Transcriptional Induction of Mammalian ER Quality Control Proteins Is Mediated by Single or Combined Action of ATF6α and XBP1

By Keisuke Yamamoto, Takashi Sato, Toshie Matsui, Masanori Sato, T. Okada, Hiderou Yoshida, Akihiro Harada, Kazutoshi Mori. 2007

959 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

The Unfolded Protein Response and Cell Fate Control. (2017, positive): “fact that double deficient animals are embryonic lethal (Yamamoto et al., 2007).”
Toll-like receptor activation of XBP1 regulates innate immune responses in macrophages (2010, methodology): “The following antibodies were used for immunoblot analysis: anti-XBP1s (Poly6195; BioLegend); antibody to phosphorylated PERK (16F8), antibody to total PERK (C33E10), anti-IRE1α (14C10) and antibody to phosphorylated Jnk (9251; all from Cell Signaling); anti-Hsp90 (H114), anti-IκBβ (C20) and anti-CH”
Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “Known or suspected target genes of ATF6α include GRP78, PDI and ER degradation-enhancing α-mannosidase-like protein 1 (EDEM1), resulting in increased ER chaperone activity and degradation of misfolded protein”
A multiplexed single-cell CRISPR screening platform enables systematic dissection of the unfolded protein response (2016, positive): “ATF6 and IRE1a showed more overlap, consistent with a more common transcriptional regulatory mechanism (Yamamoto et al., 2007).”
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, neutral): “Interestingly, however, mice lacking ATF6a or ATF6b do not have amajor phenotype, whereas the dual deficiency is lethal (Wu et al., 2007; Yamamoto et al., 2007).”