A5053515605- Adipose Tissue and Metabolism
- PI3K/AKT/mTOR signaling in cancer
- Cancer, Hypoxia, and Metabolism
- Adipokines, Inflammation, and Metabolic Diseases
- Lipid metabolism and biosynthesis
- Protein Kinase Regulation and GTPase Signaling
- Muscle metabolism and nutrition
- Fungal and yeast genetics research
- Microtubule and mitosis dynamics
- Cancer, Lipids, and Metabolism
- Metabolism, Diabetes, and Cancer
- Polyamine Metabolism and Applications
- Mitochondrial Function and Pathology
- Pancreatic function and diabetes
- Diet and metabolism studies
- Ubiquitin and proteasome pathways
- Exercise and Physiological Responses
- RNA Research and Splicing
- Photosynthetic Processes and Mechanisms
- CRISPR and Genetic Engineering
- Sirtuins and Resveratrol in Medicine
- Hippo pathway signaling and YAP/TAZ
- Metabolomics and Mass Spectrometry Studies
- Genetics, Aging, and Longevity in Model Organisms
- Nuclear Structure and Function
University of Massachusetts Chan Medical School
2015-2024
Whitehead Institute for Biomedical Research
2004-2012
Massachusetts Institute of Technology
2004-2012
Allen Institute
2009-2012
Koch Institute for Integrative Cancer Research At MIT
2009-2012
Broad Institute
2005-2012
Howard Hughes Medical Institute
2009-2012
Institute of Molecular Medicine
2011
Deregulation of Akt/protein kinase B (PKB) is implicated in the pathogenesis cancer and diabetes. Akt/PKB activation requires phosphorylation Thr308 loop by phosphoinositide-dependent 1 (PDK1) Ser473 within carboxyl-terminal hydrophobic motif an unknown kinase. We show that Drosophila human cells target rapamycin (TOR) its associated protein rictor are necessary for a reduction or mammalian TOR (mTOR) expression inhibited effector. The rictor-mTOR complex directly phosphorylated on vitro...
Abstract Biologists can now prepare and image thousands of samples per day using automation, enabling chemical screens functional genomics (for example, RNA interference). Here we describe the first free, open-source system designed for flexible, high-throughput cell analysis, CellProfiler. CellProfiler address a variety biological questions quantitatively, including standard assays count, size, per-cell protein levels) complex morphological cell/organelle shape or subcellular patterns DNA staining).
Rapamycin, an inhibitor of mechanistic target rapamycin complex 1 (mTORC1), extends the life spans yeast, flies, and mice. Calorie restriction, which increases span insulin sensitivity, is proposed to function by inhibition mTORC1, yet paradoxically, chronic administration substantially impairs glucose tolerance action. We demonstrate that disrupted a second mTOR complex, mTORC2, in vivo mTORC2 was required for insulin-mediated suppression hepatic gluconeogenesis. Further, decreased mTORC1...
A flurry of reports indicates that we are entering a new phase in the development mammalian target rapamycin (mTOR)-based therapies for oncology. Here, summarize exciting findings regarding mTOR signaling and outlook inhibitors as tools to study pathway drugs clinic.
Neural crest cells are embryonic progenitors that generate numerous cell types in vertebrates. With single-cell analysis, we show mouse trunk neural become biased toward neuronal lineages when they delaminate from the tube, whereas cranial acquire ectomesenchyme potential dependent on activation of transcription factor Twist1. The choices make to sensory, glial, autonomic, or mesenchymal can be formalized as a series sequential binary decisions. Each branch decision tree involves initial...
The developmental origin of adipose tissue and what controls its distribution is poorly understood. By lineage tracing gene expression analysis in mice, we provide evidence that mesenchymal precursors expressing Myf5—which are thought to give rise only brown adipocytes skeletal muscle—also a subset white adipocytes. Furthermore, individual fats contain mixture adipocyte progenitor cells derived from Myf5+ Myf5neg lineages, the number which varies with depot location. Subsets originating both...
Abstract Adipose tissue de novo lipogenesis (DNL) positively influences insulin sensitivity, is reduced in obesity, and predicts resistance. Therefore, elucidating mechanisms controlling adipose DNL could lead to therapies for type 2 diabetes. Here, we report that mechanistic target of rapamycin complex (mTORC2) functions white (WAT) control expression the lipogenic transcription factor ChREBPβ. Conditionally deleting essential mTORC2 subunit Rictor mature adipocytes decreases ChREBPβ...