ATF6 Activated by Proteolysis Binds in the Presence of NF-Y (CBF) Directly to the cis-Acting Element Responsible for the Mammalian Unfolded Protein Response

By Hiderou Yoshida, T. Okada, K. Haze, H. Yanagi, T. Yura, M. Negishi, K. Mori. Molecular and Cellular Biology, 2000

978 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/88fb3c5bc75a87e0167bf729d6d1e3a5a1164a0b

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Citations in the corpus

CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum. (2004, background): “The CHOP promoter also receives positive input from other components of the UPR (Wang et al. 1998b; Yoshida et al. 2000), and CHOP protein is post-translationally activated by the p38 kinase (Wang and Ron 1996).”
The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “Thus, ATF6 can cooperate with XBP-1 to activate CHOP (39).”
TRB3, a novel ER stress‐inducible gene, is induced via ATF4–CHOP pathway and is involved in cell death (2005, background): “On the other hand, ER stress response element (ERSE) was identified as a sequence of 19 nucleotides, the consensus of which is CCAAT-N9-CCAAG, in the CHOP and ER chaperone promoters (Yoshida et al, 2000).”
The molecular biology and nomenclature of the activating transcription factor/cAMP responsive element binding family of transcription factors: activating transcription factor proteins and homeostasis. (2001, methodology): “This ternary complex has a slower mobility than that of the binary complex between DNA and NF-Y (or YY-1) ( Yoshida et al., 2000, 2001; Li et al., 2000).”
The unfolded protein response: controlling cell fate decisions under ER stress and beyond (2012, background): “The activity of ATF6f, and its specificity for ER stress response elements in the promoter regions of target genes, is determined by its direct interaction with different transcription factors, including NF-Y (also known as CBF), YY1, TATA-binding protein (TBP”
Islet amyloid polypeptide, islet amyloid, and diabetes mellitus. (2011, background): “The different pathways are regulated by the three sensors ATF6 (activating transcription factor 6 alpha), IRE1 (inositol requiring 1), and PERK (PKR like ER kinase).”
XBP-1 Regulates a Subset of Endoplasmic Reticulum Resident Chaperone Genes in the Unfolded Protein Response (2003, background): “UPRE reporter (5xATF6GL3), pCGNATF6, and pCGNAF6(1-373) were previously described (57).”
Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, neutral): “These transducers are two protein kinases IRE1 (inositol-requiring kinase 1) (129, 159), and PERK (double-stranded RNA-activated protein kinase-like ER kinase) (42), and the transcription factor ATF6 (activating transcription factor 6) (159, 160).”
Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease. (2018, background): “involved in protein folding and ERAD, but can also activate the transcription of XBP1u (44, 45).”
Roles of CHOP/GADD153 in endoplasmic reticulum stress (2004, background): “pATF6a(N) and pATF6b(N) contain a bZIP domain and bind to the ER stress response element (ERSE) consensus sequence 50CCAAT-N9-CCACG-3 0 as a homo- or heterodimer interacting with NF-Y trimer.(36,37) Activated Ire1a and Ire1b cleave the substrate precursor XBP-1 mRNA to mature XBP-1 mRNA by their end”
ER stress regulation of ATF6 localization by dissociation of BiP/GRP78 binding and unmasking of Golgi localization signals. (2002, neutral): “(Ma and Hendershot, 2001; Mori, 2000; Patil and Walter, 2001).”