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1 HLA-B-associated transcript 3) as a TGF-beta receptor-interacting protein.
2                              The Cannabinoid Receptor Interacting Protein 1 (Cnrip1) was discovered a
3                   A SNP within the glutamate receptor interacting protein 1 (GRIP1) gene presented a
4  subunit of the AMPAR and requires glutamate receptor interacting protein 1 (GRIP1) interaction with
5                                    Glutamate receptor interacting protein 1 (GRIP1) is a neuronal sca
6 P90/DLG/ZO-1 (PDZ) domain 2 of the glutamate receptor interacting protein 1 (GRIP1) through its intra
7 ssary for synaptic accumulation of glutamate receptor interacting protein 1 (GRIP1), a crucial scaffo
8                  Here we show that glutamate receptor interacting protein 1 (GRIP1), an AMPAR-binding
9 ch repeat and Ig-like domain-containing Nogo receptor interacting protein 1 (LINGO-1) is a negative r
10 ch repeat and Ig-like domain-containing Nogo receptor interacting protein 1 (LINGO-1) is a negative r
11          The recent discovery of the role of receptor interacting protein 1 (RIP1) kinase in tumor ne
12                      The death domain kinase receptor interacting protein 1 (RIP1) plays a key role i
13 2 is necessary for the polyubiquitination of receptor interacting protein 1 (RIP1) that then serves a
14              In this study, we show that the receptor interacting protein 1 (RIP1), a central compone
15 d both K48- and K63-linked ubiquitination of receptor interacting protein 1 (RIP1).
16                                We found that receptor interacting protein 1 and 3 (RIP1 and RIP3) kin
17 singly, TRADD is required for recruitment of receptor interacting protein 1 and TNFR-associated facto
18 ation (c.279delG, p.Trp93fs*) of the nuclear receptor interacting protein 1 gene (NRIP1) in all seven
19 oxicity was also abolished by necrostatin or receptor interacting protein 1 knock down.
20 uit fly, the PDZ7 domain of GRIP1 (glutamate receptor interacting protein 1) from rat and the PDZ2 do
21 naling complex and for the ubiquitination of receptor interacting protein 1.
22                                    Glutamate receptor-interacting protein 1 (GRIP1) and GRIP2 are clo
23 r recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that bind
24                  Overexpression of glutamate receptor-interacting protein 1 (GRIP1) rescues ephrinB3
25 lating the formation of a complex containing receptor-interacting protein 1 (RIP1) and receptor-inter
26 f Casp8 prevents proteolytic cleavage of the receptor-interacting protein 1 (RIP1) in hepatocytes and
27 ily promote K11-linked polyubiquitination of receptor-interacting protein 1 (RIP1) in vitro and in vi
28 f necroptosis, which could be blocked by the receptor-interacting protein 1 (RIP1) inhibitor, necrost
29                                     Although receptor-interacting protein 1 (RIP1) is well known as a
30 retroviral expression of TAK1, inhibition of receptor-interacting protein 1 (RIP1) kinase activity wi
31 tatin-1 (Nec-1), a specific inhibitor of the receptor-interacting protein 1 (RIP1) kinase domain, pre
32                                 Finally, the receptor-interacting protein 1 (RIP1) may be involved in
33       Ubiquitination and deubiquitination of receptor-interacting protein 1 (RIP1) play an important
34 NF) receptor-associated factor 2 (TRAF2) and receptor-interacting protein 1 (RIP1) play critical role
35  has been attributed to ubiquitin editing of receptor-interacting protein 1 (RIP1) to influence activ
36 rongly reduced in murine fibroblasts lacking receptor-interacting protein 1 (RIP1), a known M45-inter
37 mbly of a death-signaling complex containing receptor-interacting protein 1 (RIP1), FADD, and caspase
38                          Here we report that receptor-interacting protein 1 (RIP1)-regulated interleu
39 romises the formation of the downstream TRIF/receptor-interacting protein 1 (RIP1)/TBK1 complex.
40 e of necrostatin-1, a selective inhibitor of receptor-interacting protein 1 (RIP1, also known as RIPK
41 additional cell death pathways, necroptosis (receptor-interacting protein 1 [RIP1] and RIP3 mRNAs) an
42 sis, a form of programmed necrosis involving receptor-interacting protein 1 and the mixed lineage kin
43 king the inhibition of polyubiquitination of receptor-interacting protein 1 in TNF receptor 1 complex
44 mice and THP-1 macrophages in vitro with the receptor-interacting protein 1 kinase (RIP1) inhibitor n
45 id receptor coactivator-1 and glucocorticoid receptor-interacting protein 1 to inhibit hCAR activity.
46                    Although TNFalpha-induced receptor-interacting protein 1 ubiquitination is indeed
47 he absence of TRAF2 and TRAF5 expression and receptor-interacting protein 1 ubiquitination.
48 ges leads to reduced ubiquitination of RIP1 (receptor-interacting protein 1), suggesting a role for L
49  formation of 2 cell death complexes, RIP 1 (receptor-interacting protein 1)-FADD (Fas-associated pro
50 ys, such as hypoxia-inducing factor-1-alpha, receptor-interacting protein 1, and apoptosis-inducing f
51  factor 6, TNF receptor-associated factor 2, receptor-interacting protein 1, Hemo-oxidized iron regul
52 ule, interferon regulatory factor 3 (IRF-3), receptor-interacting protein 1, IFNbeta-1, and nucleotid
53                   PMN lysis was dependent on receptor-interacting protein 1, suggesting that PMN-SA u
54 receptor coactivator 1 or the glucocorticoid receptor-interacting protein 1.
55 nd hepatocyte death in vitro, independent of receptor-interacting protein 1.
56 teractions with TNFR-associated factor 6 and receptor-interacting protein 1.
57 riments show that WNV-E acts at the level of receptor-interacting protein 1.
58 ation is dependent upon its interaction with receptor-interacting protein 1.
59 itochondria, the role of necroptosis through receptor-interacting proteins 1 and 3 (RIPK1 and RIPK3)
60  Mechanistically, Traf2 critically regulates receptor-interacting proteins 1 and 3 and mixed lineage
61 nd resulted in the downregulation of nuclear receptor interacting protein-1 (NRIP1), which influences
62                                We identified receptor interacting protein-1 (RIP1) as a novel API2-MA
63 how that the AMPAR-binding protein glutamate receptor-interacting protein-1 (GRIP1) is essential for
64 NF-alpha/Fas-induced cell death is a type of receptor-interacting protein-1 (RIP-1)-dependent program
65 -associated death domain protein (TRADD) and receptor-interacting protein-1 (RIP1) in TRAIL signaling
66        We identified TRIP12 (thyroid hormone receptor-interacting protein 12), an E3 ubiquitin-protei
67  In this study, we demonstrated that thyroid receptor interacting protein 13 (TRIP13) is a critical m
68 0-Mad2 subcomplex and identify it as Thyroid Receptor Interacting Protein 13 (TRIP13), an AAA-ATPase
69               The AAA-ATPase thyroid hormone receptor interacting protein 13 (TRIP13), jointly with t
70                      In this study, we found receptor interacting protein 140 (RIP140) can regulate t
71                                              Receptor interacting protein 140 (RIP140) is a nuclear r
72             T3 repression of Crabp1 requires receptor interacting protein 140 (RIP140).
73 ment of histone deacetylase-containing/GRIP1/receptor-interacting protein 140 (RIP140) complex in dif
74 onal carcinoma cell line P19, which involves receptor-interacting protein 140 (RIP140) for heterochro
75 urons induces rapid translocation of nuclear receptor-interacting protein 140 (RIP140) to the cytopla
76 coactivator 1alpha or 1beta and repressed by receptor-interacting protein 140.
77                                  Cannabinoid receptor interacting protein 1a (CRIP1a) is a CB1 recept
78                                  Cannabinoid receptor-interacting protein 1a (CRIP1a) binds to the CB
79 icated in the breakdown of 2-AG; cannabinoid receptor-interacting protein 1a (CRIP1a), a protein that
80 it a higher expression of IRAK1, IRAK-M, and receptor interacting protein 2 (Rip2).
81 nd their common downstream adaptor molecule, receptor interacting protein 2 (RIP2; also known as RIPK
82  now show that MDP induces ubiquitylation of receptor- interacting protein 2 (RIP2) in primary macrop
83                                              Receptor-interacting protein 2 (RIP2) is a kinase that m
84                                              Receptor-interacting protein 2 (Rip2) is a transcription
85  1 (NOD1) interacts with its adaptor protein receptor-interacting protein 2 (RIP2) to propagate immun
86 pensable for recruiting a downstream kinase, receptor-interacting protein 2 (RIP2), that activates nu
87 ient in the gene coding for the NLR adaptor, receptor-interacting protein 2 (RIP2).
88 8 as well as NOD1 and its signaling molecule receptor-interacting protein 2 (RIP2).
89 on of MAPKs, and deficient ubiquitination of receptor-interacting protein 2 in response to MDP.
90  reduced in the absence of NOD proteins, but receptor-interacting protein 2 is not involved in CD8 si
91 protein 2) binds to the protein kinase RIP2 (receptor-interacting protein 2) to coordinate NF-kappaB
92 njury was seen with a deficiency of Nod2 and receptor-interacting protein 2, and the simultaneous def
93 of IkappaB kinase (IKKbeta) and its upstream receptor-interacting protein 2, whereas IKKbeta inhibito
94 , and in their downstream signaling molecule receptor-interacting protein 2.
95 ulation and NF-kappaB activation, indicating receptor-interacting protein 2/IKKbeta signaling plays c
96              Responses were mediated through receptor interacting protein-2 (RIP2)- and tumor necrosi
97 ifferentiation primary response gene 88, and receptor-interacting protein-2 but reduced the expressio
98 rated that a super-low dose of LPS activates receptor interacting protein 3 kinase (RIP3), a key mole
99 IF) and led to persistent phosphorylation of receptor-interacting protein 3 (Rip3) kinase, which resu
100  was correlated with increased expression of receptor-interacting protein 3 (RIP3), a master regulato
101 ne products due to mu1 knockdown potentiates receptor-interacting protein 3 (RIP3)-dependent cell dea
102 ia and that Gpx4 is essential for preventing receptor-interacting protein 3 (RIP3)-dependent necropto
103 ng receptor-interacting protein 1 (RIP1) and receptor-interacting protein 3 (RIP3).
104 lly, inhibition of STIM1 signaling prevented receptor-interacting protein 3-dependent (RIP3-dependent
105 lpha and CD95 ligand, but was independent of receptor-interacting protein 3.
106 +) exchange regulatory factor 2, and thyroid receptor interacting protein 6, which has been shown pre
107 of two proteins in the zyxin family, thyroid receptor-interacting protein 6 (TRIP6) and lipoma-prefer
108    In this study, a role for thyroid hormone receptor-interacting protein 6 (TRIP6) in sealing zone f
109 LIM domain-containing TRIP6 (Thyroid Hormone Receptor-interacting Protein 6) is a focal adhesion mole
110  Fisetin also inhibited TNF-induced TAK1 and receptor-interacting protein activation, events that lie
111 e by the "death" adaptor protein caspase and receptor interacting protein adaptor with death domain (
112 cular mechanisms leading to aryl hydrocarbon receptor interacting protein (AIP) mutation-induced aggr
113 partners, we found that the aryl hydrocarbon receptor-interacting protein (AIP) directly associates w
114                             Aryl hydrocarbon receptor-interacting protein (AIP) mutations lead to som
115 RISPR screen identified the aryl hydrocarbon receptor-interacting protein (AIP), a co-chaperone prote
116  homozygous deletion of the aryl hydrocarbon receptor-interacting protein (AIP), a survivin-associate
117 cluding Hsp90, p23, and the aryl hydrocarbon receptor-interacting protein (AIP), also known as ARA9 a
118                      These G protein-coupled receptor-interacting proteins also facilitate fine-tunin
119 re, we have identified AIP (aryl hydrocarbon receptor interacting protein) as a new binding partner o
120 ng protein adaptor with death domain (CRADD)/receptor interacting protein-associated ICH-1/CED-3 homo
121 -induced protein with a death domain (PIDD), receptor-interacting protein-associated ICH-1/CED-3 homo
122 r show that RIP1 (the Ser/Thr protein kinase receptor-interacting protein) associates with the GAP do
123 primary keratinocytes (KCs) as the vitamin D receptor-interacting protein complex.
124  of two structurally related CB1 cannabinoid receptor interacting proteins (CRIP1a and CRIP1b) that b
125  factor receptor (TNFR) superfamily, through receptor-interacting protein-dependent K63-linked ubiqui
126      Using VDR affinity beads, the vitamin D receptor interacting protein (DRIP)/mediator complex was
127 kout mice and chimeras revealed that Eph-Eph receptor-interacting proteins (ephrins) are expressed bo
128                   We identified a novel NMDA receptor-interacting protein, GIPC (GAIP-interacting pro
129 with one of the PDZ domains of the Glutamate receptor interacting protein (Grip), another factor requ
130 -associated protein (GABARAP), and glutamate receptor interacting protein (GRIP).
131 on, two AMPAR-interacting proteins-glutamate receptor-interacting protein (GRIP) and protein interact
132                                    Glutamate receptor-interacting protein (GRIP) is a neuronal scaffo
133 brane through its interaction with glutamate receptor-interacting protein (GRIP), a PDZ domain protei
134 g domains for left-handed helix (Z-form) and receptor-interacting protein homotypic interaction motif
135  of RAMPs highlight the need to consider all receptor-interacting proteins in future drug development
136      PRIP (peroxisome proliferator-activator receptor interacting protein) is a nuclear receptor coac
137 ty of NEMO to bind to K63-linked polyUb RIP (receptor-interacting protein) is necessary for efficient
138   Our findings suggest that BAT3, a TGF-beta receptor-interacting protein, is capable of modulating T
139              Programmed necrosis mediated by receptor interacting protein kinase (RIP)3 (also called
140 d cIAP2 (cIAP1/2), leading to the release of receptor interacting protein kinase (RIPK1) from the act
141 Degradation of cIAPs triggers the release of receptor interacting protein kinase (RIPK1) from TNF rec
142 he necroptosis inhibitor Nec-1, which blocks receptor interacting protein kinase 1 (RIP kinase 1), al
143 ding tumor necrosis factor receptor (TNFR1), receptor interacting protein kinase 1 (RIP1), RIP3, phos
144 D and caspase 8, and the necroptosis kinases receptor interacting protein kinase 1 (RIPK1) and RIPK3.
145 emonstrated that the scaffolding function of receptor interacting protein kinase 1 (RIPK1) and tumor
146     In contrast, inhibition and knockdown of receptor interacting protein kinase 1 (RIPK1) had no eff
147                                              Receptor interacting protein kinase 1 (RIPK1) has an ess
148                                              Receptor interacting protein kinase 1 (RIPK1) is a criti
149 by tumor necrosis factor (TNF) signaling via receptor interacting protein kinase 1 (RIPK1)- and caspa
150 iven by two serine threonine kinases, RIPK1 (Receptor Interacting Protein Kinase 1) and RIPK3, and a
151 ction model, such variant procaspase-1 binds receptor interacting protein kinase 2 (RIP2) via Caspase
152                                              Receptor interacting protein kinase 2 (RIPK2) is critica
153 itment of additional proteins (such as RIP2, receptor interacting protein kinase 2), which is further
154             Recent findings suggest that the receptor interacting protein kinase 3 (RIP3) acts as a s
155 orm of nonapoptotic cell death driven by the receptor interacting protein kinase 3 (RIPK3) and its su
156 sis is a cell death pathway regulated by the receptor interacting protein kinase 3 (RIPK3) and the mi
157 ptosis, functions as a negative regulator of receptor interacting protein kinase 3 (RIPK3), an essent
158 l survival, caspase-8-mediated apoptosis, or receptor interacting protein kinase 3 (RIPK3)-dependent
159 pases, while necroptosis is dependent on the receptor interacting protein kinase 3 (RIPK3).
160 ll death defined by activation of the kinase receptor interacting protein kinase 3 and its downstream
161 ed phosphorylation and decreased cleavage of receptor interacting protein kinase-1 (Rip1), leading to
162 8, revealing a new regulatory axis affecting receptor interacting protein kinase-1 (RIPK1)>CASPASE-8
163                                              Receptor Interacting Protein Kinase-1 (RIPK1), a key pla
164 osis is mediated by the kinase activities of receptor interacting protein kinase-1 and receptor inter
165 ch is transduced by the kinase activities of receptor interacting protein kinase-1 and receptor inter
166                                              Receptor interacting protein kinase-3 (RIP3) is an essen
167 ath pathway downstream of the protein kinase Receptor Interacting Protein Kinase-3 (RIPK3).
168 nt mice is completely rescued by ablation of receptor interacting protein kinase-3 (RIPK3).
169 of receptor interacting protein kinase-1 and receptor interacting protein kinase-3, eventually leadin
170 of receptor interacting protein kinase-1 and receptor interacting protein kinase-3, which eventually
171                                              Receptor-interacting protein kinase (RIP) 3 (also called
172                                      Because receptor-interacting protein kinase (RIP) 3-mediated nec
173 inase (FAK) which then interact with AKT and receptor-interacting protein kinase (RIP), respectively.
174                                Inhibition of receptor-interacting protein kinase (RIP)1 by necrostati
175  NF-kappaB is shown to depend on the adaptor receptor-interacting protein kinase (RIP)1, acting via a
176                                              Receptor-interacting protein kinase (RIPK) 1 functions a
177 es neutrophil extracellular traps (NETs) via receptor-interacting protein kinase (RIPK) 1/3- and mixe
178 l of peritonitis, we show in this study that receptor-interacting protein kinase (RIPK) 3 impacts pyr
179                                              Receptor-interacting protein kinase (RIPK)-1 is involved
180 ochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-mediated nec
181 on by APAP was p53 independent, and required receptor-interacting protein kinase 1 (RIP1) and c-Jun N
182  cells by inhibiting the interaction between receptor-interacting protein kinase 1 (RIP1) and RIP3, a
183 ck the Fas-associated death domain (FADD) or receptor-interacting protein kinase 1 (RIP1) cell death
184 noic acid receptor gamma (RARgamma) controls receptor-interacting protein kinase 1 (RIP1)-initiated c
185                                              Receptor-interacting protein kinase 1 (RIPK1) and RIPK3
186                                              Receptor-interacting protein kinase 1 (RIPK1) induces ap
187                                              Receptor-interacting protein kinase 1 (RIPK1) is a serin
188                                              Receptor-interacting protein kinase 1 (RIPK1) is an impo
189                                Inhibition of receptor-interacting protein kinase 1 (RIPK1) kinase act
190       Knock-in expression of kinase inactive receptor-interacting protein kinase 1 (RIPK1) prevented
191                                              Receptor-interacting protein kinase 1 (RIPK1) promotes c
192                                              Receptor-interacting protein kinase 1 (RIPK1) regulates
193 s acidic neuronal necroptosis via recruiting receptor-interacting protein kinase 1 (RIPK1) to its C t
194 ed apoptosis requires the kinase activity of receptor-interacting protein kinase 1 (RIPK1), a key reg
195 ath known as necroptosis that is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3 and
196 programmed cell death and innate immunity is receptor-interacting protein kinase 1 (RIPK1), which has
197                                      Rather, receptor-interacting protein kinase 1, a kinase also lin
198   Activation of macrophages required DR5 and receptor-interacting protein kinase 1.
199 n to directly binding its downstream targets receptor-interacting protein kinase 2 (RIP2) and autopha
200 reporting conflicting requirements for RIP2 (receptor-interacting protein kinase 2) in autophagy indu
201  Ly6/PLAUR domain-containing protein 6, in a receptor-interacting protein kinase 2-TGF-beta-activated
202                                              Receptor-interacting protein kinase 3 (RIP3 or RIPK3) ha
203                                              Receptor-interacting protein kinase 3 (RIP3) and its sub
204                  We further demonstrate that receptor-interacting protein kinase 3 (RIP3), which is h
205 shed by caspase-8 compromise and mediated by receptor-interacting protein kinase 3 (RIP3).
206                                          The receptor-interacting protein kinase 3 (RIP3/RIPK3) has e
207 tein expression of the necroptosis mediators receptor-interacting protein kinase 3 (RIPK3) and mixed
208 otein with death domain (FADD) combined with receptor-interacting protein kinase 3 (RIPK3) deficiency
209      Besides causing necroptotic cell death, receptor-interacting protein kinase 3 (RIPK3) has an alt
210                                              Receptor-interacting protein kinase 3 (RIPK3) is a serin
211                                              Receptor-interacting protein kinase 3 (RIPK3) mediates n
212                         RNA interference for receptor-interacting protein kinase 3 (RIPK3) or mixed l
213                                          The receptor-interacting protein kinase 3 (RIPK3) plays cruc
214                                              Receptor-interacting protein kinase 3 (RIPK3)-mediated n
215 c approach, we demonstrate the presence of a receptor-interacting protein kinase 3 (RIPK3)-mixed line
216 m of cell death that critically requires the receptor-interacting protein kinase 3 (RIPK3).
217 rammed necrosis, or "necroptosis", driven by receptor-interacting protein kinase 3 (RIPK3).
218                                              Receptor-interacting protein kinase 4 (RIPK4) and interf
219                                              Receptor-interacting protein kinase 4 (RIPK4) is require
220 ted kinase (PKK), which is also known as the receptor-interacting protein kinase 4, as a suppressor o
221 D), Fas-associated death domain protein, and receptor-interacting protein kinase proteins form the si
222 nteract via a CARD-CARD interaction with the receptor-interacting protein kinase RIP2, an inducer of
223 at MLKL-mediated death is independent of the receptor-interacting protein kinase RIPK3.
224       Instead, robust cross-priming required receptor-interacting protein kinase-1 (RIPK1) signaling
225 because the molecules initiating it [such as receptor-interacting protein kinase-1 (RIPK1), RIPK3, or
226 y assays and immunohistochemistry for RIPK1 (receptor-interacting protein kinase-1), MLKL (mixed line
227                                              Receptor-interacting protein kinase-3 (RIP3 or RIPK3) is
228 nonapoptotic form of cell death initiated by receptor-interacting protein kinase-3 (RIPK3) and mixed
229                                              Receptor-interacting protein kinase-3 (RIPK3) is an acti
230            Here, we show that modulating the receptor-interacting protein kinase-3 (Ripk3) pathway ma
231 ological cell suicide mechanism initiated by receptor-interacting protein kinase-3 (RIPK3) phosphoryl
232 ation of mixed lineage kinase-like (MLKL) by receptor-interacting protein kinase-3 (RIPK3) results in
233 onents of the necroptotic pathway, including receptor-interacting protein kinase-3 (RIPK3), mixed lin
234 l approach, we demonstrate the presence of a receptor-interacting protein kinase-3 (RIPK3)-a mixed li
235 tosis, in which dying cells are generated by receptor-interacting protein kinase-3 and caspase-8 dime
236  is represented by necroptosis, in which the receptor-interacting protein kinase-3 and its substrate
237 sure and, more recently, also in relation to receptor-interacting protein kinase-driven necroptosis,
238 ting Fas-associated death domain protein and receptor-interacting protein kinase.
239                                          The receptor interacting protein kinases-1 (RIPK1) and RIPK3
240        Recent studies have demonstrated that receptor-interacting protein kinases (RIPKs) RIPK1 and R
241  of programmed necrosis that is regulated by receptor-interacting protein kinases (RIPs).
242 dence points to unregulated signaling by the receptor-interacting protein kinases-1 (RIPK1) and RIPK3
243 LCA) caused by mutations in Aryl hydrocarbon receptor interacting protein like-1 (Aipl1) is a severe
244 photoreceptor-specific gene aryl hydrocarbon receptor interacting protein-like 1 (Aipl1) are associat
245 the photoreceptor-expressed aryl hydrocarbon receptor interacting protein-like 1 (AIPL1) are associat
246  P351Delta12 human isoform, aryl hydrocarbon receptor interacting protein-like 1 (hAIPL1) mice demons
247 IPL1 and the mouse isoform, aryl hydrocarbon receptor interacting protein-like 1 (mAipl1).
248 ptor-specific gene encoding aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1) are clinical
249                             Aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1) is a distinc
250                             Aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1) is a photore
251                             Aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1) is a photore
252 n the chaperone activity of aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1), and mutatio
253 the enzyme itself or AIPL1 (aryl hydrocarbon receptor-interacting protein-like 1), leads to retinal d
254                                        RICK (receptor-interacting protein-like interacting caspase-li
255                  Defects in aryl hydrocarbon receptor interacting protein-like1 (AIPL1) are associate
256  identify LRR and Ig domain-containing, Nogo receptor-interacting protein (LINGO-1) as a potent axona
257 eviously, LRR and Ig domain-containing, Nogo receptor-interacting protein (LINGO-1) has been identifi
258 iated factor 2, TGF-beta-activated kinase 1, receptor-interacting protein, NF-kappaB-inducing kinase,
259                                      Nuclear receptor interacting protein (Nrip1), also known as RIP1
260                      We have identified an N receptor-interacting protein, NRIP1, that directly inter
261 the recruitment of PPARalpha and the nuclear receptor-interacting protein, nuclear receptor corepress
262 ct of multiple ligands, association with the receptor-interacting protein receptor activity-modifying
263 f TLR2, TLR3, TLR4, TLR5, or TLR9 results in receptor interacting protein (RIP) 3 kinase-dependent pr
264                        Wild-type C57BL/6 and receptor interacting protein (RIP) 3(-/-) mice were rand
265                           Here, we show that receptor interacting protein (RIP) kinase-mediated necro
266                             It is known that receptor interacting protein (RIP) kinases, RIP1 and RIP
267                                              Receptor interacting protein (RIP)3 kinase (also called
268 e cytomegalovirus M45 protein interacts with receptor-interacting protein (RIP) 1 and RIP3 via a RIP
269                                              Receptor-interacting protein (RIP) and cellular Fas-asso
270                                          The receptor-interacting protein (RIP) family kinase RIP4 in
271 ing motifs, one of which is related to RHIM [receptor-interacting protein (RIP) homotypic interaction
272 of IFN-regulatory factors (DAI) that contain receptor-interacting protein (RIP) homotypic interaction
273                        Because this involves receptor-interacting protein (RIP) kinase 1/3, this stud
274                                              Receptor-interacting protein (RIP) kinase 3 (RIPK3)-depe
275                  In this study, we show that receptor-interacting protein (RIP) kinase mediates necro
276  The complex interplay between caspase-8 and receptor-interacting protein (RIP) kinase RIP 3 (RIPK3)
277       Here we provide genetic evidence for a receptor-interacting protein (RIP) kinase-caspase-8-depe
278 , which plays a key role in the execution of receptor-interacting protein (RIP) kinase-dependent necr
279 type I interferon (IFN-I) response to induce receptor-interacting protein (RIP) kinase-mediated necro
280 ase-11, IL-1R-associated kinases (IRAK), and receptor-interacting protein (RIP) kinases contribute to
281 /Fas-mediated signaling pathway regulated by receptor-interacting protein (RIP), a kinase that shuttl
282 ern recognition receptor that assembles with receptor-interacting protein (RIP)-2 kinase in response
283 e-2, or the caspase-2 adaptor protein RAIDD (receptor-interacting protein (RIP)-associated Ich-1/CED
284 ase-8, TNFR-associated factor 2 (TRAF2), and receptor-interacting protein (RIP).
285 t the principal components of the necrosome, receptor-interacting protein (RIP)1 and RIP3, are highly
286  and type II (gamma) IFNs induce precipitous receptor-interacting protein (RIP)1/RIP3 kinase-mediated
287                      The pronecrotic kinase, receptor interacting protein (RIP1, also called RIPK1) m
288                                              Receptor-interacting protein (RIP1) and p38 mitogen-acti
289                                              Receptor-interacting protein (RIP1) is a serine/threonin
290                                          The receptor-interacting protein RIP140 interacts with the t
291 ced anti-inflammation engineered by lowering receptor interacting protein (RIP140) expression in macr
292 milar to programmed necrosis that depends on receptor interacting protein (Ripk1).
293      In particular, we focus on the roles of receptor-interacting proteins, scaffold proteins, synapt
294 n ID-related gene encoding the synaptic NMDA-receptor interacting protein synapse-associated protein
295 TO-ETHYLENE SENSITIVITY1 (RTE1), an ethylene receptor interacting protein that regulates the activity
296              In an attempt to discover novel receptor interacting proteins, the C-terminal tail of th
297       Two such proteins, mannose 6-phosphate receptor-interacting protein TIP47 and Arfaptin2, were f
298 tic Wnt-receiving cell to target dGRIP, a Wg-receptor-interacting protein, to postsynaptic sites.
299 y, we cloned the tomato ortholog of TGF-beta Receptor Interacting Protein (TRIP1), which was previous
300 uman PIMT (peroxisome proliferator-activated receptor-interacting protein with methyltransferase) pro

 
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