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1 87.5% versus 50%, control versus psi(epsilon)RACK).
2 ns such as receptors for activated C kinase (RACKs).
3 r hidden when active epsilonPKC binds to its RACK.
4 he binding of each isozyme to its respective RACK.
5 ills the criteria previously established for RACKs.
6 s for activated C kinase collectively called RACKs.
7 items to automobile rooftops and to bicycle racks.
8 verbal message were displayed above bicycle racks.
9 , mitogen-activated protein kinase kinase 5, RACK 1, apolipoprotein C-III, and the gene encoding the
10 ins such as receptor for activated C kinase (RACK) 1 are involved in the targeting of signaling prote
11 ein receptor for activated protein kinase C (RACK)-1 has been linked to a variety of signaling system
13 ion (Ki = 11.5 +/- 5 microM) with respect to RACK-1 (receptor for activated C kinase-1), an adaptor p
16 type I IFN signaling because mutation of the RACK-1 binding site in the IFN-alpha receptor 2/beta sub
21 Our findings suggest a mechanism by which RACK-1 directs the dynactin-dependent redistribution of
32 is elegans Receptor of Activated C Kinase 1 (RACK-1) is required for cytokinesis, germline membrane o
33 , UV-treated control PKC alpha bound well to RACK-1, whereas UV/DECA-inactivated PKC alpha had reduce
35 s increases the interaction between NR2B and RACK-1, which is also dependent on tPA, further suggesti
36 ment of synthetic peptides modeled after the RACK-1-binding site in the C2 region of PKC beta induced
40 silonPKC first translocates and binds to its RACK and subsequently the epsilonPKC/epsilonRACK complex
41 % versus 14+/-1%, control versus psi(epsilon)RACK) and resulted in fewer cases of ventricular fibrill
42 proteins (receptors for activated C kinases (RACKs)) and demonstrates a direct connection between the
43 dation of the Zapotec state, the first skull rack, and the building of a fortress in conquered territ
45 addition, pretreatment of platelets with eta-RACK antagonistic peptides, a specific inhibitor of nPKC
48 Furthermore, administration of psi(epsilon)RACK before ischemia followed by deltaV1-1 during reperf
50 ypothesized that in inactive epsilonPKC, the RACK-binding site is engaged in an intramolecular intera
51 y shown that at least part of the PKCepsilon RACK-binding site on PKCepsilon lies within the unique V
52 eraction between the psiepsilonRACK site and RACK-binding site within epsilonPKC is critical and rate
53 In contrast, pretreatment with psi(epsilon)RACK but not deltaV1-1, followed by a 10-minute washout
55 d pi-stacked arrays of dimers undergo a wine-rack compression, but the dimer remains intact up to 8 G
56 epsilon-protein kinase C (PKC), psi(epsilon)RACK, conferred cardioprotection against ischemia-reperf
57 continuous systemic delivery of psi(epsilon)RACK confers sustained cardioprotection against ischemia
59 ns, at different levels ranging from rack-to-rack down to chip-to-chip and intra-chip interconnection
60 be a result of inhibition of its binding to RACKs due to Nef binding, could contribute to the variou
61 inistration of deltaV1-1 but not psi(epsilon)RACK during reperfusion improved cardiac function and de
66 e at least some of the proteins that bind to RACKs, including PKC itself, regulate cell growth, modul
67 ction, continuous treatment with psi(epsilon)RACK induced a sustained preconditioned state during the
70 tal (which results in a so-called entatic or rack-induced state) modifies the folding of the metallat
72 that the protein scaffold creates an entatic/rack-induced state, which gives rise to a rigid environm
73 translocation of PKCepsilon and PKCbetaI by RACK interference peptides attenuated EGF-mediated preve
78 l growth, modulating their interactions with RACKs may help elucidate signaling pathways leading to c
79 mate; this structural frustration implies a "rack" mechanism for the 290 mV (vs NHE) reduction potent
80 f these lasers have only been validated with rack-mounted support equipment, assembled with fibre las
82 bound polypeptides by causing expansion (or racking) of some regions and compaction of others, most
83 gp120-triggered transient activation of the Rack-PAK-LIMK pathway, and that knockdown of LIMK throug
85 in human platelets pretreated with PKC-theta RACK peptide, which may contribute to the lower levels o
86 V1-1) and epsilon-PKC activator (psi(epsilon)RACK) peptides for ischemia/reperfusion damage in isolat
87 s, such as receptors for activated C kinase (RACKs), play an important role in regulating the localiz
88 Our findings indicate that INAD functions as RACK (receptor for activated PKC), allowing eye-PKC to p
89 platelets, PKC-theta-selective antagonistic (RACK; receptor for activated C kinase) peptide significa
96 onnections, at different levels ranging from rack-to-rack down to chip-to-chip and intra-chip interco
98 solated mouse hearts and whether psi(epsilon)RACK treatment reduces infarct size or lethal arrhythmia
99 schemia-reperfusion in vivo, and psi(epsilon)RACK was administered by intracoronary injection during
101 on V1 region to clone a PKCepsilon-selective RACK, which was identified as the COPI coatomer protein,
103 1 and a point mutant that does not bind Src (RACK Y246F) with green fluorescent protein and expressed
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