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70] Similarly, ATF4 being transcriptional regulator of the cellular hypoxic response to the UPR also showed resistance to bortezomib which actually a UPR-apoptosis mediator through autophagy induction as a survival key in HCC.
Role of ATF4 in regulation of autophagy and resistance to drugs and hypoxia.
Among the genes that are transcriptionally regulated by ATF4, ATF6, and XBP1, CHOP10 is one of the mostly expressed inducible genes during ER stress (Oyadomari and Mori 2004).
ATF4 is a substrate of RSK2 and an essential regulator of osteoblast biology; implication for Coffin-Lowry Syndrome.
Nevertheless, the downstream molecule of PERK, mRNAs encoding ATF4, paradoxically sustain translational efficiency, which induces transcription of target genes encoding enzymes involved in amino acid metabolism, enzymes required for protein folding and degradation, GADD34 phosphatase, and the transcription factor C/EBP homologous protein (CHOP/DDIT) (Han et al.
Furthermore, some of these proteins alter the activity of the UPR stress sensors (IRE1[alpha], PERK, and ATF6) as well as the activity/levels of downstream signaling mediators and transcription factors, including cleaved ATF6, ATF4, and spliced XBP1.
ATF4 could be stimulated from ERS activation indirectly or protein synthesis attenuation by eIF2B mutation directly.
Key words: ATF4, cadmium, eIF2[alpha], endoplasmic reticulum stress, Grp78, heavy metal, LLC-PK1 cells, siRNA.
Conclusions: Our results indicated that during H/R stress, CRT translocation increases cell apoptosis and LDH leakage, aggravates ER disorder, up-regulates expression of nuclear transcription factors, Nrf2 and ATF4, and activates ERS-associated apoptosis.
Inducible enhancement of memory storage and synaptic plasticity in transgenic mice expressing an inhibitor of ATF4 (CREB-2) and C/EBP proteins.
The first contains members of the Jun, Fos, and ATF subgroups of transcription factors (C-FOS, FOSB, C-JUN, JUNB, ATF3, ATF4, ATF5) that form AP-1 dimers implicated in the regulation of cell proliferation and survival (Shaulian and Karin 2001).
When ATF4 is ubiquitously expressed at low basal level, its initiation of translation at the authentic start codon is dependent on the upregulated phosphorylation of eIF2[alpha] by ER stress .
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