occurs independently of nuclear factors in a cell-free system. |
1(0,0,0,1) | Details |
| 19777442 | Pucci B, Indelicato M, Paradisi V, Reali V, Pellegrini L, Aventaggiato M, Karpinich NO, Fini M, Russo MA, Farber JL, Tafani M: ERK-1 MAP kinase prevents TNF-induced apoptosis through bad phosphorylation and inhibition of Bax translocation in HeLa Cells. J Cell Biochem. 2009 Dec 1;108(5):1166-74. By contrast, HeLa wt and K71R clones released cytochrome c. |
1(0,0,0,1) | Details |
| 17363499 | Ding WX, Ni HM, Chen X, Yu J, Zhang L, Yin XM: A coordinated action of Bax, PUMA, and p53 promotes MG132-induced mitochondria activation and apoptosis in colon cancer cells. Mol Cancer Ther. 2007 Mar;6(3):1062-9. Consistently, inhibition of translation by cycloheximide could also effectively abolish the accumulation of p53 and PUMA and suppress MG132-induced Bax activation and apoptosis. Genetic deletion of either p53 or PUMA led to a marked suppression of apoptosis induced by these inhibitors, accompanied with reduced Bax activation and cytochrome c release. |
1(0,0,0,1) | Details |
| 16675490 | Chang AY, Chan JY, Chou JL, Li FC, Dai KY, Chan SH: Heat shock protein 60 in rostral ventrolateral medulla reduces cardiovascular fatality during endotoxaemia in the rat. J Physiol. 2006 Jul 15;574(Pt 2):547-64. Epub 2006 May 4. Pretreatment with a microinjection of actinomycin D or cycloheximide into bilateral RVLM significantly blunted this HSP60 increase, whereas real-time PCR showed progressive augmentation of hsp60 mRNA. We conclude that HSP60 redistributed from mitochondrion to cytosol in the RVLM confers neuroprotection against fatal cardiovascular depression during endotoxaemia via reduced activation of the cytochrome c-caspase-3 cascade of apoptotic signalling through enhanced interactions with mitochondrial or cytosolic Bax or Bcl-2. |
1(0,0,0,1) | Details |
| 16215688 | Singh S, Khar A: Differential gene expression during apoptosis induced by a serum factor: role of mitochondrial F0-F1 ATP synthase complex. Apoptosis. 2005 Dec;10(6):1469-82. However, cytochrome C release during apoptosis was found to be completely independent of intracellular ATP content. |
1(0,0,0,1) | Details |
| 18056701 | Fei Q, McCormack AL, Di Monte DA, Ethell DW: Paraquat neurotoxicity is mediated by a Bak-dependent mechanism. . J Biol Chem. 2008 Feb 8;283(6):3357-64. Epub 2007 Dec 4. PQ induced morphological and biochemical features that were consistent with apoptosis, including dose-dependent cytochrome c release, with subsequent caspase-3 and poly (ADP- polymerase cleavage. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. |
1(0,0,0,1) | Details |
| 16546987 | Tang R, Faussat AM, Majdak P, Marzac C, Dubrulle S, Marjanovic Z, Legrand O, Marie JP: Semisynthetic homoharringtonine induces apoptosis via inhibition of protein synthesis and triggers rapid myeloid cell leukemia-1 down-regulation in myeloid leukemia cells. Mol Cancer Ther. 2006 Mar;5(3):723-31. The decrease of mitochondrial membrane potential and the release of cytochrome c were observed in the apoptotic cells induced by ssHHT. The Mcl-1 turnover was only induced by ssHHT and cycloheximide, but not by daunorubicin and cytosine arabinoside, and could be restored by proteasome inhibitors. |
1(0,0,0,1) | Details |
| 15685448 | Tahara E Jr, Tahara H, Kanno M, Naka K, Takeda Y, Matsuzaki T, Yamazaki R, Ishihara H, Yasui W, Barrett JC, Ide T, Tahara E: G1P3, an interferon inducible gene 6-16, is expressed in gastric cancers and inhibits mitochondrial-mediated apoptosis in gastric cancer cell line TMK-1 cell. Cancer Immunol Immunother. 2005 Aug;54(8):729-40. Epub 2005 Feb 1. One of exceptional gastric cancer cell line, TMK-1, which do not express detectable 6-16, is sensitive to apoptosis induced by cycloheximide (CHX), 5-fluorouracil (5-FU) and serum-deprivation. This anti-apoptotic function is expressed through inhibition of the depolarization of mitochondrial membrane potential and release of cytochrome c. |
1(0,0,0,1) | Details |
| 15629159 | Li Z, Wang H, Zong H, Sun Q, Kong X, Jiang J, Gu J: Downregulation of beta1,4-galactosyltransferase 1 inhibits CDK11 (p58)-mediated apoptosis induced by cycloheximide. Biochem Biophys Res Commun. 2005 Feb 11;327(2):628-36. Knock down of beta1,4-GT 1 also inhibited the release of cytochrome c from mitochondria and caspase-3 processing. |
1(0,0,0,1) | Details |
| 16158421 | Jin HO, Park IC, An S, Lee HC, Woo SH, Hong YJ, Lee SJ, Park MJ, Yoo DH, Rhee CH, Hong SI: Up-regulation of Bak and Bim via JNK downstream pathway in the response to in human glioblastoma cells. J Cell Physiol. 2006 Feb;206(2):477-86. In addition, de novo protein synthesis was required for the initiation of apoptosis in that the protein synthesis inhibitor, cycloheximide (CHX), inhibited NO-induced apoptotic cell death as well as up-regulation of Bak and Bim. |
0(0,0,0,0) | Details |
| 17532486 | Lin HY, Shen SC, Lin CW, Yang LY, Chen YC: Baicalein inhibition of peroxide-induced apoptosis via ROS-dependent heme oxygenase 1 gene expression. Biochim Biophys Acta. 2007 Jul;1773(7):1073-86. Epub 2007 Apr 22. In the present study, baicalein (BE) but not its glycoside, baicalin (BI), induced heme oxygenase-1 (HO-1) gene expression at both the mRNA and protein levels, and the BE-induced HO-1 protein was blocked by adding cycloheximide (CHX) or actinomycin D (Act D). |
0(0,0,0,0) | Details |
| 17804721 | Endo H, Murata K, Mukai M, Ishikawa O, Inoue M: Activation of insulin-like growth factor signaling induces apoptotic cell death under prolonged hypoxia by enhancing endoplasmic reticulum stress response. Cancer Res. 2007 Sep 1;67(17):8095-103. IGF-induced cell death under hypoxic conditions was prevented by treatment with cycloheximide, suggesting that de novo protein synthesis is required. |
0(0,0,0,0) | Details |
| 17879164 | Shaltouki A, Freer M, Mei Y, Weyman CM: Increased expression of the pro-apoptotic Bcl2 family member PUMA is required for mitochondrial release of cytochrome C and the apoptosis associated with skeletal myoblast differentiation. Apoptosis. 2007 Dec;12(12):2143-54. Inclusion of cycloheximide inhibits the release of cytochrome C, the activation of caspase 9 and apoptosis. |
84(1,1,1,4) | Details |
| 17535899 | Fu NY, Sukumaran SK, Yu VC: Inhibition of ubiquitin-mediated degradation of MOAP-1 by apoptotic stimuli promotes Bax function in mitochondria. Proc Natl Acad Sci U S A. 2007 Jun 12;104(24):10051-6. Epub 2007 May 29. Mitochondria depleted of short-lived proteins by cycloheximide (CHX) become resistant to Bax-mediated cytochrome c release. |
83(1,1,1,3) | Details |
| 17245642 | Chen SP, Wu JL, Su YC, Hong JR: Anti-Bcl-2 family members, zfBcl-x (L) and zfMcl-1a, prevent cytochrome c release from cells undergoing betanodavirus-induced secondary necrotic cell death. Apoptosis. 2007 Jun;12(6):1043-60. To identify the mediator (s) of this necrotic process, a protein synthesis inhibitor (cycloheximide; CHX; 0.33 microg/ml) was used to block cytochrome c release as well as PS exposure and mitochondrial membrane permeability transition pore (MMP) loss. |
34(0,1,1,4) | Details |
| 18546202 | Pucci B, Bertani F, Karpinich NO, Indelicato M, Russo MA, Farber JL, Tafani M: Detailing the role of Bax translocation, cytochrome c release, and perinuclear clustering of the mitochondria in the killing of HeLa cells by TNF. J Cell Physiol. 2008 Nov;217(2):442-9. Induction of cell death in HeLa cells with TNF and cycloheximide (CHX) required an adequate ATP supply and was accompanied by decrease in intracellular pH, translocation of Bax, perinuclear clustering of the mitochondria, and cytochrome c release. |
8(0,0,1,3) | Details |
| 15670574 | Kadohara K, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Acetoxycycloheximide (E-73) rapidly induces apoptosis mediated by the release of cytochrome c via activation of c-Jun N-terminal kinase. Biochem Pharmacol. 2005 Feb 15;69(4):551-60. Epub 2004 Dec 28. Cycloheximide (CHX) is an inhibitor of protein synthesis and commonly used to modulate death receptor-mediated apoptosis or to induce apoptosis in a number of normal and transformed cells. |
5(0,0,0,5) | Details |
| 19112105 | Kadohara K, Nagumo M, Asami S, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Caspase-8 mediates mitochondrial release of pro-apoptotic proteins in a manner independent of its proteolytic activity in apoptosis induced by the protein synthesis inhibitor acetoxycycloheximide in human leukemia Jurkat cells. J Biol Chem. 2009 Feb 27;284(9):5478-87. Epub 2008 Dec 26. The protein synthesis inhibitor acetoxycycloheximide (Ac-CHX) has been previously shown to induce rapid apoptosis mediated by the release of cytochrome c in human leukemia Jurkat cells. |
2(0,0,0,2) | Details |
| 16109713 | Rahmani M, Davis EM, Bauer C, Dent P, Grant S: Apoptosis induced by the kinase inhibitor BAY 43-9006 in human leukemia cells involves down-regulation of Mcl-1 through inhibition of translation. J Biol Chem. 2005 Oct 21;280(42):35217-27. Epub 2005 Aug 18. Here we report that treatment with BAY 43-9006 results in marked cytochrome c and AIF release into the cytosol, caspase-9, -8, -7, and -3 activation, and apoptosis in human leukemia cells (U937, Jurkat, and K562). Inhibition of protein synthesis by cycloheximide or proteasome function with MG132 and pulse-chase studies with [35S] demonstrated that BAY 43-9006 did not diminish Mcl-1 protein stability, nor did it enhance Mcl-1 ubiquitination, but instead markedly attenuated Mcl-1 translation in association with the rapid and potent dephosphorylation of the eIF4E translation initiation factor. |
2(0,0,0,2) | Details |
| 20123115 | Pushpanjali P, Ramaiah KV: PKC activation contributes to caspase-mediated eIF2alpha phosphorylation and cell death. Biochim Biophys Acta. 2010 May;1800(5):518-525. Epub 2010 Feb 1. Status of eIF2alpha phosphorylation and cytochrome c levels are analyzed by western blots. However, PMA enhances late stages of UV-irradiation or cycloheximide-induced caspase activation, eIF2alpha phosphorylation and apoptosis in Sf9 cells. |
2(0,0,0,2) | Details |
| 16579440 | Smutok OV, Os'mak GS, Gaida GZ, Gonchar MV: [Screening of yeasts producing stable L-lactate cytochrome c oxidoreductase and regulation of enzyme synthesis]. Mikrobiologiia. 2006 Jan-Feb;75(1):29-34. L-Lactate induces de novo synthesis of FC b2, as proved by the use of cycloheximide, an inhibitor of protein synthesis. |
2(0,0,0,2) | Details |
| 15528219 | Kaur M, Agarwal C, Singh RP, Guan X, Dwivedi C, Agarwal R: Skin cancer chemopreventive agent, {alpha}-santalol, induces apoptotic death of human epidermoid carcinoma A431 cells via caspase activation together with dissipation of mitochondrial membrane potential and cytochrome c release. Carcinogenesis. 2005 Feb;26(2):369-80. Epub 2004 Nov 4. Pre-treatment of cells with caspase-8 or -9 inhibitor, pan caspase inhibitor or cycloheximide totally blocked alpha-santalol-caused caspase-3 activity and cleavage, but only partially reversed apoptotic cell death. |
2(0,0,0,2) | Details |
| 17324936 | Saeki M, Irie Y, Ni L, Itsuki Y, Terao Y, Kawabata S, Kamisaki Y: Calcineurin potentiates the activation of procaspase-3 by accelerating its proteolytic maturation. J Biol Chem. 2007 Apr 20;282(16):11786-94. Epub 2007 Feb 26. Overexpression of calcineurin B in HEK293 cells potentiated processing of caspase-3 and apoptosis triggered by tumor necrosis factor-alpha and cycloheximide treatment. In a cell-free system, overexpression of calcineurin B in HEK293 cells markedly increased processing of caspase-3 by cytochrome c. |
2(0,0,0,2) | Details |
| 17311906 | Yang C, Kaushal V, Shah SV, Kaushal GP: Mcl-1 is downregulated in cisplatin-induced apoptosis, and proteasome inhibitors restore Mcl-1 and promote survival in renal tubular epithelial cells. Am J Physiol Renal Physiol. 2007 Jun;292(6):F1710-7. Epub 2007 Feb 20. Cisplatin-induced loss of Mcl-1 occurs at the same time as the mitochondrial release of cytochrome c, activation of caspase-3, and initiation of apoptosis. Treatment of cells with cycloheximide, a protein synthesis inhibitor, revealed rapid turnover of Mcl-1. |
2(0,0,0,2) | Details |
| 16432762 | Xia Y, Novak R, Lewis J, Duckett CS, Phillips AC: Xaf1 can cooperate with TNFalpha in the induction of apoptosis, independently of interaction with XIAP. Mol Cell Biochem. 2006 Jun;286(1-2):67-76. Epub 2006 Jan 24. Xaf1 expression promotes cytochrome c release that cannot be blocked by inhibition of caspase activity. |
2(0,0,0,2) | Details |
| 20017956 | Cho SH, Chung KS, Choi JH, Kim DH, Lee KT: Compound K, a metabolite of ginseng saponin, induces apoptosis via caspase-8-dependent pathway in HL-60 human leukemia cells. BMC Cancer. 2009 Dec 18;9:449. Interestingly, the activation of caspase-3 and -8 and DNA fragmentation were significantly prevented in the presence of cycloheximide, suggesting that Compound K-induced apoptosis is dependent on de novo protein synthesis. In addition, compound-K induced a series of intracellular events associated with both the mitochondrial- and death receptor-dependent apoptotic pathways, namely, (1) the activation of caspases-3, -8, and -9; (2) the loss of mitochondrial membrane potential; (3) the release of cytochrome c and Smac/DIABLO to the cytosol; (4) the translocation of Bid and Bax to mitochondria; and (5) the downregulations of Bcl-2 and Bcl-xL. |
2(0,0,0,2) | Details |
| 19151744 | Liu HY, Wang ZM, Bai Y, Wang M, Li Y, Wei S, Zhou QH, Chen J: Different BAG-1 isoforms have distinct functions in modulating chemotherapeutic-induced apoptosis in breast cancer cells. Acta Pharmacol Sin. 2009 Feb;30(2):235-41. Epub 2009 Jan 19. In the detection of the expression of K-ras, Hsp70, cytochrome c, Raf-1, ER-alpha, and Bcl-2 in MCF-7 cells by Western blot, only Bcl-2 protein expression was significantly increased in MCF-7 cells transfected with BAG-1 p50 and p46, respectively. The mechanism by which BAG-1 affected the function of Bcl-2 was exploredby using the cycloheximide chase assay. |
1(0,0,0,1) | Details |
| 18078929 | Brumatti G, Yon M, Castro FA, Bueno-da-Silva AE, Jacysyn JF, Brunner T, Amarante-Mendes GP: Conversion of CD95 (Fas) Type II into Type I signaling by sub-lethal doses of cycloheximide. Exp Cell Res. 2008 Feb 1;314(3):554-63. Epub 2007 Nov 17. The other is related to the cleavage of Bid by low concentration of caspase-8, leading to the release of cytochrome c from mitochondria and the activation of caspase-3 by the cytochrome c/APAF-1/caspase-9 apoptosome (Type II cells). |
1(0,0,0,1) | Details |
| 15876423 | Chow JM, Shen SC, Huan SK, Lin HY, Chen YC: but not rutin and quercitrin, prevention of H2O2-induced apoptosis via anti-oxidant activity and heme oxygenase 1 gene expression in macrophages. Biochem Pharmacol. 2005 Jun 15;69(12):1839-51. Results of Western blotting show that QE but not its glycoside rutin (RUT) and quicitrin-induced HO-1 protein expression in a time- and dose-dependent manner, and HO-1 protein induced by QE was blocked by an addition of cycloheximide or actinomycin D. Additionally, QE protects cells from H (2) O (2)-induced a decrease in the mitochondrial membrane potential and a release of cytochrome c from mitochondria to cytosol by DiOC6 and Western blotting assay, respectively. |
1(0,0,0,1) | Details |
| 17700538 | Deniaud A, Sharaf el dein O, Maillier E, Poncet D, Kroemer G, Lemaire C, Brenner C: Endoplasmic reticulum stress induces -dependent permeability transition, mitochondrial outer membrane permeabilization and apoptosis. Oncogene. 2008 Jan 10;27(3):285-99. Epub 2007 Aug 13. Sustained Ca2+ accumulation in the mitochondrial matrix induced by ER stress triggered signs of proapoptotic mitochondrial alteration, namely permeability transition, dissipation of the electrochemical potential, matrix swelling, relocalization of Bax to mitochondria and the release of cytochrome c and apoptosis-inducing factor from mitochondria. The specificity of this apoptosis pathway was validated in cells using a panel of pharmacological agents that chelate Ca2+ (BAPTA-AM) or inhibit receptor (IP (3) R; 2-aminoethoxydiphenyl borate), voltage-dependent anion channel (VDAC) (4,4'-diisothiocyanatostilbene-2,2'-disulfonate, the permeability transition pore (cyclosporin A and bongkrekic acid), caspases (z-VAD-fmk) and protein synthesis (cycloheximide). |
1(0,0,0,1) | Details |
| 16091589 | Yui S, Saeki T, Kanamoto R, Iwami K: Characteristics of apoptosis in HCT116 colon cancer cells induced by J Biochem. 2005 Aug;138(2):151-7. Our results indicate that hydrophobic bile acids induce apoptosis in HCT116 cells by releasing cytochrome c from mitochondria via an undefined but specific mechanism, and that UDCA protects HCT116 cells by acting downstream of cytochrome c release. Pretreatment with cycloheximide failed to inhibit apoptosis, suggesting that protein synthesis is not involved in the apoptotic response. |
1(0,0,0,1) | Details |
| 18339020 | Long F, Wang Y, Qi HH, Zhou X, Jin XQ: Rapid non-genomic effects of glucocorticoids on oxidative stress in a guinea pig model of asthma. Respirology. 2008 Mar;13(2):227-32. These rapid effects were not blocked by the GC receptor antagonist RU486 and/or the protein synthesis inhibitor cycloheximide. production was measured by cytochrome c reduction assay. |
1(0,0,0,1) | Details |