L
Lih-Ling Lin
Researcher at Genetics Institute, Inc.
Publications - 7
Citations - 4047
Lih-Ling Lin is an academic researcher from Genetics Institute, Inc.. The author has contributed to research in topics: Phosphorylation & Phospholipase A2. The author has an hindex of 4, co-authored 4 publications receiving 3973 citations.
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Journal ArticleDOI
cPLA2 is phosphorylated and activated by MAP kinase.
TL;DR: Treatment of cells with agents that stimulate the release of arachidonic acid causes increased serine phosphorylation and activation of cytosolic phospholipase A2 (cPLA2).
Journal ArticleDOI
A novel arachidonic acid-selective cytosolic PLA2 contains a Ca2+-dependent translocation domain with homology to PKC and GAP
James D. Clark,Lih-Ling Lin,Ronald W. Kriz,Chakkodabylu S. Ramesha,Lisa A. Sultzman,Alice Y. Lin,Nina Milona,John L. Knopf +7 more
TL;DR: The cloning and expression of a cDNA encoding a high molecular weight cytosolic phospholipase A2 (cPLA2) that has no detectable sequence homology with the secreted forms of PLA2 is reported and it is demonstrated that cPLA2 selectively cleaves arachidonic acid from natural membrane vesicles and translocates to membrane vESicles in response to physiologically relevant changes in free calcium.
Journal ArticleDOI
Cytosolic phospholipase A2 is coupled to hormonally regulated release of arachidonic acid.
TL;DR: The treatment of Chinese hamster ovary cells overexpressing cPLA2 with ATP or thrombin resulted in an increased release of arachidonic acid as compared with parental CHO cells, demonstrating the hormonal coupling of c PLA2.
Book ChapterDOI
Phospholipase C isozymes: structural and functional similarities.
Ronald W. Kriz,Lih-Ling Lin,Lisa A. Sultzman,Christine Ellis,Carl-Henrik Heldin,Tony Pawson,John L. Knopf +6 more
TL;DR: The overexpression of PLC Gamma 1 in Rat-2 cells results in increased phosphatidylinositol breakdown in response to PDGF treatment, demonstrating that PLC gamma 1 mediates this response.
Journal ArticleDOI
Identification of Pathogenic Immune Cell Subsets Associated With Checkpoint Inhibitor–Induced Myocarditis
Han-zhang Zhu,Francisco X Galdos,Daniel Lee,Sarah Waliany,Y. V. Huang,J J Ryan,Katherine Dang,Joel W. Neal,Heather A. Wakelee,Sunil Reddy,Sandy Srinivas,Lih-Ling Lin,Ronald M. Witteles,Holden T. Maecker,Mark M. Davis,Patricia K. Nguyen,Sean M. Wu +16 more
TL;DR: Clonal cytotoxic Temra CD8+ cells are significantly increased in the blood of patients with ICI myocarditis, corresponding to an analogous increase in effector cytot toxic CD8+, which may serve as attractive diagnostic/therapeutic targets for reducing life-threatening cardiac immune-related adverse events in ICI-treated patients with cancer.