| Name | cIAP1 |
|---|---|
| Synonyms | API 1; API1; Apoptosis inhibitor 1; BIRC 2; BIRC2; Baculoviral IAP repeat containing protein 2; C IAP1; HIAP 2… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 18485876 | Wang L, Du F, Wang X: TNF-alpha induces two distinct caspase-8 activation pathways. Cell. 2008 May 16;133(4):693-703. Cycloheximide promotes caspase-8 activation by eliminating endogenous caspase-8 inhibitor, c-FLIP, while Smac mimetic does so by triggering autodegradation of cIAP1 and cIAP2 (cIAP1/2), leading to the release of receptor interacting protein kinase (RIPK1) from the activated TNF receptor complex to form a caspase-8-activating complex consisting of RIPK1, FADD, and caspase-8. |
32(0,1,1,2) | 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. Hypotheses have been proposed to explain this molecularly, including the up-regulation of host anti-apoptotic proteins such as cellular Inhibitor of Apoptosis Protein (IAP) 2 and the Bcl-2 protein 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). |
2(0,0,0,2) | Details |
| 15856013 | Yuan H, Fu F, Zhuo J, Wang W, Nishitani J, An DS, Chen IS, Liu X: Human papillomavirus type 16 E6 and E7 oncoproteins upregulate c-IAP2 gene expression and confer resistance to apoptosis. Oncogene. 2005 Jul 28;24(32):5069-78. Here, we report that the transcription of the inhibitor of apoptosis gene, cellular inhibitor of apoptosis protein 2, (c-IAP2), is significantly upregulated in HPV16 E6/E7-immortalized human oral keratinocytes (HOK16E6E7). Overexpression of c-IAP2 in normal human oral keratinocyte conferred resistance to tumor necrosis factor-alpha (TNF-alpha)/cycloheximide (CHX)-induced apoptosis, suggesting the increased c-IAP2 expression in HOK16E6E7 may protect the cells from TNF-alpha-mediated cell death. |
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 |
| 16082387 | de Leseleuc L, Denis F: Inhibition of apoptosis by Nur77 through NF-kappaB activity modulation. . Cell Death Differ. 2006 Feb;13(2):293-300. Nur77 overexpression leads to NF-kappaB-dependent induction of the antiapoptotic gene cIAP1. |
1(0,0,0,1) | Details |
| 16876795 | Kato T, Kutsuna H, Oshitani N, Kitagawa S: delays neutrophil apoptosis via stabilization of Mcl-1. . FEBS Lett. 2006 Aug 21;580(19):4582-6. Epub 2006 Jul 21. Spontaneous neutrophil apoptosis and Mcl-1 degradation were prevented by (cAMP) agonists (dibutyryl cAMP and (1)), and the effects of cAMP agonists on neutrophils were highly resistant to cycloheximide, a protein synthesis inhibitor, although slight increase in Mcl-1 mRNA expression was induced by cAMP agonists. |
0(0,0,0,0) | 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. |
0(0,0,0,0) | Details |