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Benjamin F. Cravatt

Researcher at Scripps Research Institute

Publications -  698
Citations -  69790

Benjamin F. Cravatt is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Fatty acid amide hydrolase & Anandamide. The author has an hindex of 131, co-authored 666 publications receiving 61932 citations. Previous affiliations of Benjamin F. Cravatt include Pfizer & Indiana University.

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Disruption of Fatty Acid Amide Hydrolase Activity Prevents the Effects of Chronic Stress on Anxiety and Amygdalar Microstructure

TL;DR: In this article, the extent to which the endocannabinoid system, which is known to regulate emotional behavior and neuroplasticity, contributes to changes in amygdalar structure and function following chronic stress was investigated.
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A Tandem Orthogonal Proteolysis Strategy for High-Content Chemical Proteomics

TL;DR: It is indicated that a wide range of functional residues are targeted by sulfonate ester probes and highlight the value of TOP-based chemical proteomics for the characterization of proteins and the residues that regulate their activity.
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Carcinoma and stromal enzyme activity profiles associated with breast tumor growth in vivo

TL;DR: A functional proteomic analysis of the human breast cancer line MDA-MB-231 grown in culture and as orthotopic xenograft tumors in the mammary fad pad of immunodeficient mice indicates that the in vivo environment of the mouse mammary fat pad cultivates the growth ofhuman breast cancer cells with elevated tumorigenic properties.
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Highly selective inhibitors of monoacylglycerol lipase bearing a reactive group that is bioisosteric with endocannabinoid substrates.

TL;DR: A distinct class of O-hexafluoroisopropyl (HFIP) carbamates are reported that inhibits MAGL in vitro and in vivo with excellent potency and greatly improved selectivity, including showing no detectable cross-reactivity with FAAH.
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Evaluation of fatty acid amide hydrolase inhibition in murine models of emotionality.

TL;DR: The present results indicate that the pharmacological inhibition or genetic deletion of FAAH is ineffective in standard mouse models of emotional reactivity.