Peter‐James H. Zushin

ORCID: 0000-0002-1915-2181
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About
Contact & Profiles
Research Areas
  • Adipose Tissue and Metabolism
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Peroxisome Proliferator-Activated Receptors
  • Metabolism, Diabetes, and Cancer
  • Cancer, Lipids, and Metabolism
  • Mitochondrial Function and Pathology
  • Lipid metabolism and biosynthesis
  • Pancreatic function and diabetes
  • Peptidase Inhibition and Analysis
  • Diabetes Treatment and Management
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Adipokines, Inflammation, and Metabolic Diseases
  • 3D Printing in Biomedical Research
  • Cellular Mechanics and Interactions
  • Proteoglycans and glycosaminoglycans research
  • Microfluidic and Bio-sensing Technologies
  • RNA modifications and cancer
  • Metabolomics and Mass Spectrometry Studies
  • Cell Adhesion Molecules Research
  • Drug Transport and Resistance Mechanisms
  • Muscle metabolism and nutrition
  • Polymer Surface Interaction Studies
  • Clinical Nutrition and Gastroenterology
  • Cholesterol and Lipid Metabolism
  • Regulation of Appetite and Obesity

University of California, Berkeley
2017-2024

Stanford University
2024

Beth Israel Deaconess Medical Center
2020

Harvard University
2014-2020

Brigham and Women's Hospital
2014-2018

Berkeley College
2017

University of Akron
2009

Organs-on-a-chip possess a promising future as drug screening assays and testbeds for disease modeling in the context of both single-organ systems multi-organ-chips.

10.1039/c6lc01590e article EN Lab on a Chip 2017-01-01

The inappropriate release of free fatty acids from obese adipose tissue stores has detrimental effects on metabolism, but key molecular mechanisms controlling FFA adipocytes remain undefined. Although obesity promotes systemic inflammation, we find activation the inflammation-associated Mitogen Activated Protein kinase ERK occurs specifically in tissues mice, and provide evidence that adipocyte may explain exaggerated lipolysis observed obesity.We genetic pharmacological inhibition MEK/ERK...

10.1016/j.molmet.2018.03.012 article EN cc-by Molecular Metabolism 2018-03-29

Understanding how loci identified by genome wide association studies (GWAS) contribute to pathogenesis requires new mechanistic insights. Variants within CDKAL1 are strongly linked an increased risk of developing type 2 diabetes and obesity. Investigations in mouse models have focused on the function Cdkal1 as a tRNALys modifier downstream effects loss pro-insulin translational fidelity pancreatic β−cells. However, is broadly expressed other metabolically relevant tissues, including adipose...

10.1016/j.molmet.2017.07.013 article EN cc-by Molecular Metabolism 2017-07-31

Abstract Coenzyme Q (CoQ) is essential for mitochondrial respiration and required thermogenic activity in brown adipose tissues (BAT). CoQ deficiency leads to a wide range of pathological manifestations, but mechanistic consequences specific tissues, such as BAT, remain poorly understood. Here, we show that pharmacological or genetic BAT stress signals causing accumulation cytosolic RNAs activation the eIF2α kinase PKR, resulting integrated response (ISR) with suppression UCP1 induction...

10.1038/s44318-023-00008-x article EN cc-by The EMBO Journal 2024-01-11

Abstract Chronic white adipose tissue (WAT) inflammation has been recognized as a critical early event in the pathogenesis of obesity‐related disorders. This process is characterized by increased residency proinflammatory M1 macrophages WAT. However, lack an isogenic human macrophage‐adipocyte model limited biological studies and drug discovery efforts, highlighting need for stem cell‐based approaches. Here, induced pluripotent cell (iPSC) derived (iMACs) adipocytes (iADIPOs) are cocultured...

10.1002/smll.202203725 article EN cc-by-nc-nd Small 2023-04-27

Hyaluronic acid (HA), the primary component of brain extracellular matrix, is increasingly used to model neuropathological processes, including glioblastoma (GBM) tumor invasion. While elastic hydrogels based on crosslinked low-molecular-weight (LMW) HA are widely exploited for this purpose and have proven valuable discovery screening, tissue both viscoelastic rich in high-MW (HMW) HA, it remains unclear how these differences influence To address question, comprised either HMW (1.5 MDa) or...

10.1002/adma.202404885 article EN Advanced Materials 2024-11-07

Abstract Altered lipid metabolism is a common hallmark of various cancers, including intrahepatic cholangiocarcinoma (ICC), highly lethal carcinoma that lacks effective treatment options. To elucidate the changes in ICC, we coupled expression firefly luciferase gene (FFL) to AKT1 (AKT-FFL) via an IRES linker, and then hydrodynamically injected mice with AKT-FFL Notch1 intracellular cytoplasmic domain (NICD) establish luciferase-positive ICC model. This model not only enabled us monitor...

10.1158/1541-7786.mcr-23-0389 article EN Molecular Cancer Research 2024-02-15

Hyaluronic acid (HA), the primary component of brain extracellular matrix, is increasingly used to model neuropathological processes, including glioblastoma (GBM) tumor invasion. While elastic hydrogels based on crosslinked low-molecular-weight (LMW) HA are widely exploited for this purpose and have proven valuable discovery screening, tissue both viscoelastic rich in high-MW (HMW) HA, it remains unclear how these differences influence To address question, comprised either HMW (1.5 MDa) or...

10.1101/2024.04.04.588167 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-04-06

Coenzyme Q (CoQ, aka ubiquinone) is a key component of the mitochondrial electron transport chain (ETC) and membrane-incorporated antioxidant. CoQ10 deficiencies encompass heterogeneous spectrum clinical phenotypes can be caused by hereditary mutations in biosynthesis pathway or result from pharmacological interventions such as HMG-CoA Reductase inhibitors, statins, which are widely used to treat hypercholesterolemia prevent cardiovascular disease. How CoQ deficiency affects individual...

10.3390/antiox12010014 article EN cc-by Antioxidants 2022-12-22

Impaired white adipose tissue (WAT) function has been recognized as a critical early event in obesity-driven disorders, but high buoyancy, fragility, and heterogeneity of primary adipocytes have largely prevented their use drug discovery efforts highlighting the need for human stem cell-based approaches. Here, cells are utilized to derive metabolically functional 3D (iADIPO) microphysiological system (MPS). Surprisingly, previously reported WAT differentiation approaches create insulin...

10.1002/smll.202103157 article EN Small 2021-11-10

Abstract Human genetics has been instrumental in identification of genetic variants linked to type 2 diabetes. Recently a rare, putative loss-of-function mutation the orphan G-protein coupled receptor 151 ( GPR151 ) was found be associated with lower odds ratio for diabetes, but mechanism behind this association remained elusive. Here we show that Gpr151 is fasting- and glucagon-responsive hepatic gene which regulates gluconeogenesis. ablation mice leads suppression gluconeogenesis genes...

10.1038/s41467-022-35069-9 article EN cc-by Nature Communications 2022-12-01

<div>Abstract<p>Altered lipid metabolism is a common hallmark of various cancers, including intrahepatic cholangiocarcinoma (ICC), highly lethal carcinoma that lacks effective treatment options. To elucidate the changes in ICC, we coupled expression firefly luciferase gene (FFL) to <i>AKT1</i> (<i>AKT-FFL</i>) via an IRES linker, and then hydrodynamically injected mice with AKT-FFL <i>Notch1</i> intracellular cytoplasmic domain...

10.1158/1541-7786.c.7267993.v1 preprint EN 2024-06-04

<div>Abstract<p>Altered lipid metabolism is a common hallmark of various cancers, including intrahepatic cholangiocarcinoma (ICC), highly lethal carcinoma that lacks effective treatment options. To elucidate the changes in ICC, we coupled expression firefly luciferase gene (FFL) to <i>AKT1</i> (<i>AKT-FFL</i>) via an IRES linker, and then hydrodynamically injected mice with AKT-FFL <i>Notch1</i> intracellular cytoplasmic domain...

10.1158/1541-7786.c.7267993 preprint EN 2024-06-04
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