Name | XIAP |
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Synonyms | API 3; API3; Apoptosis inhibitor 3; BIRC 4; BIRC4; Baculoviral IAP repeat containing protein 4; HILP; IAP Like protein… |
Name | cycloheximide |
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CAS |
PubMed | Abstract | RScore(About this table) | |
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18647593 | Ozaki Y, Kato T, Kitagawa M, Fujita H, Kitagawa S: Calpain inhibition delays neutrophil apoptosis via cyclic AMP-independent activation of protein kinase A and protein kinase A-mediated stabilization of Mcl-1 and X-linked inhibitor of apoptosis (XIAP). Arch Biochem Biophys. 2008 Sep 15;477(2):227-31. Epub 2008 Jul 11. Calpain inhibitors (PD150606 and N-acetyl- - -Nle-CHO) prevented spontaneous neutrophil apoptosis and degradation of Mcl-1 and XIAP, and the effects of calpain inhibitors on neutrophils were resistant to cycloheximide. |
35(0,1,1,5) | Details |
17435549 | Turner DJ, Alaish SM, Zou T, Rao JN, Wang JY, Strauch ED: Bile salts induce resistance to apoptosis through NF-kappaB-mediated XIAP expression. Ann Surg. 2007 Mar;245(3):415-25. Exposure of normal intestinal epithelial cells (IEC-6) to the conjugated bile salts taurodeoxycholate (TDCA) and (TCDCA) resulted in an increase in resistance to tumor necrosis factor (TNF)-alpha and cycloheximide (CHX)-induced apoptosis, and NF-kappaB activation. |
7(0,0,0,7) | Details |
15578516 | Marienfeld C, Yamagiwa Y, Ueno Y, Chiasson V, Brooks L, Meng F, Patel T: Translational regulation of XIAP expression and cell survival during hypoxia in human cholangiocarcinoma. Gastroenterology. 2004 Dec;127(6):1787-97. Translational processes were deregulated by cycloheximide or rapamycin or by targeted deletion of eukaryotic initiation factor (eIF)-4E, a rate-limiting translational initiation factor using small interfering RNA (siRNA). |
5(0,0,0,5) | 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. |
3(0,0,0,3) | Details |
18069034 | Ying S, Christian JG, Paschen SA, Hacker G: Chlamydia trachomatis can protect host cells against apoptosis in the absence of cellular Inhibitor of Apoptosis Proteins and Mcl-1. Microbes Infect. 2008 Jan;10(1):97-101. Epub 2007 Oct 18. To test for the importance of these proteins, we used mouse embryonic fibroblasts from gene-targeted mice that were deficient in cIAP1, cIAP2, cIAP1/cIAP2, XIAP, or Mcl-1. Infection with Chlamydia trachomatis protected all cells equally well against apoptosis, which was induced either with tumour necrosis factor/cycloheximide (IAP-knock-out cells) or staurosporine (Mcl-1-knock-out). |
1(0,0,0,1) | Details |
16912191 | Ma Y, Yu WD, Kong RX, Trump DL, Johnson CS: Role of nongenomic activation of phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase/extracellular signal-regulated kinase 1/2 pathways in 1,25D3-mediated apoptosis in squamous cell carcinoma cells. Cancer Res. 2006 Aug 15;66(16):8131-8. These effects were nongenomic: they occurred rapidly and were not inhibited by cycloheximide or actinomycin D. In addition, siRNA-Akt transfection followed by 1,25D3 treatment induced apoptosis much sooner than 1,25D3 alone. siRNA-Akt and 1,25D3 induced caspase-10 activation, suppressed the expression of c-IAP1 and XIAP, and promoted 1,25D3-induced caspase-3 activation. |
1(0,0,0,1) | Details |
17097066 | Lee TJ, Lee JT, Park JW, Kwon TK: Acquired TRAIL resistance in human breast cancer cells are caused by the sustained cFLIP (L) and XIAP protein levels and ERK activation. Biochem Biophys Res Commun. 2006 Dec 29;351(4):1024-30. Epub 2006 Nov 7. The selected TRAIL-resistant cells were cross-resistant to TNF-alpha/cycloheximide but remained sensitive to DNA-damage drugs such as oxaliplatin and etoposide. |
3(0,0,0,3) | 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. The antiapoptotic factors involved in macrophage survival following toxin challenge include inhibitors of apoptosis proteins and X-linked inhibitor of apoptosis protein. 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. |
1(0,0,0,1) | Details |
18439101 | Kato T, Noma H, Kitagawa M, Takahashi T, Oshitani N, Kitagawa S: Distinct role of c-Jun N-terminal kinase isoforms in human neutrophil apoptosis regulated by tumor necrosis factor-alpha and granulocyte-macrophage colony-stimulating factor. J Interferon Cytokine Res. 2008 Apr;28(4):235-43. TNF-alpha-induced JNK phosphorylation was sustained in the presence of cycloheximide, which was accompanied by accelerated neutrophil apoptosis. |
0(0,0,0,0) | Details |
15541727 | McNeish IA, Lopes R, Bell SJ, McKay TR, Fernandez M, Lockley M, Wheatley SP, Lemoine NR: Survivin interacts with Smac/DIABLO in ovarian carcinoma cells but is redundant in Smac-mediated apoptosis. Exp Cell Res. 2005 Jan 1;302(1):69-82. This down-regulation does not result from transcriptional changes, as determined by quantitative real-time PCR, but cycloheximide treatment indicates that survivin half-life is reduced from 6 to 2 h, which is secondary to ubiquitination and proteasomal degradation. |
0(0,0,0,0) | Details |