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  1. Article ; Online: Molecular mechanism of activation of class IA phosphoinositide 3-kinases (PI3Ks) by membrane-localized HRas.

    Siempelkamp, Braden D / Rathinaswamy, Manoj K / Jenkins, Meredith L / Burke, John E

    The Journal of biological chemistry

    2017  Volume 292, Issue 29, Page(s) 12256–12266

    Abstract: Class IA PI3Ks are involved in the generation of the key lipid signaling molecule phosphatidylinositol 3,4,5-trisphosphate ( ... ...

    Abstract Class IA PI3Ks are involved in the generation of the key lipid signaling molecule phosphatidylinositol 3,4,5-trisphosphate (PIP
    MeSH term(s) Amino Acid Substitution ; Animals ; Class I Phosphatidylinositol 3-Kinases/chemistry ; Class I Phosphatidylinositol 3-Kinases/genetics ; Class I Phosphatidylinositol 3-Kinases/metabolism ; Deuterium Exchange Measurement ; Enzyme Activation ; Humans ; Lipid Bilayers/metabolism ; Liposomes ; Models, Molecular ; Mutagenesis, Site-Directed ; Peptide Fragments/chemistry ; Peptide Fragments/genetics ; Peptide Fragments/metabolism ; Phosphatidylinositol 3-Kinases/chemistry ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Point Mutation ; Protein Conformation ; Protein Interaction Domains and Motifs ; Protein Transport ; Proto-Oncogene Proteins p21(ras)/chemistry ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/metabolism ; Second Messenger Systems ; Sf9 Cells ; Spodoptera
    Chemical Substances Lipid Bilayers ; Liposomes ; Peptide Fragments ; Phosphatidylinositol Phosphates ; Recombinant Proteins ; phosphatidylinositol 3,4,5-triphosphate ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CA protein, human (EC 2.7.1.137) ; PIK3CD protein, human (EC 2.7.1.137) ; HRAS protein, human (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2017-05-17
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M117.789263
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
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  2. Article ; Online: Investigation of CH3NH3PbI3 degradation rates and mechanisms in controlled humidity environments using in situ techniques.

    Yang, Jinli / Siempelkamp, Braden D / Liu, Dianyi / Kelly, Timothy L

    ACS nano

    2015  Volume 9, Issue 2, Page(s) 1955–1963

    Abstract: Perovskite solar cells have rapidly advanced to the forefront of solution-processable photovoltaic devices, but the CH3NH3PbI3 semiconductor decomposes rapidly in moist air, limiting their commercial utility. In this work, we report a quantitative and ... ...

    Abstract Perovskite solar cells have rapidly advanced to the forefront of solution-processable photovoltaic devices, but the CH3NH3PbI3 semiconductor decomposes rapidly in moist air, limiting their commercial utility. In this work, we report a quantitative and systematic investigation of perovskite degradation processes. By carefully controlling the relative humidity of an environmental chamber and using in situ absorption spectroscopy and in situ grazing incidence X-ray diffraction to monitor phase changes in perovskite degradation process, we demonstrate the formation of a hydrated intermediate containing isolated PbI6(4-) octahedra as the first step of the degradation mechanism. We also show that the identity of the hole transport layer can have a dramatic impact on the stability of the underlying perovskite film, suggesting a route toward perovskite solar cells with long device lifetimes and a resistance to humidity.
    Language English
    Publishing date 2015-02-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1936-086X
    ISSN (online) 1936-086X
    DOI 10.1021/nn506864k
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Conformational disruption of PI3Kδ regulation by immunodeficiency mutations in

    Dornan, Gillian L / Siempelkamp, Braden D / Jenkins, Meredith L / Vadas, Oscar / Lucas, Carrie L / Burke, John E

    Proceedings of the National Academy of Sciences of the United States of America

    2017  Volume 114, Issue 8, Page(s) 1982–1987

    Abstract: Activated PI3K Delta Syndrome (APDS) is a primary immunodeficiency disease caused by activating mutations in either the leukocyte-restricted p110δ catalytic ( ...

    Abstract Activated PI3K Delta Syndrome (APDS) is a primary immunodeficiency disease caused by activating mutations in either the leukocyte-restricted p110δ catalytic (
    Language English
    Publishing date 2017-02-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1617244114
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1148: Show issues Location:
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  4. Article ; Online: Ras Binder Induces a Modified Switch-II Pocket in GTP and GDP States.

    Gentile, Daniel R / Rathinaswamy, Manoj K / Jenkins, Meredith L / Moss, Steven M / Siempelkamp, Braden D / Renslo, Adam R / Burke, John E / Shokat, Kevan M

    Cell chemical biology

    2017  Volume 24, Issue 12, Page(s) 1455–1466.e14

    Abstract: Covalent inhibitors of K-Ras(G12C) have been reported that exclusively recognize the GDP state. Here, we utilize disulfide tethering of a non-natural cysteine (K-Ras(M72C)) to identify a new switch-II pocket (S-IIP) binding ligand (2C07) that engages the ...

    Abstract Covalent inhibitors of K-Ras(G12C) have been reported that exclusively recognize the GDP state. Here, we utilize disulfide tethering of a non-natural cysteine (K-Ras(M72C)) to identify a new switch-II pocket (S-IIP) binding ligand (2C07) that engages the active GTP state. Co-crystal structures of 2C07 bound to H-Ras(M72C) reveal binding in a cryptic groove we term S-IIG. In the GppNHp state, 2C07 binding to a modified S-IIP pushes switch I away from the nucleotide, breaking the network of polar contacts essential for adopting the canonical GTP state. Biochemical studies show that 2C07 alters nucleotide preference and inhibits SOS binding and catalyzed nucleotide exchange. 2C07 was converted to irreversible covalent analogs, which target both nucleotide states, inhibit PI3K activation in vitro, and function as occupancy probes to detect reversible engagement in competition assays. Targeting both nucleotide states opens the possibility of inhibiting oncogenic mutants of Ras, which exist predominantly in the GTP state in cells.
    MeSH term(s) Binding Sites ; Guanosine Diphosphate/chemistry ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/chemistry ; Guanosine Triphosphate/metabolism ; Humans ; Models, Molecular ; Molecular Structure ; Mutation ; Proto-Oncogene Proteins p21(ras)/chemistry ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism
    Chemical Substances Guanosine Diphosphate (146-91-8) ; Guanosine Triphosphate (86-01-1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2017-10-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2451-9448
    ISSN (online) 2451-9448
    DOI 10.1016/j.chembiol.2017.08.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Novel PIK3CD mutations affecting N-terminal residues of p110δ cause activated PI3Kδ syndrome (APDS) in humans.

    Takeda, Andrew J / Zhang, Yu / Dornan, Gillian L / Siempelkamp, Braden D / Jenkins, Meredith L / Matthews, Helen F / McElwee, Joshua J / Bi, Weimin / Seeborg, Filiz O / Su, Helen C / Burke, John E / Lucas, Carrie L

    The Journal of allergy and clinical immunology

    2017  Volume 140, Issue 4, Page(s) 1152–1156.e10

    MeSH term(s) Adolescent ; Adult ; Child ; Class I Phosphatidylinositol 3-Kinases/genetics ; Female ; Humans ; Immunologic Deficiency Syndromes/genetics ; Male ; Mutation
    Chemical Substances Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CD protein, human (EC 2.7.1.137)
    Language English
    Publishing date 2017-04-13
    Publishing country United States
    Document type Case Reports ; Letter ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2017.03.026
    Database MEDical Literature Analysis and Retrieval System OnLINE

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