Endoplasmic reticulum stress activates cleavage of CREBH to induce a systemic inflammatory response.

By Kezhong Zhang, Xiaohua Shen, Jun Wu, K. Sakaki, T. Saunders, D. Rutkowski, Sung Hoon Back, Randal J. Kaufman. Cell, 2006

833 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/1a8b6b1c7aa9ad9b99b197cb625268df3bd2da4f

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Citations in the corpus

The impact of the unfolded protein response on human disease (2012, background): “…ATF6 (1) Hypoferremia and spleen iron sequestration; (2) Hyperlipidemia; (3) Liver knockdown: fasting hyperglycemia (1) Extreme hypertriglyceridemia Zhang et al., 2006; Vecchi et al., 2009; J.H. Lee et al., 2011 PERK N.A. (1) Neonatal hyperglycemia (1) Wolcott-Rallison syndrome; (2) Supranuclear…”
Toll-like receptor activation of XBP1 regulates innate immune responses in macrophages (2010, background): “Some ER-stress markers have also been detected after sustained LPS stimulatio”
Aberrant Mucin Assembly in Mice Causes Endoplasmic Reticulum Stress and Spontaneous Inflammation Resembling Ulcerative Colitis (2008, background): “Direct biochemical links between ER stress and both local and systemic inflammation suggest that ER stress directly promotes inflammation [57,58], Figure 10.”
Endoplasmic reticulum stress signaling in disease. (2006, background): “Following from the identification of ATF6, there have been several related transcription factors identified, which share similar domain structures and localization to the ER [Luman (35, 113, 154), OASIS (88), CREBH (225), ATF6b (59), CREB4 (178)].”
The endoplasmic reticulum stress response in immunity and autoimmunity (2008, background): “Similar to ATF6, CREBH undergoes intramembrane proteolysis in response to ER stress, releasing an N-terminal fragment that transits to the nucleus, where it acts on the UPR”
Inflammation and metabolic disorders (2006, background): “Second, inflammatory mediators can trigger ER stress and lead to propagation of general stress response”
Decoding cell death signals in liver inflammation. (2013, background): “Interestingly, the hepatic ER stress response per se exerts pro-inflammatory functions, both as it allows for the activation of the pro-inflammatory hepatocytespecific transcription factor CREBH [79] and as it sensitizes liver-resident macrophages to stimulation by Toll-like receptor 4 (TLR4) agonis”
Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, positive): “These studies identified CREBH as a novel ER-localized transcription factor that has an essential role in induction of innate immune response genes and links for the first time ER stress to inflammatory responses (164).”
The Endoplasmic Reticulum: Folding, Calcium Homeostasis, Signaling, and Redox Control (2006, neutral): “…histone deacetylase complex 1; HIF, hypoxia-inducible factors; HSP, heat-shock-protein; InsP3, inositol 1,4,5-trisphosphate; InsP3R, inositol-1,4,5-trisphosphate receptor; INSIG-1, insulin-induced gene 1 protein; IRE, inositol requiring kinase; JAB-1, Jun activation domain-binding protein; JNK,…”
Endoplasmic Reticulum Stress in Liver Disease (2010, background): “The ER membrane-localized hepatocyte-specific bZIP-transcription factor CREBH (cyclic-AMP-responsive-element-binding protein H) is cleaved by RIP upon ER stress, similarly to ATF6a [80,161].”
From endoplasmic-reticulum stress to the inflammatory response (2008, background): “Recently, CREBH, another RIP-regulated bZIP-containing transcription factor, was identified to mediate the acute-phase response in the live”
Autophagy Is Activated for Cell Survival after Endoplasmic ReticulumStress (2006, background): “Recently, it was reported that transmembrane transcription factors localized to the ER membrane (OASIS, CREB-H, and Tisp40/AIbZIP) function as tissue-specific ER stress transducers (1, 13, 42 ).”