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Articles by Sarah Warburton in JoVE
JoVE General
प्रोटिओमिक्स P2X2 ligand-gated कटियन चैनल के साथ बातचीत प्रोटीन की पहचान
1Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, 2Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, 3Department of Anesthesiology, Medicine and Physiology, David Geffen School of Medicine, University of California, Los Angeles
हम करने के लिए मस्तिष्क प्रोटीन है कि एटीपी gated P2X2 रिसेप्टर्स की पूरी लंबाई सी टर्मिनस करने के लिए बाध्य की पहचान के लिए एक सरल प्रोटोकॉल का वर्णन. एक्सटेंशन और सभी P2X रिसेप्टर्स करने के लिए इस दृष्टिकोण के व्यवस्थित आवेदन P2X रिसेप्टर संकेतन का एक बेहतर समझ के लिए नेतृत्व की उम्मीद है.
Other articles by Sarah Warburton on PubMed
Examining the Proteins of Functional Retinal Lipofuscin Using Proteomic Analysis As a Guide for Understanding Its Origin
To elucidate the origins of biologically active retinal lipofuscin (RLF) by examining its protein composition.
Proteomic and Phototoxic Characterization of Melanolipofuscin: Correlation to Disease and Model for Its Origin
Melanolipofuscin (MLF) is a complex granule, exhibiting properties of both melanosomes and lipofuscin (LF) granules, which accumulates in retinal pigment epithelial (RPE) cells and may contribute to the etiology of age-related macular degeneration (AMD). MLF accumulation has been reported by Feeney-Burns to more closely reflect the onset of AMD than the accumulation of lipofuscin. In an effort to assess the possible contribution MLF may have to the onset of AMD, we analyzed the phototoxicity and protein composition of MLF and compared those results to that of LF.
Cardiovascular Initiative of the Human Proteome Organisation, 5th Workshop October 2007, Seoul, Korea
The Cardiovascular Initiative (CVI) of the Human Proteome Organisation (HUPO) held its fifth workshop prior to the Sixth Annual HUPO World Congress in Seoul, Korea in October 2007. The objectives of this report are as follows: to trace the (relatively brief) history of the CVI for those who may not be acquainted with it; to highlight lectures given by members of the CVI during this Workshop; and to make the community aware of the aims of this Initiative, including collaborative projects currently under consideration.
Loss of Bmx Nonreceptor Tyrosine Kinase Prevents Pressure Overload-induced Cardiac Hypertrophy
Bmx nonreceptor tyrosine kinase has an established role in endothelial and lymphocyte signaling; however, its role in the heart is unknown. To determine whether Bmx participates in cardiac growth, we subjected mice deficient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC). In comparison with wild-type mice, which progressively developed massive hypertrophy following TAC, Bmx knockout mice were resistant to TAC-induced cardiac growth at the organ and cell level. Loss of Bmx preserved cardiac ejection fraction and decreased mortality following TAC. These findings are the first to demonstrate a necessary role for the Tec family of tyrosine kinases in the heart and reveal a novel regulator (Bmx) of pressure overload-induced hypertrophic growth.
Protein Phosphatase 2Cm is a Critical Regulator of Branched-chain Amino Acid Catabolism in Mice and Cultured Cells
The branched-chain amino acids (BCAA) are essential amino acids required for protein homeostasis, energy balance, and nutrient signaling. In individuals with deficiencies in BCAA, these amino acids can be preserved through inhibition of the branched-chain-alpha-ketoacid dehydrogenase (BCKD) complex, the rate-limiting step in their metabolism. BCKD is inhibited by phosphorylation of its E1alpha subunit at Ser293, which is catalyzed by BCKD kinase. During BCAA excess, phosphorylated Ser293 (pSer293) becomes dephosphorylated through the concerted inhibition of BCKD kinase and the activity of an unknown intramitochondrial phosphatase. Using unbiased, proteomic approaches, we have found that a mitochondrial-targeted phosphatase, PP2Cm, specifically binds the BCKD complex and induces dephosphorylation of Ser293 in the presence of BCKD substrates. Loss of PP2Cm completely abolished substrate-induced E1alpha dephosphorylation both in vitro and in vivo. PP2Cm-deficient mice exhibited BCAA catabolic defects and a metabolic phenotype similar to the intermittent or intermediate types of human maple syrup urine disease (MSUD), a hereditary disorder caused by defects in BCKD activity. These results indicate that PP2Cm is the endogenous BCKD phosphatase required for nutrient-mediated regulation of BCKD activity and suggest that defects in PP2Cm may be responsible for a subset of human MSUD.
Target Identification Using Drug Affinity Responsive Target Stability (DARTS)
Identifying the molecular targets for the beneficial or detrimental effects of small-molecule drugs is an important and currently unmet challenge. We have developed a method, drug affinity responsive target stability (DARTS), which takes advantage of a reduction in the protease susceptibility of the target protein upon drug binding. DARTS is universally applicable because it requires no modification of the drug and is independent of the mechanism of drug action. We demonstrate use of DARTS to identify known small-molecule-protein interactions and to reveal the eukaryotic translation initiation machinery as a molecular target for the longevity-enhancing plant natural product resveratrol. We envisage that DARTS will also be useful in global mapping of protein-metabolite interaction networks and in label-free screening of unlimited varieties of compounds for development as molecular imaging agents.
