Regulation of Hepatic Lipogenesis by the Transcription Factor XBP1
By Ann-Hwee Lee, E. Scapa, D. Cohen, Laurie H. Glimcher. Science, 2008
964 citations recorded by the source corpus.
Subfields: Biochemistry, Cell Biology, Endocrinology, Diabetes and Metabolism
View Paper: https://www.semanticscholar.org/paper/53eab4c7efc30437967a7e6517ad1c5d2d20c3ae
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Biochemistry
- Gerald I. Shulman
- V. Samuel
- Liangyou Rui
- G. Hotamışlıgil
- R. Kaufman
- Fabio Martinon
- R. Medzhitov
- M. Kotas
In Cell Biology
- R. Kaufman
- C. Hetz
- G. Hotamışlıgil
- Laurie H. Glimcher
- J. Cubillos-Ruiz
- Sarah Bettigole
- Gerald I. Shulman
- Herbert Tilg
In Endocrinology, Diabetes and Metabolism
- Liangyou Rui
- Gerald I. Shulman
- G. Hotamışlıgil
- V. Samuel
- Herbert Tilg
- A. Moschen
- R. Kaufman
- Haiming Cao
Citations in the corpus
- The impact of the unfolded protein response on human disease (2012, background): “XBP1s also regulates fatty acid synthesis by inducing expression of critical lipogenic enzymes, including stearoyl-CoA desaturase-1 (Lee et al., 2008).”
- Endoplasmic reticulum stress: molecular mechanism and therapeutic targets (2023, background): “47,48 PERK/eIF2 α regulates glucose and lipid metabolism through C/EBP β and C/EBP α which directly regulate glucose production and PPAR γ .”
- Endoplasmic Reticulum Stress in Liver Disease (2010, background): “Liver specific deletion of Xbp1 reduces serum lipids in mice and decreases de novo lipogenesis in the liver [71].”
- Integrating Mechanisms for Insulin Resistance: Common Threads and Missing Links (2012, positive): “In contrast, liver-specific deletion of XBP1s (DXBP1s) reduced hepatic and plasma lipid concentrations in mice, associated with reduced expression of lipogenic enzymes (Lee et al., 2008).”
- The unfolded protein response: controlling cell fate decisions under ER stress and beyond (2012, background): “For example, XBP1 positively controls hepatic lipogenesis at basal levels, affecting cholesterol and triglyceride levels, possibly by directly transactivating key genes in this metabolic pathwa”
- Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP‐1c (2010, background): “The genetic deletion of XBP1 in liver leads to a decrease of the de novo lipid synthesis [65].”
- Energy Metabolism in the Liver (2014, positive): “Transient inhibition of both ACC1 and ACC2 in the liver decreases levels of hepatic malonyl-CoA and lipogenesis, increases β oxidation, and protects against hepatic steatosis (236).”
- Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “Ablation of XBP1 expression in the liver results in hypocholesterolaemia and hypotriglyceridaemia, demonstrating that XBP1 is a regulator of lipogenesis and implying that XBP1 activation following ER stress in the liver may contribute to dyslipidaemia”
- ER Stress Sensor XBP1 Controls Anti-tumor Immunity by Disrupting Dendritic Cell Homeostasis (2015, background): “Consistent with previous reports linking XBP1 and lipid biosynthesis (Lee et al., 2008; Sriburi et al., 2004), we found that enhanced intracellular lipid accumulation by tDCs required ROS generation and IRE1a/XBP1 activation.”
- Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, positive): “For example, genes involved in glucose output and glycogen synthesis such as glycogen synthase 1 are targets of XBP1 (Acosta-Alvear et al., 2007; Lee et al., 2008).”