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PMID |
Sentence |
1 |
17569614
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Resveratrol induces apoptosis by up-regulating the expression of Bax, Bak, PUMA, Noxa, Bim, p53, TRAIL, TRAIL-R1/DR4 and TRAIL-R2/DR5 and simultaneously down-regulating the expression of Bcl-2, Bcl-XL, Mcl-1 and survivin.
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2 |
17569614
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Resveratrol causes growth arrest at G1 and G1/S phases of cell cycle by inducing the expression of CDK inhibitors p21/WAF1/CIP1 and p27/KIP1.
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3 |
19164757
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Like bortezomib, EerI-induced cytotoxicity requires the up-regulation of the Bcl-2 homology3 (BH3)-only pro-apoptotic protein NOXA.
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4 |
19164757
|
First, these agents elicit an integrated stress response program at the ER to activate the CREB/ATF transcription factors ATF3 and ATF4.
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5 |
19164757
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We show that ATF3 and ATF4 form a complex capable of binding to the NOXA promoter, which is required for NOXA activation.
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6 |
19164757
|
Second, EerI and bortezomib also block ubiquitination of histone H2A to relieve its inhibition on NOXA transcription.
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7 |
19164757
|
Like bortezomib, EerI-induced cytotoxicity requires the up-regulation of the Bcl-2 homology3 (BH3)-only pro-apoptotic protein NOXA.
|
8 |
19164757
|
First, these agents elicit an integrated stress response program at the ER to activate the CREB/ATF transcription factors ATF3 and ATF4.
|
9 |
19164757
|
We show that ATF3 and ATF4 form a complex capable of binding to the NOXA promoter, which is required for NOXA activation.
|
10 |
19164757
|
Second, EerI and bortezomib also block ubiquitination of histone H2A to relieve its inhibition on NOXA transcription.
|
11 |
19164757
|
Like bortezomib, EerI-induced cytotoxicity requires the up-regulation of the Bcl-2 homology3 (BH3)-only pro-apoptotic protein NOXA.
|
12 |
19164757
|
First, these agents elicit an integrated stress response program at the ER to activate the CREB/ATF transcription factors ATF3 and ATF4.
|
13 |
19164757
|
We show that ATF3 and ATF4 form a complex capable of binding to the NOXA promoter, which is required for NOXA activation.
|
14 |
19164757
|
Second, EerI and bortezomib also block ubiquitination of histone H2A to relieve its inhibition on NOXA transcription.
|