Jiandie D. Lin

ORCID: 0000-0001-8069-5647
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About
Contact & Profiles
Research Areas
  • Adipose Tissue and Metabolism
  • Pancreatic function and diabetes
  • Adipokines, Inflammation, and Metabolic Diseases
  • Lipid metabolism and biosynthesis
  • Peroxisome Proliferator-Activated Receptors
  • Metabolism, Diabetes, and Cancer
  • Liver Disease Diagnosis and Treatment
  • Mitochondrial Function and Pathology
  • Circadian rhythm and melatonin
  • Autophagy in Disease and Therapy
  • Cancer-related molecular mechanisms research
  • Growth Hormone and Insulin-like Growth Factors
  • Endoplasmic Reticulum Stress and Disease
  • Dietary Effects on Health
  • Regulation of Appetite and Obesity
  • Lipid metabolism and disorders
  • Genetics, Aging, and Longevity in Model Organisms
  • Muscle Physiology and Disorders
  • Cardiovascular Disease and Adiposity
  • Diet, Metabolism, and Disease
  • Immune Cell Function and Interaction
  • Immune cells in cancer
  • Cancer, Hypoxia, and Metabolism
  • Diabetes and associated disorders
  • Chromatin Remodeling and Cancer

University of Michigan
2016-2025

Ann Arbor Center for Independent Living
2012-2023

Michigan Medicine
2021-2022

Michigan United
2012-2014

Washtenaw Community College
2012

UiT The Arctic University of Norway
2012

Harvard University Press
2004-2008

Gachon University
2008

Cellular Research (United States)
2008

Dana-Farber Cancer Institute
2002-2006

The YAP transcription coactivator has been implicated as an oncogene and is amplified in human cancers. Recent studies have established that phosphorylated inhibited by the Hippo tumor suppressor pathway. Here we demonstrate TEAD family factors are essential mediating YAP-dependent gene expression. also required for YAP-induced cell growth, oncogenic transformation, epithelial-mesenchymal transition. CTGF identified a direct target important growth. Moreover, functional relationship between...

10.1101/gad.1664408 article EN Genes & Development 2008-06-25

Maintaining muscle size and fiber composition requires contractile activity. Increased activity stimulates expression of the transcriptional coactivator PGC-1α (peroxisome proliferator-activated receptor γ 1α), which promotes fiber-type switching from glycolytic toward more oxidative fibers. In response to disuse or denervation, but also in fasting many systemic diseases, muscles undergo marked atrophy through a common set changes. FoxO family transcription factors play critical role this...

10.1073/pnas.0607795103 article EN Proceedings of the National Academy of Sciences 2006-10-20

Skeletal muscle adapts to chronic physical activity by inducing mitochondrial biogenesis and switching proportions of fibers from type II I. Several major factors involved in this process have been identified, such as the calcium/calmodulin-dependent protein kinase IV (CaMKIV), calcineurin A (CnA), transcriptional component peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α). Transgenic expression PGC-1α recently has shown dramatically increase content I skeletal muscle, but...

10.1073/pnas.1232352100 article EN Proceedings of the National Academy of Sciences 2003-05-22

Peroxisome proliferator-activated receptor gamma coactivator (PGC)-1alpha is a of nuclear receptors and other transcription factors that regulates several components energy metabolism, particularly certain aspects adaptive thermogenesis in brown fat skeletal muscle, hepatic gluconeogenesis, fiber type switching muscle. PGC-1alpha has been shown to induce mitochondrial biogenesis when expressed muscle cells, preliminary analysis suggested this molecule may specifically increase the fraction...

10.1074/jbc.m301850200 article EN cc-by Journal of Biological Chemistry 2003-07-01

Peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1) plays a critical role in regulating multiple aspects of energy metabolism, including adaptive thermogenesis, mitochondrial biogenesis, and fatty acid β-oxidation. Recently, this coactivator nuclear receptors/transcription factors has been shown to control hepatic gluconeogenesis, an important component the pathogenesis both type-1 type-2 diabetes. We described here cloning novel bona fide homologue PGC-1, PGC-1β (PGC-1 was...

10.1074/jbc.c100631200 article EN cc-by Journal of Biological Chemistry 2002-01-01

The induction of peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha), a key regulator mitochondriogenesis, is well-established under multiple physical exercise regimens, including, endurance, resistance, and sprint training. We wanted to determine if increased expression PGC-1alpha in muscle sufficient improve performance during vivo. demonstrate that muscle-specific improves the voluntary as well forced challenges. Additionally, transgenic mice exhibit an...

10.1152/japplphysiol.01231.2007 article EN Journal of Applied Physiology 2008-02-01

Metabolic dysfunction–associated steatohepatitis (MASH), formerly known as nonalcoholic (NASH), is an advanced stage of metabolic fatty liver disease. The pathogenic mechanisms MASH center on hepatocyte injury and the ensuing immune response within microenvironment. Recent work has implicated TREM2 + macrophages in various disease conditions, substantial induction NASH-associated (NAMs) serves a hallmark Despite this, through which NAMs contribute to pathogenesis remain poorly understood....

10.1126/scitranslmed.adk1866 article EN Science Translational Medicine 2024-03-13

The transcriptional coactivator PPAR gamma 1 α (PGC-1α) is a key regulator of metabolic processes such as mitochondrial biogenesis and respiration in muscle gluconeogenesis liver. Reduced levels PGC-1α humans have been associated with type II diabetes. contains negative regulatory domain that attenuates its activity. This regulation removed by phosphorylation p38 MAPK, an important kinase downstream cytokine signaling β-adrenergic brown fat. We describe here the identification p160 myb...

10.1101/gad.1152204 article EN Genes & Development 2004-01-26
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