White adipose tissue (WAT) is a highly dynamic organ and can respond rapidly to alterations in nutrient excess and deprivation, thereby fulfilling its major role in whole body energy homeostasis. Dysfunctional WAT leads to the etiology of a large number of metabolic disorders including type II diabetes and other metabolic syndrome. As the major cell type in WAT, a healthy, highly metabolic responsible adipocyte itself is essential in maintaining adipose tissue functions. However, it has been known that the functions of adipocyte start to fail under many pathophysiological conditions, such as obesity, metabolic stress, aging, lipodystrophy and others. The long term goal of my research is to understand what are the key factors and mechanisms that control adipocyte cellular functional set limit, beyond which WAT fails to function properly? To identify and characterize novel regulators, high throughput gene expression profiling, protein interaction mapping by proteomic mass spectrometry, CRISPR/RNAi screening and other systems-based approaches will be employed. My goal is to integrate the data obtained from these approaches and apply them back to in vivo mouse models. Studies for the molecular components and details of these regulatory machineries will help us to understand the mechanisms and factors that control adipocyte functional homeostasis, and furthermore to develop the potential biomarkers and drug targets for diagnosis, prognosis, and therapy to improve adipocyte quality and treat human obesity related metabolic diseases.
- Member, Evans Center for Interdisciplinary Biomedical Research, Boston University
- Gunma University, PhD
- China Medical University, MB
- Published on 12/15/2020
Wang H, Wan X, Pilch PF, Ellisen LW, Fried SK, Liu L. An AMPK-dependent, non-canonical p53 pathway plays a key role in adipocyte metabolic reprogramming. Elife. 2020 12 15; 9. PMID: 33320092.
- Published on 2/28/2020
Liu L. Lessons from cavin-1 deficiency. Biochem Soc Trans. 2020 02 28; 48(1):147-154. PMID: 31922193.
- Published on 5/24/2019
Wang H, Pilch PF, Liu L. Cavin-1/PTRF mediates insulin-dependent focal adhesion remodeling and ameliorates high-fat diet-induced inflammatory responses in mice. J Biol Chem. 2019 07 05; 294(27):10544-10552. PMID: 31126986.
- Published on 1/12/2018
Williams JJL, Alotaiq N, Mullen W, Burchmore R, Liu L, Baillie GS, Schaper F, Pilch PF, Palmer TM. Interaction of suppressor of cytokine signalling 3 with cavin-1 links SOCS3 function and cavin-1 stability. Nat Commun. 2018 01 12; 9(1):168. PMID: 29330478.
- Published on 3/9/2017
Ding SY, Liu L, Pilch PF. Muscular dystrophy in PTFR/cavin-1 null mice. JCI Insight. 2017 03 09; 2(5):e91023. PMID: 28289716.
- Published on 12/13/2016
Wang H, Liu L, Lin JZ, Aprahamian TR, Farmer SR. Browning of White Adipose Tissue with Roscovitine Induces a Distinct Population of UCP1+ Adipocytes. Cell Metab. 2016 Dec 13; 24(6):835-847. PMID: 27974179.
- Published on 8/16/2016
Liu L, Pilch PF. PTRF/Cavin-1 promotes efficient ribosomal RNA transcription in response to metabolic challenges. Elife. 2016 Aug 16; 5. PMID: 27528195.
- Published on 9/18/2015
Jedrychowski MP, Liu L, Laflamme CJ, Karastergiou K, Meshulam T, Ding SY, Wu Y, Lee MJ, Gygi SP, Fried SK, Pilch PF. Adiporedoxin, an upstream regulator of ER oxidative folding and protein secretion in adipocytes. Mol Metab. 2015 Nov; 4(11):758-70. PMID: 26629401.
- Published on 7/18/2014
Liu L, Hansen CG, Honeyman BJ, Nichols BJ, Pilch PF. Cavin-3 knockout mice show that cavin-3 is not essential for caveolae formation, for maintenance of body composition, or for glucose tolerance. PLoS One. 2014; 9(7):e102935. PMID: 25036884.
- Published on 2/7/2014
Ding SY, Lee MJ, Summer R, Liu L, Fried SK, Pilch PF. Pleiotropic effects of cavin-1 deficiency on lipid metabolism. J Biol Chem. 2014 Mar 21; 289(12):8473-83. PMID: 24509860.
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