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1 ily anti-apoptosis proteins is a 'BH3 alone' pro-apoptotic protein.
2 ng and enzymatic activity of procaspase-3, a pro-apoptotic protein.
3 gy to Bax and Bak, has been proposed to be a pro-apoptotic protein.
4 death, is a member of the BH3-only family of pro-apoptotic proteins.
5 e required to induce apoptosis by activating pro-apoptotic proteins.
6 guously into the Bax-like Bcl-2 subfamily of pro-apoptotic proteins.
7 as reduced expression and/or inactivation of pro-apoptotic proteins.
8 ents in the hydrophobic groove that binds to pro-apoptotic proteins.
9 activation of BNIP3 and BNIP3L, which encode pro-apoptotic proteins.
10 proteins interact with certain BCL-2 family pro-apoptotic proteins.
11 complementary set of anti-proliferative and pro-apoptotic proteins.
12 s the founding member of the BH3-only family pro-apoptotic proteins.
15 was associated with increased expression of pro-apoptotic proteins and decreased expression of antia
16 member of the BH3-contaning BCL-2 family of pro-apoptotic proteins and functions in mitochondria.
18 rst report to demonstrate that inhibition of pro-apoptotic proteins and induction of autophagy sensit
19 (IAPs) physically interact with a variety of pro-apoptotic proteins and inhibit apoptosis induced by
20 IAPs physically interact with a variety of pro-apoptotic proteins and inhibit apoptosis induced by
21 he activated Akt then phosphorylates several pro-apoptotic proteins and prevents apoptosis mediated b
22 the active Bcl-2 homology 3 (BH3) domains of pro-apoptotic proteins and the threshold for cytochrome
24 ell apoptosis through induction of CHOP, the pro-apoptotic protein, and sensitizes cells to lipopolys
25 diated cell death using purified recombinant pro-apoptotic proteins, and cell-free extracts from the
26 s, the pore opens, increasing the release of pro-apoptotic proteins, and ultimately resulting in cell
30 n of p90RSK and decreased phosphorylation of pro-apoptotic protein BAD (BCL2-antagonist of cell death
32 ated phosphorylation and inactivation of the pro-apoptotic protein Bad as well as transcription of su
33 e Rsks, catalyzed the phosphorylation of the pro-apoptotic protein BAD at serine 112 both in vitro an
34 s also led to reduced phosphorylation of the pro-apoptotic protein BAD at the protein phosphatase 2A
35 trated that Rsk1 directly phosphorylated the pro-apoptotic protein Bad at the serine residues that, w
37 In particular, the formula explains how the pro-apoptotic protein BAD lowers the threshold at which
38 However, the kinase can phosphorylate the pro-apoptotic protein BAD on serine 112, which accounts
39 modules revealed that phosphorylation of the pro-apoptotic protein Bad was elevated in mitochondria.
40 poptosis through increased activation of the pro-apoptotic protein Bad, a change in the conformation
41 vel of the anti-apoptotic protein Bcl-2, the pro-apoptotic protein Bad, or the inactivated form of Ba
42 of Akt and prolonged phosphorylation of the pro-apoptotic protein Bad, resulting in enhanced cell su
43 uzumab treatment, but rather inactivated the pro-apoptotic protein BAD, the BCl-2-associated death pr
44 gnal, in part through phosphorylation of the pro-apoptotic protein BAD, TPCK reduced BAD phosphorylat
49 hospho-Erk1/2) proteins, and upregulated the pro-apoptotic proteins (Bad, Bim, Bax and Bid) leading t
50 mitochondria, MCL-1 interacts with the major pro-apoptotic protein BAK and prevents BAK-BAK homo-olig
52 e crypts and an accompanying increase in the pro-apoptotic protein Bak was expressed in intestinal ep
54 i-apoptotic proteins Bcl-2 and Mcl-1 and the pro-apoptotic protein Bak, whereas Bax expression is rel
58 ation of the cell death pathway demonstrated pro-apoptotic protein Bax 'activation' and caspase cleav
60 Sequential steps in the activation of the pro-apoptotic protein Bax are described for cells with d
64 ed by the fact that removal of the intrinsic pro-apoptotic protein Bax rescues the germ-cell apoptosi
66 he anti-apoptotic protein Bcl-2 binds to the pro-apoptotic protein Bax to prevent Bax homo-oligomeriz
67 ential of a pharmacological activator of the pro-apoptotic protein BAX to suppress acute myeloid leuk
68 membranes are unaffected by addition of the pro-apoptotic protein Bax under a variety of conditions.
70 ast, the intensity of immunostaining for the pro-apoptotic protein Bax was not significantly altered
71 oth cellular and mitochondrial levels of the pro-apoptotic protein Bax were increased severalfold as
72 oposide resulted in the up-regulation of the pro-apoptotic protein Bax, a result that was prevented b
73 een the tumor suppressor protein p53 and the pro-apoptotic protein Bax, in human melanoma cell lines
74 ough a newly identified BH3 domain, with the pro-apoptotic protein Bax, their co-translocation to the
75 port that ARC co-immunoprecipitated with the pro-apoptotic protein Bax, which causes cytochrome c rel
84 rial apoptotic pathway acts through two core pro-apoptotic proteins Bax (Bcl2-associated X protein) a
86 d from cells deficient in one or both of the pro-apoptotic proteins Bax and Bak show that at least on
87 spectively, whereas immunopositivity for the pro-apoptotic proteins Bax and Bak was found in 44 (92%)
89 f these events represses the function of the pro-apoptotic proteins Bax and Bak, which are required f
91 -apoptotic proteins BCL-2 and BCL-XL and the pro-apoptotic proteins BAX and BCL-XS in T/null-cell ALC
92 ses in the mitochondrial levels of activated pro-apoptotic proteins Bax and Bid, and to a lesser exte
94 s associated with elevated expression of the pro-apoptotic proteins Bax, Bad, and TRAIL (tumor necros
95 pha) significantly reduced the expression of pro-apoptotic proteins (Bax and PUMA) and autophagic pro
96 ins functioned to inhibit the ability of the pro-apoptotic protein, Bax to induce PCD in plants and y
97 f 1, 2 and 10mg/kg could alter the levels of pro-apoptotic protein, Bax, anti-apoptotic protein, Bcl-
100 t shares a conserved domain, BH3, with other pro-apoptotic proteins, Bax, Bak, Bid, and Hrk, and cert
102 s correlates with increased abundance of the pro-apoptotic proteins BCL2L11 and BBC3, and with decrea
104 nduced cleavage of both procaspase-8 and the pro-apoptotic protein Bid, indicating that Bcl-2 functio
109 On the other hand, ectopic expression of the pro-apoptotic protein Bik led to decreased Ca(m) load an
113 s significantly reduced the induction of the pro-apoptotic protein Bim both in vitro and in mice.
114 rtinib treatment increased expression of the pro-apoptotic protein Bim by as much as 144% in Z119 cel
116 beta-induced apoptosis and expression of the pro-apoptotic protein Bim in WEHI 231 B lymphocytes.
117 hat was 'rescued' by genetic deletion of the pro-apoptotic protein Bim or transgenic expression of Bc
118 tion may arise through the inhibition of the pro-apoptotic protein Bim, which is normally repressed b
121 mor cell apoptosis, increasing levels of the pro-apoptotic protein Bim/Bod, and cleavage of caspase-7
124 ulation and suppresses the expression of the pro-apoptotic protein BimEL, as has been observed in Her
127 coding not only antiviral, inflammatory, and pro-apoptotic proteins but also proteins of other functi
128 stress with the additional expression of the pro-apoptotic protein C/EBP-homologous protein/growth ar
129 lear membrane protein lamin A, expression of pro-apoptotic proteins c-Jun N-terminal kinase 3, caspas
130 ic genetic model Caenorhabditis elegans, the pro-apoptotic protein CED-4 activates the CED-3 caspase
131 In this manner, treatments that increase pro-apoptotic protein expression increase the efficacy o
132 related with CO-induced up-regulation of the pro-apoptotic protein FADD as well as activation of casp
133 c PYD interaction between NLRP12 PYD and the pro-apoptotic protein Fas-associated factor 1 (FAF-1), w
135 channels may be one mechanism for releasing pro-apoptotic proteins from mitochondria during the indu
136 -cell survival in part via inhibition of the pro-apoptotic proteins glycogen synthase kinase-3alpha/b
140 s been shown to be an important activity for pro-apoptotic proteins in Drosophila (Reaper, HID, and G
142 olytic degradation of the BH3-only family of pro-apoptotic proteins in the mitochondrial pathway.
143 ks the ability of BCL-XL to bind and inhibit pro-apoptotic proteins, in combination with a MEK inhibi
147 eclin-1 contains a BH3-only motif typical of pro-apoptotic proteins, it is a negligible modulator of
149 , EBER-1, binds to the growth inhibitory and pro-apoptotic protein kinase R (PKR) and blocks activati
150 ment binding protein (phospho-CREB), and the pro-apoptotic protein kinases extracellular signal-regul
151 and is the founding member of a subfamily of pro-apoptotic proteins known as "BH3-alone" proteins.
153 rom 11 of 41 tumor lines that expressed this pro-apoptotic protein migrated in gels as a clear double
154 physiology, thereby promoting the release of pro-apoptotic proteins normally contained within this or
155 Bortezomib induced an upregulation of the pro-apoptotic protein Noxa, loss of mitochondrial transm
156 bination treatment induced expression of the pro-apoptotic protein Noxa- and caspase-dependent degrad
162 1 also induced the phosphorylation of Bad (a pro-apoptotic protein of the Bcl-2 family), which was in
163 Furthermore, the expression levels of the pro-apoptotic proteins of CHOP/GADD153 and caspase-12 we
164 eted NSCLC cells show elevated expression of pro-apoptotic proteins of the Bcl-2 family, caspase recr
166 onsequent DNA fragmentation, accumulation of pro-apoptotic proteins (p27, p53, p89 PARP fragments), a
168 We report that Akt physically binds to the pro-apoptotic protein Par-4 via the Par-4 leucine zipper
170 uggesting that E1B 19K may act to antagonize pro-apoptotic proteins rather than as an effector of sur
171 ng with cytochrome c and other mitochondrial pro-apoptotic proteins represent important regulatory ch
172 we identify a novel protein, named Parcs for pro-apoptotic protein required for cell survival, that i
173 imer formation occurs through binding of the pro-apoptotic protein's BH3 domain into the hydrophobic
174 2 family antiapoptotic proteins with various pro-apoptotic proteins, several of which are also member
176 ns of key mitophagic/autophagic proteins and pro-apoptotic protein such as ROS, VDAC1, LC-3II and Cas
177 y interacting with and negatively regulating pro-apoptotic proteins such as Bax and Bad, as a target
178 their pro-apoptotic functions through BH1-3 pro-apoptotic proteins such as BAX and BAK, while their
179 hich bind to the BH3 alpha-helical domain of pro-apoptotic proteins such as Bax, Bak, Bad, and Bim, a
186 perties of a small molecule mimic of Smac, a pro-apoptotic protein that functions by relieving inhibi
189 dings identify Par-4 as a novel example of a pro-apoptotic protein that selectively inhibits oncogeni
190 -ATPase (SERCA), and decreases levels of the pro-apoptotic protein thioredoxin-interacting protein (T
193 rane (OM), thus promoting recruitment of the pro-apoptotic proteins truncated Bid (tBid) and Bax for
194 the "BCL-2 homology (BH) 3-only" members of pro-apoptotic proteins, truncated BID (tBID) has been im
195 e SW48 cells increased the expression of the pro-apoptotic proteins, whereas the SW480 cells increase
197 hondrial calcium overload and the release of pro-apoptotic proteins, which triggers delayed cell deat
198 sive gene 3)) is a human caspase-independent pro-apoptotic protein with some similarity to apoptosis-
199 The Bcl-2 family includes both anti- and pro-apoptotic proteins with opposing biological function
200 -apoptotic proteins to counter expression of pro-apoptotic proteins, WM samples expressed both pro- a
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