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Trevor J. Biden

Researcher at Garvan Institute of Medical Research

Publications -  103
Citations -  9109

Trevor J. Biden is an academic researcher from Garvan Institute of Medical Research. The author has contributed to research in topics: Protein kinase C & Insulin. The author has an hindex of 46, co-authored 102 publications receiving 7757 citations. Previous affiliations of Trevor J. Biden include St. Vincent's Health System & University of New South Wales.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Endoplasmic reticulum stress contributes to beta cell apoptosis in type 2 diabetes.

D. R. Laybutt, +7 more
- 01 Feb 2007 - 
TL;DR: Evidence that endoplasmic reticulum (ER) stress occurs in type 2 diabetes and is required for aspects of the underlying beta cell failure is provided.
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Ceramide generation is sufficient to account for the inhibition of the insulin-stimulated PKB pathway in C2C12 skeletal muscle cells pretreated with palmitate

Carsten Schmitz-Peiffer, +2 more
- 20 Aug 1999 - 
TL;DR: It is concluded that palmitate-induced insulin resistance occurs by a mechanism distinct from that of unsaturated FFAs, and involves elevation of ceramide byde novo synthesis, leading to PKB inhibition without affecting IRS-1 function.
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Molecular cloning and characterization of PKC iota, an atypical isoform of protein kinase C derived from insulin-secreting cells.

Lisa Selbie, +3 more
- 15 Nov 1993 - 
TL;DR: This study identifies new PKC isoforms in the insulin-secreting cell line RINm5F that might be activated by the alterations in lipid metabolism that accompany nutrient-stimulated insulin release and suggests that PKC iota should be included in the atypical subgroup of PKCs whose definitive member is PKC zeta.
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Alterations in the expression and cellular localization of protein kinase C isozymes epsilon and theta are associated with insulin resistance in skeletal muscle of the high-fat-fed rat.

Carsten Schmitz-Peiffer, +6 more
- 01 Feb 1997 - 
TL;DR: While insulin infusion in glucose-clamped rats increased the proportion of PKC θ in the particulate fraction of red muscle, this was potentiated by fat-feeding, suggesting that the translocation is a consequence of altered lipid flux rather than a proximal event in insulin signaling.