ATF4


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ATF4

A gene on chromosome 22q13.1 that encodes a transcription activator protein belonging to a family of DNA-binding proteins, which includes the AP-1 family of transcription factors, cAMP-response element binding proteins (CREBs) and CREB-like proteins.
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When the researchers knocked out ATF4 in cells or mice they found tumours continued to increase the amount of 4E-BP - and eventually died from stress.
Significant correlations among the protein levels of PDL1, eIF2[alpha], and ATF4 and between those of IRF1 and PDL1 were observed in the tumor tissues of both subgroups and in the normal tissue of SCC.
ATF4 Was Increased in Mouse Corneas Infected by Intrastromal Injection.
[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.
Alteration of PERK and ATF4 signaling is responsible for ER stress-associated redox imbalance and affects the disulfide bond formation (ERO1, endoplasmic reticulum oxidoreductin; PDI, protein disulfide isomerase) that influences antioxidant activation in ER [2].
ER stress caused by the accumulation of unfolded proteins triggers the unfolded protein response (UPR) which in turn modulates both transcription and translation of key regulators (e.g., ATF4) of the cellular stress response [37].
Most of the transcription factors that presented differences between the studied groups (ATF4, CDX2, DDIT3, HSF1, OTX2, POU5F1, XBP1, HAND1, NANOG, NFKB2, SOX2, and SOD2) also have important functions in RNA metabolic processes, regulating the frequency, rate, and extent of chemical reactions involving RNA [33, 35].
Furthermore, the mRNA expression levels of ER stress responsive genes (Grp78, chop, Xbp-1s, Atf4, and Erdj4) were significantly lower in HFD-fed obese mice treated with DNJ than in control mice treated with the vehicle (Figure 4(b)).
33'-diindolylmethane induces activating transcription factor 3 (ATF3) via ATF4 in human colorectal cancer cells.
Redfern, "Regulation of endoplasmic reticulum stress-induced cell death by ATF4 in neuroectodermal tumor cells," Journal of Biological Chemistry, vol.
Meanwhile, upregulation of ATF4 and CHOP, known as a hallmark of one of the three pathways of endoplasmic reticulum stress (ER stress) response, was also observed.
To investigate whether UPR, especially CHOP10 induction, is involved in the suppression of terminal adipogenesis by [iAs.sup.3+], the expression of ATF4 and CHOP10 were measured in 3T3-L1 cells.