Pavel Krejci

Summary

Affiliation: Cedars-Sinai Medical Center
Country: USA

Publications

  1. pmc NF449 is a novel inhibitor of fibroblast growth factor receptor 3 (FGFR3) signaling active in chondrocytes and multiple myeloma cells
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
    J Biol Chem 285:20644-53. 2010
  2. ncbi Fibroblast growth factors 1, 2, 17, and 19 are the predominant FGF ligands expressed in human fetal growth plate cartilage
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, California 90048, USA
    Pediatr Res 61:267-72. 2007
  3. pmc Breast cancer-specific mutations in CK1epsilon inhibit Wnt/beta-catenin and activate the Wnt/Rac1/JNK and NFAT pathways to decrease cell adhesion and promote cell migration
    Silvie Foldynová-Trantírková
    Biology Centre AS CR, V, V, I, and University of South Bohemia, Branisovska 31, Ceske Budejovice, Czech Republic
    Breast Cancer Res 12:R30. 2010
  4. ncbi Bisindolylmaleimide I suppresses fibroblast growth factor-mediated activation of Erk MAP kinase in chondrocytes by preventing Shp2 association with the Frs2 and Gab1 adaptor proteins
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, California 90048, USA
    J Biol Chem 282:2929-36. 2007
  5. ncbi Simple, mammalian cell-based assay for identification of inhibitors of the Erk MAP kinase pathway
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, SSB 3, 8700 Beverly Blvd, Los Angeles, CA 90048, USA
    Invest New Drugs 25:391-5. 2007
  6. pmc Analysis of STAT1 activation by six FGFR3 mutants associated with skeletal dysplasia undermines dominant role of STAT1 in FGFR3 signaling in cartilage
    Pavel Krejci
    Department of Animal Physiology and Immunology, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic
    PLoS ONE 3:e3961. 2008
  7. pmc Fibroblast growth factor inhibits interferon gamma-STAT1 and interleukin 6-STAT3 signaling in chondrocytes
    Pavel Krejci
    Institute of Experimental Biology, Masaryk University, 61137 Brno, Czech Republic
    Cell Signal 21:151-60. 2009
  8. pmc FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence
    Pavel Krejci
    Institute of Experimental Biology, Masaryk University, 61137 Brno, Czech Republic
    Bone 47:102-10. 2010
  9. ncbi STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes
    Pavel Krejci
    Institute of Experimental Biology, Masaryk University, 61137 Brno, Czech Republic
    J Cell Sci 121:272-81. 2008
  10. ncbi Interaction of fibroblast growth factor and C-natriuretic peptide signaling in regulation of chondrocyte proliferation and extracellular matrix homeostasis
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
    J Cell Sci 118:5089-100. 2005

Collaborators

  • William R Wilcox
  • Vitezslav Bryja
  • Deborah Krakow
  • Jiri Mayer
  • Michael Doubek
  • David Chitayat
  • David L Rimoin
  • John M Graham
  • Daniel H Cohn
  • Alois Kozubik
  • Igor Cervenka
  • Ondrej Bernatik
  • Marketa Kaucka
  • Fatih Ezgu
  • Ralph S Lachman
  • Hane Lee
  • Amy E Merrill
  • Gunnar Schulte
  • Silvie Foldynová-Trantírková
  • Katerina Pejchalova
  • Yvona Brychtova
  • Pavlína Janovská
  • Sarka Pospisilova
  • Jirina Prochazkova
  • Karla Plevova
  • Jan Verner
  • Boris Tichy
  • Petra Ovesna
  • Sarka Pavlova
  • Archana Mishra
  • Jana Kotaskova
  • Kristine D Estrada
  • Brian Idoni
  • Haynes Robinson
  • Stuart W Tompson
  • Hannah Deixler
  • Anna Sarukhanov
  • Natalia Camacho
  • Karen M Lyons
  • Cynthia J Curry
  • Stanley F Nelson
  • Jan Masek
  • Ranjani Sri Ganji
  • Jacomijn P Dijksterhuis
  • Tilman Polonio
  • Joshua Wolf
  • Peter Konik
  • J Silvio Gutkind
  • Eva Brumovská
  • Wulf Blankenfeldt
  • Tomas Dolezal
  • Lukas Trantirek
  • Petra Sekyrova
  • Katerina Tmejová

Detail Information

Publications22

  1. pmc NF449 is a novel inhibitor of fibroblast growth factor receptor 3 (FGFR3) signaling active in chondrocytes and multiple myeloma cells
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
    J Biol Chem 285:20644-53. 2010
    ..Our data identify NF449 as a novel antagonist of FGFR3 signaling, useful for FGFR3 inhibition alone or in combination with inhibitors that target the ATP binding site...
  2. ncbi Fibroblast growth factors 1, 2, 17, and 19 are the predominant FGF ligands expressed in human fetal growth plate cartilage
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, California 90048, USA
    Pediatr Res 61:267-72. 2007
    ..We conclude that FGF1, 2, 17, and 19 are the predominant FGF ligands present in developing human cartilage that are, with the exception of FGF19, experimentally capable of inhibiting chondrocyte proliferation...
  3. pmc Breast cancer-specific mutations in CK1epsilon inhibit Wnt/beta-catenin and activate the Wnt/Rac1/JNK and NFAT pathways to decrease cell adhesion and promote cell migration
    Silvie Foldynová-Trantírková
    Biology Centre AS CR, V, V, I, and University of South Bohemia, Branisovska 31, Ceske Budejovice, Czech Republic
    Breast Cancer Res 12:R30. 2010
    ..Because CK1epsilon is a crucial regulator of the Wnt signaling cascades, we determined how these CK1epsilon mutations interfere with the Wnt pathway and affect the behavior of epithelial breast cancer cell lines...
  4. ncbi Bisindolylmaleimide I suppresses fibroblast growth factor-mediated activation of Erk MAP kinase in chondrocytes by preventing Shp2 association with the Frs2 and Gab1 adaptor proteins
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, California 90048, USA
    J Biol Chem 282:2929-36. 2007
    ..Moreover, treatment with PKClambda/zeta pseudosubstrate lead to significant reduction of FGF2-mediated activation of Erk, suggesting involvement of an atypical PKC...
  5. ncbi Simple, mammalian cell-based assay for identification of inhibitors of the Erk MAP kinase pathway
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, SSB 3, 8700 Beverly Blvd, Los Angeles, CA 90048, USA
    Invest New Drugs 25:391-5. 2007
    ..A major advantage of this system is exclusion of toxic compounds as false-positive hits, given the nature of the RCS response to inhibition of the Erk pathway, i.e. growth...
  6. pmc Analysis of STAT1 activation by six FGFR3 mutants associated with skeletal dysplasia undermines dominant role of STAT1 in FGFR3 signaling in cartilage
    Pavel Krejci
    Department of Animal Physiology and Immunology, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic
    PLoS ONE 3:e3961. 2008
    ..Other pathways such as ERK should therefore be considered as central to pathological FGFR3 signaling in cartilage...
  7. pmc Fibroblast growth factor inhibits interferon gamma-STAT1 and interleukin 6-STAT3 signaling in chondrocytes
    Pavel Krejci
    Institute of Experimental Biology, Masaryk University, 61137 Brno, Czech Republic
    Cell Signal 21:151-60. 2009
    ..Since cytokine-gp130 signaling represents an important positive regulator of cartilage, its inhibition may contribute to the growth-inhibitory effect of FGFR3 in cartilage...
  8. pmc FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence
    Pavel Krejci
    Institute of Experimental Biology, Masaryk University, 61137 Brno, Czech Republic
    Bone 47:102-10. 2010
    ..Our data support a model whereby FGFR3 signaling inhibits cartilage growth via exploiting cellular responses originally designed to eliminate cells harboring activated oncogenes...
  9. ncbi STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytes
    Pavel Krejci
    Institute of Experimental Biology, Masaryk University, 61137 Brno, Czech Republic
    J Cell Sci 121:272-81. 2008
    ....
  10. ncbi Interaction of fibroblast growth factor and C-natriuretic peptide signaling in regulation of chondrocyte proliferation and extracellular matrix homeostasis
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
    J Cell Sci 118:5089-100. 2005
    ..We conclude that CNP utilizes both direct and indirect ways to counteract the effects of FGF signaling in a chondrocyte environment...
  11. ncbi C-natriuretic peptide: an important regulator of cartilage
    Katerina Pejchalova
    Medical Genetics Institute, Cedars Sinai Medical Center, 8700 Beverly Blvd, SSB 3, Los Angeles, CA 90048, USA
    Mol Genet Metab 92:210-5. 2007
    ..This review summarizes our current knowledge about the mechanism of CNP signaling in cartilage, areas for future investigation and its potential therapeutic uses...
  12. pmc Receptor tyrosine kinases activate canonical WNT/β-catenin signaling via MAP kinase/LRP6 pathway and direct β-catenin phosphorylation
    Pavel Krejci
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, California, United States of America
    PLoS ONE 7:e35826. 2012
    ..We conclude that signaling via ERK/LRP6 pathway and direct β-catenin phosphorylation at Tyr142 represent two mechanisms used by various receptor tyrosine kinase systems to activate canonical WNT signaling...
  13. pmc Mitogen-activated protein kinases promote WNT/beta-catenin signaling via phosphorylation of LRP6
    Igor Cervenka
    Institute of Experimental Biology, Faculty of Science, Masaryk University, CZ 611 37 Brno, Czech Republic
    Mol Cell Biol 31:179-89. 2011
    ..Moreover, direct phosphorylation of LRP6 by MAPKs provides a unique point for convergence between WNT/β-catenin signaling and mitogenic pathways...
  14. ncbi FGF2 inhibits proliferation and alters the cartilage-like phenotype of RCS cells
    Pavel Krejci
    Steven Spielberg Pediatric Research Center, Burns and Allen Research Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
    Exp Cell Res 297:152-64. 2004
    ..Both p21(WAF1) and p27(Kip1) accumulated upon FGF2 treatment, but this accumulation occurred at the protein level at least partially due to interaction with transcriptionally induced cyclin D1...
  15. pmc Molecular pathology of the fibroblast growth factor family
    Pavel Krejci
    Department of Immunology and Animal Physiology, Institute of Experimental Biology, Masaryk University, Brno, Czech Republic
    Hum Mutat 30:1245-55. 2009
    ..We review the current knowledge about the molecular pathology of the FGF family...
  16. ncbi The paradox of FGFR3 signaling in skeletal dysplasia: why chondrocytes growth arrest while other cells over proliferate
    Pavel Krejci
    Department of Biology, Faculty of Medicine, Masaryk University, Brno, Czech Republic Department of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic Department of Cytokinetics, Institute of Biophysics AS CR, Brno, Czech Republic Department of Orthopaedic Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA Electronic address
    Mutat Res Rev Mutat Res 759:40-8. 2014
    ..Subsequent inhibition of chondrocyte proliferation in FGFR3-related skeletal dysplasias and RASopathies is proposed to result from activation of defense mechanisms that originally evolved to safeguard mammalian organisms against cancer. ..
  17. pmc Sequential activation and inactivation of Dishevelled in the Wnt/beta-catenin pathway by casein kinases
    Ondrej Bernatik
    Institute of Experimental Biology, Masaryk University, 61137 Brno, Czech Republic
    J Biol Chem 286:10396-410. 2011
    ..We propose a multistep and multikinase model for Dvl activation in the Wnt/β-catenin pathway that uncovers a built-in de-activation mechanism that is triggered by activating phosphorylation of Dvl by CK1δ/ε...
  18. doi The planar cell polarity pathway drives pathogenesis of chronic lymphocytic leukemia by the regulation of B-lymphocyte migration
    Marketa Kaucka
    Institute of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic
    Cancer Res 73:1491-501. 2013
    ..PCP proteins represent an important class of molecules regulating pathogenic interaction of CLL cells with their microenvironment...
  19. pmc Bent bone dysplasia-FGFR2 type, a distinct skeletal disorder, has deficient canonical FGF signaling
    Amy E Merrill
    Department of Orthopedic Surgery, David Geffen School of Medicine, University of California, Los Angeles, 90048, USA
    Am J Hum Genet 90:550-7. 2012
    ..All together, these clinical and molecular findings are separate from previously characterized FGFR2 disorders and represent a distinct skeletal dysplasia...
  20. doi Mild clinical presentation and prolonged survival of a patient with fumarase deficiency due to the combination of a known and a novel mutation in FH gene
    Fatih Ezgu
    Medical Genetics Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
    Gene 524:403-6. 2013
    ..782G>T) mutation. The patient had an unusually mild clinical course without acidotic attacks. Interestingly his father who was heterozygous for the c.1431_1433dupAAA mutation in the FH gene had cutaneous leiomyoma...
  21. pmc Exome sequencing identifies PDE4D mutations in acrodysostosis
    Hane Lee
    Department of Human Genetics, University of California Los Angeles, CA 90095, USA
    Am J Hum Genet 90:746-51. 2012
    ..These findings demonstrate that acrodysostosis is genetically heterogeneous and underscore the exquisite sensitivity of many tissues to alterations in cAMP homeostasis...
  22. ncbi The antiapoptotic protein Api5 and its partner, high molecular weight FGF2, are up-regulated in B cell chronic lymphoid leukemia
    Pavel Krejci
    J Leukoc Biol 82:1363-4. 2007