戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
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
11                                    Nedd 4-1, XIAP, and WWP2 have been shown to maintain PTEN turnover
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
14 M, caspase-3, BCL-XL) and resistance (MCL-1, XIAP).
15 hed1/2, and Smoothened), Gli targets (Bcl-2, XIAP and Cyclin D1), and EMT markers and transcription f
16 f anti-apoptotic proteins (survivin, cIAP-2, XIAP), induced apoptosis, and arrested cells in G1.
17                                   However, a XIAP mutant that does not interact with caspase-9 had no
18                        These data included a XIAP threshold concentration at which apoptosis executio
19      Mitochondrial stress was reduced by AAV-XIAP-GFP, but did not reach a statistical significance (
20 sing recombinant adeno-associated virus (AAV-XIAP-GFP).
21      To test this scenario, we pre-activated XIAP at mitochondria via mitochondrial depolarization or
22                 Upon Wnt pathway activation, XIAP is recruited to TCF/Lef where it monoubiquitylates
23                                 In addition, XIAP and CAS mRNA expression levels were correlated in H
24            Anti-apoptotic proteins Bcl-2 and XIAP were up-regulated while pro-apoptotic BAX was down-
25  PARP, together with a decrease in Bcl-2 and XIAP.
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
28                                Syk, Akt, and XIAP antagonists may present potential new therapeutic s
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
32  this ratio but had little effect on BAX and XIAP.
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-
35           miR-34a directly inhibits Bcl2 and XIAP, both anti-apoptotic proteins.
36  constitutively on the promoters of BCL2 and XIAP, whereas p50 is recruited to these promoters only i
37 the NF-kappaB antiapoptotic targets BCL2 and XIAP.
38 nt antiproliferative activities in cIAP- and XIAP-dependent cell lines.
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
41 lular ROS and degradation of IAPs (cIAP1 and XIAP).
42 tly to the BIR3 domains of cIAP1, cIAP2, and XIAP (IC50 = 15, 21, and 15 nM, respectively).
43 imals that lack functional cIAP1, cIAP2, and XIAP are not viable, and 2 mimicked features of triple I
44  we generated a mouse with cIAP1, cIAP2, and XIAP deleted in the myeloid lineage.
45 asone cooperate to deplete cIAP1, cIAP2, and XIAP, thereby promoting assembly of the ripoptosome, a R
46 ays required inhibition of cIAP1, cIAP2, and XIAP.
47                            Loss of cIAPs and XIAP in the myeloid lineage caused overproduction of man
48 from bone marrow in the absence of cIAPs and XIAP led to detectable levels of TNF and resulted in red
49       Our results demonstrate that cIAPs and XIAP together restrain RIPK1- and RIPK3-dependent cytoki
50 ellular radiosensitivity and both DIABLO and XIAP might be potential predictive markers of radiation
51  and (v) down regulation of p-AKT, p-ERK and XIAP.
52 ations in understanding the role of HIF1 and XIAP in human disease.
53 sized as antagonists of cIAP1/2, ML-IAP, and XIAP based on the N-terminus, AVPI, of mature Smac.
54 hibitor treatments caused loss of c-IAP1 and XIAP in multiple cancer cell lines and in tumor xenograf
55                                     MDM2 and XIAP are mutually regulated.
56 e a novel signaling circuit between PERK and XIAP that operates in parallel with PERK to CHOP inducti
57 involving concomitant CHOP up-regulation and XIAP down-regulation both induced by PERK.
58 poptosis inducers TNF and staurosporine, and XIAP overexpression reduces the lag time between the adm
59 , increasing its association with BCL-XL and XIAP mRNAs to promote their nuclear export.
60 ies and are highly effective in antagonizing XIAP in cell-free functional assays.
61 e find dramatic suppression of antiapoptosis XIAP proteins in response to chronic ER stress.
62 down of the X-linked inhibitor of apoptosis (XIAP) and partially reverted by XIAP overexpression.
63 tients with X-linked inhibitor of apoptosis (XIAP) deficiency.
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
66             X-linked inhibitor of apoptosis (XIAP) is the most potent naturally occurring specific in
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
69         The X-linked inhibitor of apoptosis (XIAP) protein has been identified as a key genetic drive
70 ic proteins X-linked inhibitor of apoptosis (XIAP), phospho-Akt (pAkt), and phospho-BAD.
71 ions in the X-linked inhibitor of apoptosis (XIAP).
72 HIF1alpha), X-linked inhibitor of apoptosis (XIAP)], promoting cell cycle arrest [growth arrest and D
73                            During apoptosis, XIAP is antagonized by SMAC, which is released from the
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
76 omain and bind to cIAP1 and cIAP2 as well as XIAP.
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.
79 pression of a mutant CSR1 that does not bind XIAP.
80      The miRNA miR-23a was predicted to bind XIAP mRNA.
81  indicated that the C-terminus of CSR1 binds XIAP with high affinity.
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
85 ize NOD2 and cell death phenotypes driven by XIAP.
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
89  occurred at Lys-138, which was inhibited by XIAP domain.
90 on of cancer cell invasion and metastasis by XIAP.
91 ated that the regulation of cell motility by XIAP depends on its interaction with the Rho GDP dissoci
92 f apoptosis (XIAP) and partially reverted by XIAP overexpression.
93 ulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, whi
94                                Consequently, XIAP E3 ligase activity recruits endolysosomes into mito
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
98 y proteins and mitochondrial depolarization, XIAP can permeabilize and enter mitochondria.
99  Surprisingly, the UbV selective for dimeric XIAP formed a dimer to stimulate E3 activity by stabiliz
100 UBE4B, phosphorylated active CBL, or dimeric XIAP.
101 d framework to rapidly test newly discovered XIAP variants.
102                    Endogenous mRNAs encoding XIAP, c-Myc, CYR61, and Pim-1, which are translated in a
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
105 s in MDM2 protein stabilization and enhanced XIAP translation.
106                             Here, we explore XIAP as an important mediator of an immune response agai
107 ot in constitutionally exogenously expressed XIAP in the same cells, excluding the possibility of ISO
108 rolonged CS/REW by the "prosurvival" factors XIAP and pAkt.
109 i-apoptotic proteins, such as BCL2, c-FLIPS, XIAP, and C-IAP2.
110 eased potency against cIAP2 and affinity for XIAP BIR3 and (ii) decreased ability to inhibit XIAP-dep
111 CS with or without UCF-101, and examined for XIAP, caspase-3, and tubular apoptosis.
112 ratio decreased for DIABLO and increased for XIAP.
113 3 ligase within RING domain was required for XIAP inhibition of phosphatase PP2A activity by up-regul
114                     Inhibitors selective for XIAP should exert pro-apoptotic effects through competit
115 d upregulation of antiapoptotic genes (e.g., XIAP and GADD45B) and downregulation of proapoptotic gen
116 onists TNFalpha or TRAIL and inhibited cIAP1>XIAP>IAP2.
117 sis protein (XIAP)-overexpressing HeLa (HeLa XIAP(Adv)) cells, only showed delayed and often no caspa
118                                        Human XIAP was delivered with bicistronic expression of green
119                 We also demonstrate that (i) XIAP polyubiquitination is dependent on the really inter
120 ay required only inhibition of X-linked IAP (XIAP) for sensitization, whereas chemotherapies that ind
121  alone and in complex with the X-linked IAP (XIAP)-BIR2-BIR3 domains.
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
128           Therefore, development of XLP-2 in XIAP-deficient patients could be partly due to sustained
129 ependent cell growth were also attenuated in XIAP-deficient cancer cells compared with those of the p
130 n of activated caspases and are decreased in XIAP-deficient individuals.
131 is the first reported whole gene deletion in XIAP, the causal gene responsible for XLP2 (X-linked lym
132 to identify a de novo whole gene deletion in XIAP.
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
135              UCF-101 significantly increased XIAP in donor kidneys and protected against apoptosis.
136    UCF-101 treatment significantly increased XIAP, significantly decreased capsase-3 protein and acti
137 P BIR3 and (ii) decreased ability to inhibit XIAP-dependent signaling pathways.
138               When the enzyme was inhibited, XIAP was degraded rapidly in infected cells, allowing cy
139     Loss of the endogenous caspase inhibitor XIAP is observed after Syk or PI3K/Akt inhibition.
140      Finally, we report that FAIM-L inhibits XIAP auto-ubiquitinylation and maintains its stability,
141 ta reveal a transcriptional switch involving XIAP-mediated ubiquitylation of Gro/TLE that facilitates
142 ting enzyme, Ubc12, to the ubiquitin ligase, XIAP or cIAP1.
143                 Importantly, one of the MDM2/XIAP inhibitors, MX69, showed minimal inhibitory effect
144 PEI) inhibited tumor growth via AKT-mediated XIAP degradation in both subcutaneous and quasi-orthotop
145              Here, we explored mitochondrial XIAP action within the intrinsic apoptosis signaling pat
146                   Importantly, mitochondrial XIAP actions are activated cell-intrinsically by typical
147       To elucidate the role of mitochondrial XIAP action during apoptosis, we integrated our findings
148 istically, we demonstrate that mitochondrial XIAP entry requires Bax or Bak and is antagonized by pro
149 creases of XIAP, combined with mitochondrial XIAP preconditioning, would reduce MOMP signaling.
150 mechanism by which miR-24 directly modulates XIAP expression level and consequently the apoptosis thr
151                                    Moreover, XIAP knockdown in SW480 cells enhanced the basal and rad
152                                      Neither XIAP nor Bcl-2 is affected by alphavbeta6 expression.
153 etails our synthetic explorations of a novel XIAP BIR2-selective benzazepinone screening hit with a f
154 which antagonizes the inflammatory action of XIAP without inducing apoptosis.
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
157              However, the molecular basis of XIAP in the regulation of cancer cell biological behavio
158 In this study, we found that a deficiency of XIAP expression in human cancer cells by either knock-ou
159                  We found that deficiency of XIAP expression resulted in a marked reduction in cyclin
160 ted by the ubiquitination and degradation of XIAP (X-linked inhibitors of aptosis protein) by E6AP, w
161                           The BIR3 domain of XIAP binds and inhibits caspase 9, while the BIR2 domain
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
165 s critically dependent on the BIR2 domain of XIAP.
166                       Targeted knock-down of XIAP enhanced CSR1-induced cell death, while overexpress
167 stance in cancer cells via downregulation of XIAP expression, and the resulting cancer cell death ind
168 many human cancers, and forced expression of XIAP blocks apoptosis.
169                                Expression of XIAP protein, but not mRNA, was highly increased in neur
170 ; this process was mediated by expression of XIAP, which bound to cleaved caspase-3.
171                The antiapoptotic function of XIAP derives from its BIR domains, which bind to and inh
172                              Inactivation of XIAP, a direct target of ARTS, abrogated these phenotype
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
177                 In conclusion, inhibition of XIAP rescues cellular radiosensitivity and both DIABLO a
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
180       Embelin, a small-molecule inhibitor of XIAP, decreased the interaction between XIAP and caspase
181 R1 binds XIAP, preventing the interaction of XIAP with caspases.
182 IM-L requires sustained endogenous levels of XIAP to protect Type II cells as well as murine cortical
183  intestinal crypts expressed lower levels of XIAP, cIAP1, cIAP2, and cFLIP than liver tissue.
184                                  The loss of XIAP and apoptosis that results from Syk or PI3K/Akt inh
185              It is possible that the loss of XIAP and its antiapoptotic functions contributes to the
186 e kidneys ex vivo is associated with loss of XIAP and subsequent tubular cell apoptosis.
187         UCF-101 protects against the loss of XIAP during prolonged CS both in vitro and ex vivo, and
188                                      Loss of XIAP leads to increased cell death, whereas XIAP overexp
189 , which prevents the HtrA2-dependent loss of XIAP.
190 -induced cell death, while overexpression of XIAP antagonized CSR1 activity.
191               The pro-survival properties of XIAP come from binding of the BIR domains to the pro-apo
192 chanisms that determine the diverse range of XIAP expression seen in cancer remains unclear.
193  of G. cleistostachyum by down-regulation of XIAP expression and induction of apoptosis through speci
194 ent with a posttranscriptional regulation of XIAP expression.
195       Of interest, PERK's down-regulation of XIAP occurs independently of CHOP activity.
196 udies have shown that ISO down-regulation of XIAP protein expression was only observed in endogenous
197 dentified miR-24 as a candidate regulator of XIAP expression.
198 The results of this work support the role of XIAP in mediating NOD2 signaling while reconciling the r
199                     Molecularly, the role of XIAP mutations in the pathogenesis of these disorders is
200 e peptides, in a manner analogous to that of XIAP-mediated inhibition of caspases-3 and -7.
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
203         miR-23a directly bound the 3' UTR of XIAP, and miR-23a inhibition led to an increase in XIAP
204  innate-like T-cell homeostasis depending on XIAP and PLZF.
205  significantly abrogated miR-24's effects on XIAP expression.
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
208               In conclusion, targeting E6 or XIAP in combination with cisplatin can efficiently poten
209  wild-type C57BL/6 mice, cIAP2-null mice, or XIAP-null mice.
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
213 IAP synthesis through eIF2alpha and promotes XIAP degradation through ATF4.
214 in both cases, but the antiapoptotic protein XIAP prevented early activation of the caspases in cells
215 the expression of the anti-apoptotic protein XIAP.
216 ein X-linked inhibitor of apoptosis protein (XIAP) and showed cellular activity.
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
223 ced X-linked inhibitor-of-apoptosis protein (XIAP) levels in these cells.
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
226 aB- X-linked inhibitor of apoptosis protein (XIAP) signaling pathway.
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
230 P), X-linked inhibitor of apoptosis protein (XIAP), and perforin expression, respectively.
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
233 ith X-linked Inhibitor of Apoptosis Protein (XIAP), using yeast two-hybrid screening analyses.
234  in X-linked inhibitor of apoptosis protein (XIAP), with poorly understood molecular mechanisms.
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
237 the X-linked inhibitor of apoptosis protein (XIAP).
238 osome-linked inhibitor of apoptosis protein (XIAP).
239 and X-linked inhibitor of apoptosis protein (XIAP).
240 ght inhibitors that blocked the MDM2 protein-XIAP RNA interaction, leading to MDM2 degradation.
241 egulates short-lived antiapoptotic proteins, XIAP and c-FLIPL by inhibiting global protein synthesis.
242 accelerate Hsp70 drug discovery by providing XIAP as a pharmacodynamic biomarker.
243 in E6-supressed cells was related to reduced XIAP levels and not due to reduced p21 levels.
244   We also identified that ISO down-regulated XIAP gene transcription via inhibition of Sp1 transactiv
245 ing protein human antigen R (HuR), regulated XIAP mRNA stability and expression.
246             We find that PERK down-regulates XIAP synthesis through eIF2alpha and promotes XIAP degra
247  excluding the possibility of ISO regulating XIAP expression at the level of protein degradation.
248        Mechanistically, [pIC](PEI) repressed XIAP and survivin expression and activated an immune res
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
251           Recent work has consistently shown XIAP to be critical for signaling downstream of the Croh
252  occurring V30E mutant also did not suppress XIAP and HuR.
253 f cells transfected with exogenous HA-tagged XIAP.
254  depolarization or by artificially targeting XIAP to the intermembrane space.
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
258                                 We find that XIAP and Ubc13 dependent Lys63-linked polyubiquitination
259              Taken together, we propose that XIAP enters mitochondria through a novel mode of mitocho
260                          Here we report that XIAP and cIAP1 induce autophagy by upregulating the tran
261             Together, our findings show that XIAP targeting sensitizes neuroblastoma to chemotherapy-
262                          Here we showed that XIAP deficiency selectively impaired B-cell chronic lymp
263                  Recent studies suggest that XIAP is involved in immune signaling.
264 cytosol and on mitochondria, suggesting that XIAP plays a critical role in the activation and translo
265                                          The XIAP expression was maintained in ground squirrel RTECs
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
269  in different human conditions including the XIAP immunodeficiency.
270          Using a luciferase construct of the XIAP 3'UTR, we showed that miR-24 specifically coordinat
271 hat miR-24 directly targets the 3'UTR of the XIAP messenger RNA (mRNA) to exert translational repress
272 n-protein interaction (PPI) inhibitor of the XIAP:p19/p12-CASP7 complex.
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
275  that miR-24 specifically coordinates to the XIAP mRNA.
276  GDP dissociation inhibitor (RhoGDI) via the XIAP RING domain.
277 s critical for stimulating apoptosis through XIAP and survivin degradation.
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
282        SATB2 overexpression also upregulated XIAP and cyclin D1, suggesting its role in cell survival
283 offering a new molecular basis for utilizing XIAP E3 ligase as a cancer therapeutic target.
284 ent B-cell lymphoma-derived cell lines where XIAP is overexpressed and pharmacological inhibition of
285 m apoptosis in pathological situations where XIAP levels are decreased.
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
289                                        While XIAP BIR3 inhibitors have previously been reported, they
290 rence enhanced EF24-induced apoptosis, while XIAP overexpression reduced it in CCA cells.
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
294                     The binding of CSR1 with XIAP enhanced caspase-9 and caspase-3 protease activitie
295 egimens should not be used for patients with XIAP deficiency.
296 on the treatment of the cancer patients with XIAP overexpression.
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
300 aB targets of antiapoptotic proteins Bcl-xL, XIAP, and cIAP2.

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top