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Leonard F. Bjeldanes

Researcher at University of California, Berkeley

Publications -  129
Citations -  7717

Leonard F. Bjeldanes is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Diindolylmethane & 3,3'-Diindolylmethane. The author has an hindex of 50, co-authored 129 publications receiving 7422 citations. Previous affiliations of Leonard F. Bjeldanes include University of California.

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Aromatic hydrocarbon responsiveness-receptor agonists generated from indole-3-carbinol in vitro and in vivo: comparisons with 2,3,7,8-tetrachlorodibenzo-p-dioxin.

TL;DR: The aromatic hydrocarbon responsiveness-receptor Kd values are reported and it is shown that indolo[3,2-b]carbazole (ICZ) is produced from I3C in yields on the order of 0.01% in vitro and, after oral intubation, in vivo, and ICZ and related condensation products appear responsible for the enzyme-inducing effects of dietary I2C.
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Indole-3-carbinol Inhibits the Expression of Cyclin-dependent Kinase-6 and Induces a G1 Cell Cycle Arrest of Human Breast Cancer Cells Independent of Estrogen Receptor Signaling

TL;DR: The observations have uncovered a previously undefined antiproliferative pathway for I3C that implicates CDK6 as a target for cell cycle control in human breast cancer cells, and establish for the first time thatCDK6 gene expression can be inhibited in response to an extracellular antiprolifierative signal.
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Lipoxin A4: a new class of ligand for the Ah receptor.

TL;DR: The ability of the arachidonic acid metabolite, lipoxin A4, to bind to and activate the Ah receptor in Hepa-1 cells is reported and established as a new class of Ah receptors ligand, one that differs dramatically from classical Ah receptor ligands.
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Identification of the mutagens in cooked beef.

TL;DR: The PhIP, which contributes the highest mass content to the cooked meat, but has the lowest mutagenic potency, might ultimately make a significant contribution to the carcinogenicity.
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Bcl-2 family-mediated apoptotic effects of 3,3'-diindolylmethane (DIM) in human breast cancer cells.

TL;DR: It is demonstrated that DIM can induce apoptosis in breast cancer cells independent of estrogen receptor status by a process that is mediated by the modulated expression of the Bax/Bcl-2 family of apoptotic regulatory factors.