In summary, we have demonstrated that the transcription factor AP-1 (primarily its c-Jun and ATF-2 components) can be activated in rat small intestine and IEC-6 cells exposed to heat stress, and that the JNK signaling pathway is also involved in this response.
As free levels of BiP decrease in the ER, ATF-6 translocates to the Golgi apparatus where the active transcription factor component, ATF-6a, is cleaved and released.
Field and laboratory cycling testing of experimental ATFs showed that nylon components in contact with ATF underwent color changes and exhibited loss of tensile strength.
As a result, the direct components of the ATF are enhanced, which leads to an improvement in speech quality of the overall system.
It was shown in [19] that the temporal smearing and therefore the reverberation relies on the all-pass component of the overall ATF.
Phosphorylation of c-jun and ATF-2, two heterodimeric components of AP-1, also play their role in nuclear translocation of NF-κB.
However, if we develop ATF expression further, target gene regulation by ATFs may be more effective.
ATF-7 binds to mouse ATFa-associated modulator (mAM), which is a component of the ESET complex (De Graeve et al. 2000; Wang et al. 2003).
Transgenic mice overexpressing the human aTf gene (Saleh et al., 2003) showed an increase in their myelin components similar to that found in rats ICI with aTf.
cJun is also a central component of AP-1, which consists of homodimers and heterodimers of the Jun, Fos and ATF gene family members and regulates transcription through AP-1 and cAMP responsive elements (Angel et al, 1987, 1988; Curran and Franza, 1988; Sassone-Corsi et al, 1990).
