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1  genetic manipulation of Ddit3 (encoding the transcription factor CHOP).
2 of CCAAT/enhancer-binding protein homologous transcription factor (CHOP).
3 -box binding protein-1 (Xbp-1) mRNA, and the transcription factor CHOP.
4 xhibited elevated levels of the proapoptotic transcription factor CHOP.
5 um (ER stress), is a powerful inducer of the transcription factor CHOP.
6 uppressive activity of MDSCs is regulated by transcription factor Chop.
7 an endoplasmic reticulum (ER) stress-related transcription factor, CHOP.
8 s, BiP and PERK, as well as the proapoptotic transcription factor, CHOP.
9 , but is thought to drive cell death via the transcription factor, CHOP.
10 The CAAT/enhancer binding protein homologous transcription factor CHOP, also known as GADD153, is inv
11 optotic proteins was detected, including the transcription factor CHOP and Bim, an essential factor f
12 3 induction is substantially mediated by the transcription factors CHOP and ATF4.
13 rtions of the PrLDs of FUS and EWSR1 and the transcription factors CHOP and FLI.
14 y in the UPR literature: the function of the transcription factor CHOP as a protective or a prodeath
15 s is mediated by the ER stress regulator and transcription factor CHOP, but not the tumor suppressor
16 ed by Adv-DNFoxo, including the proapoptotic transcription factor CHOP (C/EBP [CCAAT/enhancer binding
17                                          The transcription factor CHOP (C/EBP homologous protein 10)
18 AT, -59 to -54) that presumptively binds the transcription factor CHOP [CAAT enhancer binding protein
19                             Induction of the transcription factor CHOP (CCAAT-binding homologous prot
20 The inhibition of the major stress-inducible transcription factor CHOP (CCAAT/enhancer-binding protei
21                 Deletion of the UPR mediator transcription factor CHOP completely rescues the motor d
22      Here we determined whether deleting the transcription factor CHOP (Ddit3-/-), which mediates ER-
23  induced by eIF2alpha-P is that encoding the transcription factor CHOP (DDIT3/GADD153).
24                                          The transcription factor CHOP (GADD153) heterodimerizes with
25            After chronic UPR activation, the transcription factor CHOP (GADD153/DDIT3) triggers cell
26 ome that features elevated expression of the transcription factor CHOP (GADD153/DDIT3).
27 ce to oxidative stress, and the proapoptotic transcription factor CHOP (GADD153/DDIT3).
28 an increased expression of the pro-apoptotic transcription factor CHOP-(gadd153), a downstream event
29 er pathways, including the expression of the transcription factor CHOP/GADD153 and its downstream tar
30 posarcomas, consists of a fusion between the transcription factor CHOP/GADD153 and the N terminus of
31                                          The transcription factor CHOP/GADD153 gene is induced by cel
32 ted samples revealed that the stress-induced transcription factor CHOP/Gadd153 was dramatically up-re
33 ess-dependent expression of the proapoptotic transcription factor chop/gadd153.
34 he data reveal a major negative role for the transcription factor CHOP in overall survival during sep
35 scription factor 4 [ATF-4], C/EBP homologous transcription factor [CHOP], oxireductase endoplasmic re
36  Atf4 or deletion of its downstream effector transcription factor Chop rescues TFH responses of Elp3-