L
Lufen Chang
Researcher at University of California, San Diego
Publications - 15
Citations - 13795
Lufen Chang is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Kinase & Signal transduction. The author has an hindex of 14, co-authored 14 publications receiving 13318 citations. Previous affiliations of Lufen Chang include City of Hope National Medical Center.
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Journal ArticleDOI
Mammalian MAP kinase signalling cascades
Lufen Chang,Michael Karin +1 more
TL;DR: Recent studies have begun to shed light on the physiological functions of MAPK cascades in the control of gene expression, cell proliferation and programmed cell death.
Journal ArticleDOI
A central role for JNK in obesity and insulin resistance
Jiro Hirosumi,Gurol Tuncman,Lufen Chang,Cem Z. Görgün,K. Teoman Uysal,Kazuhisa Maeda,Michael Karin,Gökhan S. Hotamisligil +7 more
TL;DR: It is shown that JNK activity is abnormally elevated in obesity and an absence of JNK1 results in decreased adiposity, significantly improved insulin sensitivity and enhanced insulin receptor signalling capacity in two different models of mouse obesity.
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Reactive Oxygen Species Promote TNFα-Induced Death and Sustained JNK Activation by Inhibiting MAP Kinase Phosphatases
TL;DR: It is shown that TNFalpha-induced ROS, whose accumulation is suppressed by mitochondrial superoxide dismutase, cause oxidation and inhibition of JNK-inactivating phosphatases by converting their catalytic cysteine to sulfenic acid, which results in sustained JNK activation, which is required for cytochrome c release and caspase 3 cleavage.
Journal ArticleDOI
c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis
Zuoning Han,David L. Boyle,Lufen Chang,Brydon L. Bennett,Michael Karin,Li Yang,Anthony M. Manning,Gary S. Firestein +7 more
TL;DR: The novel JNK inhibitor SP600125 completely blocked IL-1--induced accumulation of phospho-Jun and induction of c-Jun transcription in synoviocytes and in joint arthritis, indicating that JNK is an important therapeutic target for RA.
Journal ArticleDOI
The E3 Ubiquitin Ligase Itch Couples JNK Activation to TNFα-induced Cell Death by Inducing c-FLIPL Turnover
Lufen Chang,Hideaki Kamata,Giovanni Solinas,Jun-Li Luo,Shin Maeda,K. Venuprasad,Yun Cai Liu,Michael Karin +7 more
TL;DR: JNK antagonizes NF-kappaB during TNFalpha signaling by promoting the proteasomal elimination of c-FLIP(L), an inhibitor of caspase-8 and E3 ubiquitin ligase Itch.