Protein Information

Name XIAP
Synonyms API 3; API3; Apoptosis inhibitor 3; BIRC 4; BIRC4; Baculoviral IAP repeat containing protein 4; HILP; IAP Like protein…

Compound Information

Name cycloheximide
CAS

Reference List

PubMed Abstract RScore(About this table)
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-Leu-Leu-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 taurochenodeoxycholate (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