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1 XIAP and cIAP1 are members of the inhibitor of apoptosis
2 XIAP and cIAP1 are two members of the inhibitors of apop
3 XIAP gene therapy using AAV may provide a means of reduc
4 XIAP has previously emerged as a molecular discriminator
5 XIAP inhibition by lentivirus mediated RNA interference
6 XIAP is a key regulator of apoptosis, and its overexpres
7 XIAP mRNA levels were higher in females at baseline.
8 XIAP overexpression has been found in many human cancers
9 XIAP overexpression was examined by immunostaining and W
10 XIAP, its vertebrate homolog, is similarly required for
12 observed that P. gingivalis targets APAF-1, XIAP, caspase-3, and caspase-9, to inhibit epithelial ce
13 nal cancer-associated survival genes (Mcl-1, XIAP and cIAP2) in a p53 status-independent manner, whil
15 hed1/2, and Smoothened), Gli targets (Bcl-2, XIAP and Cyclin D1), and EMT markers and transcription f
26 ogates the production of cIAP-1, cIAP-2, and XIAP and HA-CD44v3-mediated cancer stem cell functions.
27 veral survival proteins (cIAP-1, cIAP-2, and XIAP) leading to self-renewal, clonal formation, and cis
29 l RTECs in which gene expression of Akt1 and XIAP was silenced lost their protection and demonstrated
30 This study identified APAF-1 apoptosome and XIAP as intracellular targets of P. gingivalis, contribu
31 eatment promoted interaction between Bax and XIAP in the cytosol and on mitochondria, suggesting that
33 , IKK, NF-kappaB, and antiapoptotic BCL2 and XIAP genes, and up-regulation of BAX and BAK proapoptoti
34 itment of p50 onto the promoters of BCL2 and XIAP is dependent upon BRCA1, but independent of its NF-
36 constitutively on the promoters of BCL2 and XIAP, whereas p50 is recruited to these promoters only i
39 Smac-mimetics reduced levels of cIAP1 and XIAP in MC38 and YAMC cells, and Smac-mimetics and TNF-r
40 ases with the E3 ubiquitin ligases cIAP1 and XIAP was hindered, leading to decreased degradation of R
43 imals that lack functional cIAP1, cIAP2, and XIAP are not viable, and 2 mimicked features of triple I
45 asone cooperate to deplete cIAP1, cIAP2, and XIAP, thereby promoting assembly of the ripoptosome, a R
48 from bone marrow in the absence of cIAPs and XIAP led to detectable levels of TNF and resulted in red
50 ellular radiosensitivity and both DIABLO and XIAP might be potential predictive markers of radiation
54 hibitor treatments caused loss of c-IAP1 and XIAP in multiple cancer cell lines and in tumor xenograf
56 e a novel signaling circuit between PERK and XIAP that operates in parallel with PERK to CHOP inducti
58 poptosis inducers TNF and staurosporine, and XIAP overexpression reduces the lag time between the adm
62 down of the X-linked inhibitor of apoptosis (XIAP) and partially reverted by XIAP overexpression.
64 -IAP2), and X-linked inhibitor of apoptosis (XIAP) in a ROS-dependent manner, and in RIP1 knockdown c
65 ed role for X-linked inhibitor of apoptosis (XIAP) in regulating this critical Wnt signaling event th
67 Because X-linked inhibitor of apoptosis (XIAP) is the primary endogenous inhibitor of caspases, i
68 ole for the X-linked inhibitor of apoptosis (XIAP) protein as a regulator of Lys63-linked polyubiquit
72 HIF1alpha), X-linked inhibitor of apoptosis (XIAP)], promoting cell cycle arrest [growth arrest and D
74 ith the mRNA that encodes the anti-apoptotic XIAP, simultaneously decreasing expression of both prote
75 inding protein with low pI); anti-apoptotic: XIAP (X-linked inhibitor of apoptosis)] are involved, we
77 eles can be replaced with disease-associated XIAP variants expressed at endogenous levels to simultan
78 r of XIAP, decreased the interaction between XIAP and caspase-3 and led to enhanced caspase activity.
82 t that cell death is induced when CSR1 binds XIAP, preventing the interaction of XIAP with caspases.
83 nown pathway members RIPK2, RELA, and BIRC4 (XIAP) as well as FRMPD2 (FERM and PDZ domain-containing
84 over, intramitochondrial Smac degradation by XIAP occurs independently of Drp1-regulated cytochrome c
86 significant level of control of the HIF1 by XIAP, with important implications in understanding the r
87 Lys63-linked ubiquitination of HIF1alpha by XIAP is dependent on the activity of E2 ubiquitin conjug
88 enotype of iNKT cells, which is inhibited by XIAP although it exerts a moderate effect in conventiona
91 ated that the regulation of cell motility by XIAP depends on its interaction with the Rho GDP dissoci
93 ulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, whi
95 ypothesized that prolonged CS would decrease XIAP, whereas upregulation of XIAP with the novel compou
96 and female Ube3A 2X ASD mice show decreased XIAP levels, increased caspase-3 activation, and elevate
97 n vitro demonstrated significantly decreased XIAP and significantly increased apoptosis, caspase-3 pr
99 Surprisingly, the UbV selective for dimeric XIAP formed a dimer to stimulate E3 activity by stabiliz
103 n expression was only observed in endogenous XIAP, but not in constitutionally exogenously expressed
104 nderstanding of the regulation of endogenous XIAP by a DR antagonist, pointing out at FAIM-L as a pro
107 ot in constitutionally exogenously expressed XIAP in the same cells, excluding the possibility of ISO
110 eased potency against cIAP2 and affinity for XIAP BIR3 and (ii) decreased ability to inhibit XIAP-dep
113 3 ligase within RING domain was required for XIAP inhibition of phosphatase PP2A activity by up-regul
115 d upregulation of antiapoptotic genes (e.g., XIAP and GADD45B) and downregulation of proapoptotic gen
117 sis protein (XIAP)-overexpressing HeLa (HeLa XIAP(Adv)) cells, only showed delayed and often no caspa
120 ay required only inhibition of X-linked IAP (XIAP) for sensitization, whereas chemotherapies that ind
122 le reconciling the role of XLP-2 and VEO-IBD XIAP mutations in inflammatory cell death and provide a
123 r, the reported effects of XLP-2 and VEO-IBD XIAP mutations on cell death have been inconsistent.
124 ll death data to show that XLP-2 and VEO-IBD XIAP mutations that exhibit a loss-of-function NOD2 phen
125 ved from DNA-programmed chemistry identified XIAP BIR2 and BIR3 domain inhibitors that displace bound
126 sting new gene (RING) catalytic domain, (ii) XIAP polyubiquitination occurs via lysine (K)-63 but not
127 sine (K)-63 but not K-48 residues, and (iii) XIAP-dependent K-63 polyubiquitination requires zinc for
129 ependent cell growth were also attenuated in XIAP-deficient cancer cells compared with those of the p
131 is the first reported whole gene deletion in XIAP, the causal gene responsible for XLP2 (X-linked lym
133 and miR-23a inhibition led to an increase in XIAP mRNA in vitro, demonstrating that XIAP is a previou
134 to reconcile the aforementioned inconsistent XIAP cell death data to show that XLP-2 and VEO-IBD XIAP
136 UCF-101 treatment significantly increased XIAP, significantly decreased capsase-3 protein and acti
141 ta reveal a transcriptional switch involving XIAP-mediated ubiquitylation of Gro/TLE that facilitates
144 PEI) inhibited tumor growth via AKT-mediated XIAP degradation in both subcutaneous and quasi-orthotop
148 istically, we demonstrate that mitochondrial XIAP entry requires Bax or Bak and is antagonized by pro
150 mechanism by which miR-24 directly modulates XIAP expression level and consequently the apoptosis thr
153 etails our synthetic explorations of a novel XIAP BIR2-selective benzazepinone screening hit with a f
155 ed a novel function of E3 ligase activity of XIAP in the up-regulation of cyclin D1 expression, provi
156 ent, orally bioavailable, dual antagonist of XIAP and cIAP1 and a structurally novel chemical probe f
158 In this study, we found that a deficiency of XIAP expression in human cancer cells by either knock-ou
160 ted by the ubiquitination and degradation of XIAP (X-linked inhibitors of aptosis protein) by E6AP, w
162 E3 ligase activity within the RING domain of XIAP is crucial for its ability to regulate cyclin D1 tr
163 of RhoGDI SUMOylation by the RING domain of XIAP may account for modulation of cancer cell invasion
164 FAIM-L interacts with the BIR2 domain of XIAP through an IAP-binding motif, the mutation of which
167 stance in cancer cells via downregulation of XIAP expression, and the resulting cancer cell death ind
173 mulations suggest that moderate increases of XIAP, combined with mitochondrial XIAP preconditioning,
174 onstitutive activation of p53, inhibition of XIAP and sensitization of cancer cells to apoptosis.
175 egulation resulted not only in inhibition of XIAP expression, but also in activation of p53, which co
176 rexpressed and pharmacological inhibition of XIAP in these cell lines reduced autophagosome biogenesi
178 sistent with this observation, inhibition of XIAP suppresses cell proliferation, resulting in cell de
179 Notably, we show that combined inhibition of XIAP, SRD5A1 and AR pathways overcomes castration resist
182 IM-L requires sustained endogenous levels of XIAP to protect Type II cells as well as murine cortical
193 of G. cleistostachyum by down-regulation of XIAP expression and induction of apoptosis through speci
196 udies have shown that ISO down-regulation of XIAP protein expression was only observed in endogenous
198 The results of this work support the role of XIAP in mediating NOD2 signaling while reconciling the r
201 effect is mediated by the ubiquitination of XIAP (X-linked inhibitor of aptosis protein) by E6AP, su
202 would decrease XIAP, whereas upregulation of XIAP with the novel compound UCF-101 would protect again
206 g of MDM2 RING protein to the IRES region on XIAP mRNA results in MDM2 protein stabilization and enha
207 nts revealed multiple Hsp70-binding sites on XIAP, suggesting that it is a direct, physical Hsp70 cli
210 ), which has high levels of selectivity over XIAP BIR3 and cIAP1 BIR2/3 and shows efficacy in a xenog
211 the biomedical significance of overexpressed XIAP in cancer development, further offering a new molec
212 e identified and studied three novel patient XIAP mutations and used this system to characterize NOD2
214 in both cases, but the antiapoptotic protein XIAP prevented early activation of the caspases in cells
217 t the X-linked inhibitory apoptosis protein (XIAP) associates with the C terminus of Ptch1 (Ptch1-C)
218 hat X-linked inhibitor of apoptosis protein (XIAP) interacted with RhoGDI via its RING domain and neg
219 X-linked inhibitor of apoptosis protein (XIAP) is a potent caspase inhibitor and an important bar
220 The X-linked inhibitor of apoptosis protein (XIAP) is a potent caspase inhibitor, best known for its
221 by X-linked inhibitor of apoptosis protein (XIAP) is a potential mechanism by which apoptosis is pre
222 The X-linked inhibitor of apoptosis protein (XIAP) is a well known potent inhibitor of apoptosis; how
224 X-linked inhibitor of apoptosis protein (XIAP) overexpression has been found to be associated wit
225 med x-linked inhibitor of apoptosis protein (XIAP) restricts bacterial colonization of this arthropod
227 bit X-linked inhibitor of apoptosis protein (XIAP) suppression of executioner caspases, respectively.
228 of X-linked inhibitor of apoptosis protein (XIAP), activation of NF-kappaB, and proteasome activity
229 een x-linked inhibitor of apoptosis protein (XIAP), an E3 ubiquitin ligase, and the E2 conjugating en
231 and X-linked inhibitor of apoptosis protein (XIAP), are obligate Hsp70 clients that are rapidly (with
232 or, X-linked inhibitor of apoptosis protein (XIAP), has been associated with chemotherapy resistance
235 nt, X-linked inhibitor of apoptosis protein (XIAP)-mediated translocation of Bax to mitochondria wher
236 to X-linked inhibitor of apoptosis protein (XIAP)-overexpressing HeLa (HeLa XIAP(Adv)) cells, only s
241 egulates short-lived antiapoptotic proteins, XIAP and c-FLIPL by inhibiting global protein synthesis.
244 We also identified that ISO down-regulated XIAP gene transcription via inhibition of Sp1 transactiv
247 excluding the possibility of ISO regulating XIAP expression at the level of protein degradation.
249 will focus on the optimization of selective XIAP BIR2 inhibitors leading to the discovery of highly
250 ffer a further theoretical basis for setting XIAP as a potential prognostic marker and specific targe
255 se in XIAP mRNA in vitro, demonstrating that XIAP is a previously uncharacterized target for miR-23a.
256 In the current study, we discovered that XIAP and its E3 ligase played a crucial role in regulati
257 Here, we report preclinical evidence that XIAP offers an effective therapeutic target in neuroblas
264 cytosol and on mitochondria, suggesting that XIAP plays a critical role in the activation and translo
266 ro recombinant protein-binding analyses, the XIAP-binding motif in CSR1 was determined to include ami
267 ewly synthesized drug is able to disrupt the XIAP:p19/p12-CASP7 complex and induce apoptosis in caspa
268 for the first time that Shigella evades the XIAP-mediated immune response by inducing the BID-depend
271 hat miR-24 directly targets the 3'UTR of the XIAP messenger RNA (mRNA) to exert translational repress
273 treat CASP3/DR malignancies by targeting the XIAP:p19/p12-CASP7 complex, but also elucidate the molec
274 profile of these compounds; it binds to the XIAP BIR3 domain, the BIR domain of ML-IAP, and the BIR3
278 with a diazabicyclic core structure bind to XIAP, cIAP1, and cIAP2 with low to subnanomolar affiniti
279 ion of compound 12 (SM-1200), which binds to XIAP, cIAP1, and cIAP2 with Ki values of 0.5, 3.7, and 5
280 CAS/imp-alpha1 transport cycle is linked to XIAP and is required to maintain tumor cell survival in
281 the brain and face is dependent in part upon XIAP mediation of Hh/Ptch1-regulated cell survival and a
284 ent B-cell lymphoma-derived cell lines where XIAP is overexpressed and pharmacological inhibition of
286 XIAP leads to increased cell death, whereas XIAP overexpression significantly enhances resistance to
287 ights into the molecular mechanisms by which XIAP regulates cancer invasion and offer a further theor
288 em for cells of the myeloid lineage in which XIAP alleles can be replaced with disease-associated XIA
291 the chemotherapy resistance associated with XIAP and cIAP1 overexpression observed in several human
292 cute the apoptotic program, yet binding with XIAP constitutively inhibits active caspase-7 (p19/p12-C
293 y cocrystal structures of key compounds with XIAP BIR2 suggested potency-enhancing structural modific
297 identifies the expression patterns of XAF1, XIAP and SRD5A1 as a predictive and actionable signature
298 d in a recent publication that reveals XAF1, XIAP, and SRD5A1 as novel predictive biomarkers and ther
299 cells, which overexpress CDK6, BCL2, Bcl-xL, XIAP, and AKT, but lack ibrutinib resistance-conferring
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