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Conference Paper: Adipocyte fatty acid-binding protein potentiates toxic lipids-induced endoplasmic reticulum stress via suppression of JAK2-dependent autophagy
| Title | Adipocyte fatty acid-binding protein potentiates toxic lipids-induced endoplasmic reticulum stress via suppression of JAK2-dependent autophagy |
|---|---|
| Authors | |
| Keywords | Medical sciences |
| Issue Date | 2014 |
| Publisher | Hong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk |
| Citation | The 19th Medical Research Conference (MRC 2014), Department of Medicine, The University of Hong Kong, 18 January 2014. In Hong Kong Medical Journal, 2014, v. 20 suppl. 1, p. 23, abstract 30 How to Cite? |
| Abstract | INTRODUCTION: Chronic inflammation is the key link between obesity and its related metabolic complications. Endoplasmic reticulum (ER) stress is the potent trigger of inflammation in obese adipose tissue but how ER stress in immune cells relates to inflammation is unclear. Adipocyte fatty acid–binding protein (A-FABP) regulates endotoxin-induced inflammation in macrophages by forming a positive feedback loop with c-Jun-N terminal kinase (JNK) which is the downstream regulator of ER stress. Defective autophagy is shown in obese liver which leads to insulin resistance and elevated ER stress. Here we investigate the role of A-FABP in association with autophagy in potentiating toxic lipids-induced ER stress in macrophages … |
| Description | Oral Presentation |
| Persistent Identifier | http://hdl.handle.net/10722/202274 |
| ISSN | 2021 Impact Factor: 1.256 2020 SCImago Journal Rankings: 0.357 |
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Hoo, RLC | - |
| dc.contributor.author | Shu, L | - |
| dc.contributor.author | Lam, KSL | - |
| dc.contributor.author | Xu, A | - |
| dc.date.accessioned | 2014-09-02T08:07:47Z | - |
| dc.date.available | 2014-09-02T08:07:47Z | - |
| dc.date.issued | 2014 | - |
| dc.identifier.citation | The 19th Medical Research Conference (MRC 2014), Department of Medicine, The University of Hong Kong, 18 January 2014. In Hong Kong Medical Journal, 2014, v. 20 suppl. 1, p. 23, abstract 30 | - |
| dc.identifier.issn | 1024-2708 | - |
| dc.identifier.uri | http://hdl.handle.net/10722/202274 | - |
| dc.description | Oral Presentation | - |
| dc.description.abstract | INTRODUCTION: Chronic inflammation is the key link between obesity and its related metabolic complications. Endoplasmic reticulum (ER) stress is the potent trigger of inflammation in obese adipose tissue but how ER stress in immune cells relates to inflammation is unclear. Adipocyte fatty acid–binding protein (A-FABP) regulates endotoxin-induced inflammation in macrophages by forming a positive feedback loop with c-Jun-N terminal kinase (JNK) which is the downstream regulator of ER stress. Defective autophagy is shown in obese liver which leads to insulin resistance and elevated ER stress. Here we investigate the role of A-FABP in association with autophagy in potentiating toxic lipids-induced ER stress in macrophages … | - |
| dc.language | eng | - |
| dc.publisher | Hong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org.hk | - |
| dc.relation.ispartof | Hong Kong Medical Journal | - |
| dc.rights | Hong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press. | - |
| dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
| dc.subject | Medical sciences | - |
| dc.title | Adipocyte fatty acid-binding protein potentiates toxic lipids-induced endoplasmic reticulum stress via suppression of JAK2-dependent autophagy | en_US |
| dc.type | Conference_Paper | en_US |
| dc.identifier.email | Hoo, RLC: rubyhoo@hku.hk | - |
| dc.identifier.email | Lam, KSL: ksllam@hku.hk | - |
| dc.identifier.email | Xu, A: amxu@hku.hk | - |
| dc.description.nature | published_or_final_version | - |
| dc.identifier.hkuros | 237137 | - |
| dc.identifier.volume | 20 | - |
| dc.identifier.issue | suppl. 1 | - |
| dc.identifier.spage | 23, abstract 30 | - |
| dc.identifier.epage | 23, abstract 30 | - |
| dc.publisher.place | Hong Kong | - |
| dc.identifier.issnl | 1024-2708 | - |