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  1. Artikel ; Online: Recent breakthroughs in computational structural biology harnessing the power of sequences and structures.

    Mészáros, Bálint / Park, Electa / Malinverni, Duccio / Sejdiu, Besian I / Immadisetty, Kalyan / Sandhu, Manbir / Lang, Benjamin / Babu, M Madan

    Current opinion in structural biology

    2023  Band 80, Seite(n) 102608

    Abstract: Recent advances in computational approaches and their integration into structural biology enable tackling increasingly complex questions. Here, we discuss several key areas, highlighting breakthroughs and remaining challenges. Theoretical modeling has ... ...

    Abstract Recent advances in computational approaches and their integration into structural biology enable tackling increasingly complex questions. Here, we discuss several key areas, highlighting breakthroughs and remaining challenges. Theoretical modeling has provided tools to accurately predict and design protein structures on a scale currently difficult to achieve using experimental approaches. Molecular Dynamics simulations have become faster and more precise, delivering actionable information inaccessible by current experimental methods. Virtual screening workflows allow a high-throughput approach to discover ligands that bind and modulate protein function, while Machine Learning methods enable the design of proteins with new functionalities. Integrative structural biology combines several of these approaches, pushing the frontiers of structural and functional characterization to ever larger systems, advancing towards a complete understanding of the living cell. These breakthroughs will accelerate and significantly impact diverse areas of science.
    Mesh-Begriff(e) Computational Biology ; Proteins/chemistry ; Molecular Dynamics Simulation
    Chemische Substanzen Proteins
    Sprache Englisch
    Erscheinungsdatum 2023-05-12
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1068353-7
    ISSN 1879-033X ; 0959-440X
    ISSN (online) 1879-033X
    ISSN 0959-440X
    DOI 10.1016/j.sbi.2023.102608
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Homozygous loss of mouse tetraspanin CD82 enhances integrin αIIbβ3 expression and clot retraction in platelets.

    Uchtmann, Kristen / Park, Electa R / Bergsma, Alexis / Segula, Justin / Edick, Mathew J / Miranti, Cindy K

    Experimental cell research

    2015  Band 339, Heft 2, Seite(n) 261–269

    Abstract: Integrin αIIbβ3 is critical for platelet-mediated blood clotting. Tetraspanins are well-established regulators of integrins and genetic loss of tetraspanin CD151 or TSSC6 in mice leads to increased bleeding due to inadequate integrin αIIbβ3 outside-in ... ...

    Abstract Integrin αIIbβ3 is critical for platelet-mediated blood clotting. Tetraspanins are well-established regulators of integrins and genetic loss of tetraspanin CD151 or TSSC6 in mice leads to increased bleeding due to inadequate integrin αIIbβ3 outside-in signaling. Conversely, mild but enhanced integrin αIIbβ3 activation and hyperaggregation is observed in CD9 and CD63 null mice respectively. CD82 is reportedly expressed in platelets; however its function is unknown. Using genetically engineered CD82 null mice, we investigated the role of the tetraspanin CD82 in platelet activation. Loss of CD82 resulted in reduced bleed times in vivo. CD82 was present on the surface of both human and mouse platelets, and its levels did not change upon platelet activation or degranulation. No differences in platelet activation, degranulation, or aggregation in response to ADP or collagen were detected in CD82 null mice. However, the kinetics of clot retraction was enhanced, which was intrinsic to the CD82-null platelets. Integrin αIIbβ3 surface expression was elevated on the platelets from CD82 null mice and they displayed enhanced adhesion and tyrosine kinase signaling on fibrinogen. This is the first report on CD82 function in platelets; which we found intrinsically modulates clot retraction, integrin αIIbβ3 expression, cell adhesion, and tyrosine signaling.
    Mesh-Begriff(e) Animals ; Blood Platelets/metabolism ; Clot Retraction/genetics ; Humans ; Kangai-1 Protein/deficiency ; Kangai-1 Protein/genetics ; Mice ; Mice, Knockout ; Platelet Glycoprotein GPIIb-IIIa Complex/genetics ; Platelet Glycoprotein GPIIb-IIIa Complex/metabolism
    Chemische Substanzen Kangai-1 Protein ; Platelet Glycoprotein GPIIb-IIIa Complex
    Sprache Englisch
    Erscheinungsdatum 2015-12-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2015.11.006
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: MEK1 activation by PAK: a novel mechanism.

    Park, Electa R / Eblen, Scott T / Catling, Andrew D

    Cellular signalling

    2007  Band 19, Heft 7, Seite(n) 1488–1496

    Abstract: Extracellular signal-Regulated Kinase (ERK) controls a variety of cellular processes, including cell proliferation and cell motility. While oncogenic mutations in Ras and B-Raf result in deregulated ERK activity and proliferation and migration in some ... ...

    Abstract Extracellular signal-Regulated Kinase (ERK) controls a variety of cellular processes, including cell proliferation and cell motility. While oncogenic mutations in Ras and B-Raf result in deregulated ERK activity and proliferation and migration in some tumor cells, other tumors exhibit elevated ERK signaling in the absence of these mutations. Here we provide evidence that PAK can directly activate MEK1 by a mechanism distinct from conventional Ras/Raf mediated activation. We find that PAK phosphorylation of MEK1 serine 298 stimulates MEK1 autophosphorylation on the activation loop, and activation of MEK1 activity towards ERK in in vitro reconstitution experiments. Serines 218 and/or 222 in the MEK1 activation loop are required for PAK-stimulated MEK1 activity towards ERK. MEK2, which is a poor target for PAK phosphorylation in cells, is not activated in this manner. Tissue culture experiments verify that this mechanism is used in suspended fibroblasts expressing mutationally activated PAK1. We speculate that aberrant signaling through PAK may directly induce anchorage-independent MEK1 activation in tumor cells lacking oncogenic Ras or Raf mutations, and that this mechanism may contribute to localized MEK signaling in focal contacts and adhesions during cell adhesion or migration.
    Mesh-Begriff(e) Animals ; COS Cells ; Cell Adhesion ; Cercopithecus aethiops ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibroblasts/cytology ; Fibroblasts/enzymology ; Fibronectins/metabolism ; Humans ; MAP Kinase Kinase 1/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins B-raf/metabolism ; Rats ; Serine/metabolism ; p21-Activated Kinases ; ras Proteins/metabolism
    Chemische Substanzen Fibronectins ; Serine (452VLY9402) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; p21-Activated Kinases (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; ras Proteins (EC 3.6.5.2)
    Sprache Englisch
    Erscheinungsdatum 2007-07
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1002702-6
    ISSN 0898-6568
    ISSN 0898-6568
    DOI 10.1016/j.cellsig.2007.01.018
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration.

    Park, Electa R / Pullikuth, Ashok K / Bailey, Evangeline M / Mercante, Donald E / Catling, Andrew D

    Cell communication and signaling : CCS

    2009  Band 7, Seite(n) 26

    Abstract: ERK signaling regulates focal adhesion disassembly during cell movement, and increased ERK signaling frequently contributes to enhanced motility of human tumor cells. We previously found that the ERK scaffold MEK Partner 1 (MP1) is required for focal ... ...

    Abstract ERK signaling regulates focal adhesion disassembly during cell movement, and increased ERK signaling frequently contributes to enhanced motility of human tumor cells. We previously found that the ERK scaffold MEK Partner 1 (MP1) is required for focal adhesion disassembly in fibroblasts. Here we test the hypothesis that MP1-dependent ERK signaling regulates motility of DU145 prostate cancer cells. We find that MP1 is required for motility on fibronectin, but not for motility stimulated by serum or EGF. Surprisingly, MP1 appears not to function through its known binding partners MEK1 or PAK1, suggesting the existence of a novel pathway by which MP1 can regulate motility on fibronectin. MP1 may function by regulating the stability or expression of paxillin, a key regulator of motility.
    Sprache Englisch
    Erscheinungsdatum 2009-11-23
    Erscheinungsland England
    Dokumenttyp Journal Article
    ISSN 1478-811X
    ISSN (online) 1478-811X
    DOI 10.1186/1478-811X-7-26
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Differential requirement for MEK Partner 1 in DU145 prostate cancer cell migration

    Bailey Evangeline M / Pullikuth Ashok K / Park Electa R / Mercante Donald E / Catling Andrew D

    Cell Communication and Signaling, Vol 7, Iss 1, p

    2009  Band 26

    Abstract: Abstract ERK signaling regulates focal adhesion disassembly during cell movement, and increased ERK signaling frequently contributes to enhanced motility of human tumor cells. We previously found that the ERK scaffold MEK Partner 1 (MP1) is required for ... ...

    Abstract Abstract ERK signaling regulates focal adhesion disassembly during cell movement, and increased ERK signaling frequently contributes to enhanced motility of human tumor cells. We previously found that the ERK scaffold MEK Partner 1 (MP1) is required for focal adhesion disassembly in fibroblasts. Here we test the hypothesis that MP1-dependent ERK signaling regulates motility of DU145 prostate cancer cells. We find that MP1 is required for motility on fibronectin, but not for motility stimulated by serum or EGF. Surprisingly, MP1 appears not to function through its known binding partners MEK1 or PAK1, suggesting the existence of a novel pathway by which MP1 can regulate motility on fibronectin. MP1 may function by regulating the stability or expression of paxillin, a key regulator of motility.
    Schlagwörter Medicine ; R ; Cytology ; QH573-671
    Sprache Englisch
    Erscheinungsdatum 2009-11-01T00:00:00Z
    Verlag BMC
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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