Research Topics
Genomes and GenesSpecies | Pavel KrejciSummaryAffiliation: Cedars-Sinai Medical Center Country: USA Publications
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Publications
NF449 is a novel inhibitor of fibroblast growth factor receptor 3 (FGFR3) signaling active in chondrocytes and multiple myeloma cellsPavel 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...
Fibroblast growth factors 1, 2, 17, and 19 are the predominant FGF ligands expressed in human fetal growth plate cartilagePavel 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...- 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 migrationSilvie 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... - Bisindolylmaleimide I suppresses fibroblast growth factor-mediated activation of Erk MAP kinase in chondrocytes by preventing Shp2 association with the Frs2 and Gab1 adaptor proteinsPavel 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... - Simple, mammalian cell-based assay for identification of inhibitors of the Erk MAP kinase pathwayPavel 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... - Analysis of STAT1 activation by six FGFR3 mutants associated with skeletal dysplasia undermines dominant role of STAT1 in FGFR3 signaling in cartilagePavel 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... - FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescencePavel 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... - Fibroblast growth factor inhibits interferon gamma-STAT1 and interleukin 6-STAT3 signaling in chondrocytesPavel 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... 
STAT1 and STAT3 do not participate in FGF-mediated growth arrest in chondrocytesPavel Krejci
Institute of Experimental Biology, Masaryk University, 61137 Brno, Czech Republic
J Cell Sci 121:272-81. 2008....- Interaction of fibroblast growth factor and C-natriuretic peptide signaling in regulation of chondrocyte proliferation and extracellular matrix homeostasisPavel 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... - C-natriuretic peptide: an important regulator of cartilageKaterina 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... - Receptor tyrosine kinases activate canonical WNT/β-catenin signaling via MAP kinase/LRP6 pathway and direct β-catenin phosphorylationPavel 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... - Mitogen-activated protein kinases promote WNT/beta-catenin signaling via phosphorylation of LRP6Igor 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... - FGF2 inhibits proliferation and alters the cartilage-like phenotype of RCS cellsPavel 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... - Molecular pathology of the fibroblast growth factor familyPavel 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... - Sequential activation and inactivation of Dishevelled in the Wnt/beta-catenin pathway by casein kinasesOndrej 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... - Bent bone dysplasia-FGFR2 type, a distinct skeletal disorder, has deficient canonical FGF signalingAmy 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... - The planar cell polarity pathway drives pathogenesis of chronic lymphocytic leukemia by the regulation of B-lymphocyte migrationMarketa 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... - Exome sequencing identifies PDE4D mutations in acrodysostosisHane 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... - The antiapoptotic protein Api5 and its partner, high molecular weight FGF2, are up-regulated in B cell chronic lymphoid leukemiaPavel Krejci
J Leukoc Biol 82:1363-4. 2007