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1. |
Rickettsia rickettsii-induced expression of cIAP2 in host endothelial cells is likely not a major contributor to protection against staurosporine-induced cell death. |
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2. |
ARIA knockdown significantly increased inhibitor of apoptosis cIAP-1 and cIAP-2 protein expression |
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3. |
cIAP2 may therefore play an important role as a target therapy in colorectal cancer |
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4. |
c-IAP1 can be targeted for degradation by two distinct processes,through degradation of the TRAF2-c-IAP1 heterodimer or through induced autoubiquitination of c-IAP1 by IAP antagonists |
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5. |
haem oxygenase-1 plays a central role in NNK-mediated cell proliferation by promoting the expression of p21(Cip1/Waf1/Cid1), inhibitor of apoptosis protein 2 and B-cell lymphoma-2 but inhibiting the activity of Bad |
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6. |
Methylation and API2/MALT1 fusion in colorectal extranodal marginal zone lymphoma. |
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7. |
TRAF2 interaction is critical for c-IAP2/MALT1-mediated increases in the NF-kappaB activity, increased expression of endogenous NF-kappaB target genes and resistance to apoptosis. |
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8. |
PERK activity inhibits the ER stress-induced apoptotic program through the induction of cellular inhibitor of apoptosis (cIAP1 and cIAP2) proteins |
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9. |
cIAP1, cIAP2, and XIAP act cooperatively via nonredundant pathways to regulate genotoxic stress-induced nuclear factor-kappaB activation. |
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10. |
API2-MALT1 transcript was confirmed to be associated with the levels of apoptosis and API2 of MALT lymphoma. |
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11. |
c-IAP2 is consistently overexpressed in nasopharyngeal carcinoma (NPC) cells; study reports that c-IAP2 plays a major role in the resistance of NPC cells to apoptosis induced by TLR3 stimulation |
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12. |
IL-3 up-regulates the expression of the antiapoptotic proteins cIAP2, Mcl-1, and Bcl-X(L) and induces a rapid and sustained de novo expression of the serine/threonine kinase Pim1 that closely correlates with cytokine-enhanced survival. |
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13. |
The ubiquitin-associated domain is required for XIAP and CIAP2-MALT1 to activate NF-kappaB. |
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14. |
c-IAP1 and c-IAP2 are required for TNFalpha-stimulated RIP1 ubiquitination and NF-kappaB activation. |
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15. |
Observational study of gene-disease association. (HuGE Navigator) |
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16. |
XIAP and HIAP-1 in myelin lesions were co-localized with microglia and T cells in multiple sclerosis |
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17. |
cIAP1 and cIAP2 promote cancer cell survival by functioning as E3 ubiquitin ligases that maintain constitutive ubiquitination of the RIP1 adaptor protein. |
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18. |
Data show that Cartilage oligomeric matrix protein protects cells against death by elevating cIAP2 proteins. |
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19. |
cIAP2 mRNA mediates translation only via ribosome bypassing 62 uAUGs. Shunting efficiency was altered by stress & was facilitated by a conserved RNA folding domain (1,470 to 1,877 nucleotides upstream) in a region not scanned by shunting ribosomes. |
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20. |
Inflammation during active ulcerative colitis causes an upregulation of cIAP2 in regenerating epithelium, rendering the cells less susceptible to Fas ligation. |
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21. |
The sequencing analysis of RT-PCR prducts confirmed the presence of the characteristic API2-MALT1 fusion transcript in patients with MALT lymphoma. |
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22. |
Levels of IAP-2 and Bax were decreased in A375 cells and HIF-1alpha was increased during hypoxia. |
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23. |
Bortezomib inhibited expression of cIAP-1, cIAP-2, and XIAP, which are regulated by NF-kappaB and function as inhibitors of apoptosis. |
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24. |
cIAP1 and cIAP2 are potential oncogenes and are overexpressed in multiple lung cancers with or without higher copy numbers |
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25. |
copy numbers of API2-MALT1 do not reflect tumor cell proportions, and that the number of copies of API2-MALT1 in a tumor cell is different for each clinical sample. |
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26. |
IAP-2, XIAP, and survivin may make an important contribution to the resistance to the apoptotic effect of cisplatin in prostate cancer |
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27. |
overexpression of PKC delta induced cIAP-2 promoter activity and increased NF-kappa B transactivation, suggesting regulation of cIAP-2 expression by a PKC delta/NF-kappa B pathway |
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28. |
Taken together, our results strongly indicated that API2-MALT1 possesses a novel mechanism of self-activation by up-regulating its own expression in t(11;18)(q21;q21)-carrying MALT lymphomas. |
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29. |
Persistent infection of epithelial cell line with Chlamydophila pneumoniae resulted in the upregulation of the NF-kappaB regulated inhibitor of apoptosis protein 2 but not inhibitor of apoptosis protein 1 and apoptosis resistance. |
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30. |
levels of c-IAP1 and c-IAP2 are regulated by Smac/DIABLO through the ubiquitin/proteasome pathway |
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31. |
cAMP can induce c-IAP2 expression in colon cancer cells through CREB phosphorylation and CRE-dependent transcription in a manner that involves activation of ERK1/2 and p38 MAPK |
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32. |
In particular, the stability of cIAP-2 is modulated by the presence of X-linked IAP and their interaction is stabilized in infected cells. |
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33. |
Fuses with MALT1 and defines a distinctive clinicopathologic subtype in pulmonary extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue. |
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34. |
Interferon-beta therapy exerts a regulatory effect on peripheral T lymphocytes through an anti-apoptosis mechanism that involves the downregulation of cellular Inhibitor of Apoptosis Protein expression. |
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35. |
Cellular inhibitors of apoptosis 1 and 2 are ubiquitin ligases for the apoptosis inducer Smac/DIABLO. |
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36. |
These results indicate that IAPs alone are not the main factor responsible for the resistance of non-small-cell lung cancer cells to treatment. |
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37. |
decreased cIAP2 may play a role in increased apoptosis in aged humans |
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38. |
demonstrates, for the first time, that BIRC3 (anti-apoptotic protein), COL3A1 (matrix protein synthesis), and CXCL3 (chemokine) were up-regulated in the thrombin-stimulated human umbilical vein endothelial cells |
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39. |
Detachment-induced upregulation of XIAP and cIAP2 delays anoikis of intestinal epithelial cells. |
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40. |
cIAP-2 is an important regulator of apoptosis in bladder cancer and its overexpression may make tumours less susceptible to therapy involving apoptosis. |
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41. |
Relative risk of death was lower for cytoplasmic c-IAP1, cytoplasmic c-IAP2, and nuclear c-IAP2 expression. It was higher for nuclear c-IAP1 expression. |
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42. |
X-linked XIAP is present in Chronic lymphocytic leukemia cells and is up-regulated in conditions where apoptosis is prevented. |
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43. |
Tax-mediated HIAP-1 overexpression is required to suppress endogenous apoptosis and, therefore, is essential for the survival of HTLV-1-transformed lymphocytes |
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44. |
Eosinophils of hypereosinophilic syndrome (HES) patients (but not normal eosinophils) express high levels of cellular IAP-2 (cIAP-2) and inhibit the caspase cascade in HES eosinophils. |
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45. |
the t(11, 18)(q21;q21) translocation creating the c-IAP2.MALT1 fusion protein activates NF-kappaB independently of TRAF1 AND TRAF2 and contributes to human malignancy in the absence of signaling adaptors that might otherwise regulate its activity |
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46. |
cIAP1 and cIAP2 bind but do not inhibit caspases |
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47. |
REVIEW: Genetic alterations involving API2 underlying the pathogenesis of MALT lymphoma |
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48. |
PR39 causes an increase in gene expression from a transfected human cDNA IAP-2 promoter in BAEC cells. PR39-induced increase in the level of IAP-2 mRNA in BAECs is due to an increase in transcription rate and mRNA stability. |
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49. |
cIAP2 expression is up-regulated by IFN-alpha and IFN-gamma through the JAK2-STAT3 pathway, and increased expression of the cIAP2 protein may contribute to an IFN-alpha- and IFN-gamma-mediated antiapoptotic effect on human neutrophils. |
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50. |
Differential expression of IAPs in B-cell lymphomas suggests differences in pathogenesis that may have implications for novel treatment strategies targeting IAPs. |
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51. |
TNF-alpha induced expression of c-IAP1 and c-IAP2 via MAP kinases, but not via NF-kappaB, and that MAP kinases participated in the inhibition of apoptosis by induction of c-IAPs in TNF-alpha-stimulated endothelial cells |
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52. |
Trp323 of BIR3 plays a pivotal role both in maintaining necessary conformation for caspase-9 interaction and to a lesser extent, recognition of Smac-type peptide. |
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53. |
LPS and TNF-alpha, enhance monocytic cell survival through the induction of the antiapoptotic c-IAP2 gene in a human promonocytic THP-1 cell line. |
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54. |
cIAP2 is an inhibitor of antigenic signaling and implicate its dysfunction in MALT lymphomas. |
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55. |
Common translocation in MALT lymphoma results in a fusion of the cIAP2 region on chromosome 11q21 with the MALT1 gene on chromosome 18q21. |
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56. |
pathway and antiapoptotic effect of up-regulation of cIAP2 by G-CSF in neutrophils, and overexpression of cIAP2 in chronic neutrophilic leukemia |
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57. |
Detection of API2-MALT1 fusion transcripts is useful for evaluating the prognosis and clinical behavior of the MALT lymphoma. |
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58. |
promotes tumor cell survival in mesothelioma |
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59. |
NF-kappa B signaling, once activated in a CD40-dependent immune response, is maintained and enhanced through deregulation of MALT1 or formation of an API2-MALT1 fusion |
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60. |
Upregulation of c-IAP2 by E6 and E7 may confer resistance to apoptosis that is necessary for sustained growth of some HPV16- and HPV18-positive cancer cells. |
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61. |
Cell cycle-dependent G2/M-phase-specific cIAP2 expression is enhanced by NF-kappaB activation, and selective down-regulation of cIAP2 causes cells blocked in mitosis with nocodazole to become susceptible to apoptosis. |
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62. |
these results indicate that unlike Smac/DIABLO, Omi/HtrA2's catalytic cleavage of IAPs is a key mechanism for it to irreversibly inactivate IAPs and promote apoptosis. |
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63. |
results reveal a physiological function of cIAP2, identify Bcl10 upregulation as a unifying molecular mechanism for MALT lymphomas, and define the mechanism and effects of this upregulation in t(11;18)-positive mucosa-associated lymphoid tissue lymphomas |