Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling
Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as trans...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Franceschi, Renny T. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer International Publishing AG 2017 |
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| Übergeordnetes Werk: |
Enthalten in: Current molecular biology reports - Berlin : Springer, 2015, 3(2017), 2 vom: 25. Apr., Seite 122-132 |
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| Übergeordnetes Werk: |
volume:3 ; year:2017 ; number:2 ; day:25 ; month:04 ; pages:122-132 |
| Links: |
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| DOI / URN: |
10.1007/s40610-017-0059-5 |
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| Katalog-ID: |
SPR036748854 |
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| 100 | 1 | |a Franceschi, Renny T. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling |
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| 520 | |a Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. | ||
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10.1007/s40610-017-0059-5 doi (DE-627)SPR036748854 (SPR)s40610-017-0059-5-e DE-627 ger DE-627 rakwb eng Franceschi, Renny T. verfasserin aut Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. MAP kinase (dpeaa)DE-He213 Transcription (dpeaa)DE-He213 Osteoblast (dpeaa)DE-He213 Chromatin (dpeaa)DE-He213 RUNX2 (dpeaa)DE-He213 Ge, Chunxi aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 2 vom: 25. Apr., Seite 122-132 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:2 day:25 month:04 pages:122-132 https://dx.doi.org/10.1007/s40610-017-0059-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 3 2017 2 25 04 122-132 |
| spelling |
10.1007/s40610-017-0059-5 doi (DE-627)SPR036748854 (SPR)s40610-017-0059-5-e DE-627 ger DE-627 rakwb eng Franceschi, Renny T. verfasserin aut Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. MAP kinase (dpeaa)DE-He213 Transcription (dpeaa)DE-He213 Osteoblast (dpeaa)DE-He213 Chromatin (dpeaa)DE-He213 RUNX2 (dpeaa)DE-He213 Ge, Chunxi aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 2 vom: 25. Apr., Seite 122-132 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:2 day:25 month:04 pages:122-132 https://dx.doi.org/10.1007/s40610-017-0059-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 3 2017 2 25 04 122-132 |
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10.1007/s40610-017-0059-5 doi (DE-627)SPR036748854 (SPR)s40610-017-0059-5-e DE-627 ger DE-627 rakwb eng Franceschi, Renny T. verfasserin aut Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. MAP kinase (dpeaa)DE-He213 Transcription (dpeaa)DE-He213 Osteoblast (dpeaa)DE-He213 Chromatin (dpeaa)DE-He213 RUNX2 (dpeaa)DE-He213 Ge, Chunxi aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 2 vom: 25. Apr., Seite 122-132 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:2 day:25 month:04 pages:122-132 https://dx.doi.org/10.1007/s40610-017-0059-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 3 2017 2 25 04 122-132 |
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10.1007/s40610-017-0059-5 doi (DE-627)SPR036748854 (SPR)s40610-017-0059-5-e DE-627 ger DE-627 rakwb eng Franceschi, Renny T. verfasserin aut Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. MAP kinase (dpeaa)DE-He213 Transcription (dpeaa)DE-He213 Osteoblast (dpeaa)DE-He213 Chromatin (dpeaa)DE-He213 RUNX2 (dpeaa)DE-He213 Ge, Chunxi aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 2 vom: 25. Apr., Seite 122-132 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:2 day:25 month:04 pages:122-132 https://dx.doi.org/10.1007/s40610-017-0059-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 3 2017 2 25 04 122-132 |
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10.1007/s40610-017-0059-5 doi (DE-627)SPR036748854 (SPR)s40610-017-0059-5-e DE-627 ger DE-627 rakwb eng Franceschi, Renny T. verfasserin aut Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer International Publishing AG 2017 Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. MAP kinase (dpeaa)DE-He213 Transcription (dpeaa)DE-He213 Osteoblast (dpeaa)DE-He213 Chromatin (dpeaa)DE-He213 RUNX2 (dpeaa)DE-He213 Ge, Chunxi aut Enthalten in Current molecular biology reports Berlin : Springer, 2015 3(2017), 2 vom: 25. Apr., Seite 122-132 (DE-627)817361065 (DE-600)2808619-3 2198-6428 nnns volume:3 year:2017 number:2 day:25 month:04 pages:122-132 https://dx.doi.org/10.1007/s40610-017-0059-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 3 2017 2 25 04 122-132 |
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Enthalten in Current molecular biology reports 3(2017), 2 vom: 25. Apr., Seite 122-132 volume:3 year:2017 number:2 day:25 month:04 pages:122-132 |
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Enthalten in Current molecular biology reports 3(2017), 2 vom: 25. Apr., Seite 122-132 volume:3 year:2017 number:2 day:25 month:04 pages:122-132 |
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Franceschi, Renny T. @@aut@@ Ge, Chunxi @@aut@@ |
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| author |
Franceschi, Renny T. |
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Franceschi, Renny T. misc MAP kinase misc Transcription misc Osteoblast misc Chromatin misc RUNX2 Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling |
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Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling MAP kinase (dpeaa)DE-He213 Transcription (dpeaa)DE-He213 Osteoblast (dpeaa)DE-He213 Chromatin (dpeaa)DE-He213 RUNX2 (dpeaa)DE-He213 |
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Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling |
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Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling |
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Franceschi, Renny T. |
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Franceschi, Renny T. Ge, Chunxi |
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Franceschi, Renny T. |
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control of the osteoblast lineage by mitogen-activated protein kinase signaling |
| title_auth |
Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling |
| abstract |
Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. © Springer International Publishing AG 2017 |
| abstractGer |
Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. © Springer International Publishing AG 2017 |
| abstract_unstemmed |
Purpose of the Review This review will provide a timely assessment of MAP kinase actions in bone development and homeostasis with particular emphasis on transcriptional control of the osteoblast lineage. Recent Findings Extracellular signal-regulated kinase (ERK) and p38 MAP kinase function as transducers of signals initiated by the extracellular matrix, mechanical loading, TGF-β, BMPs, and FGF2. MAPK signals may also affect and/or interact with other important pathways such as WNT and HIPPO. ERK and p38 MAP kinase pathways phosphorylate specific osteogenic transcription factors including RUNX2, Osterix, ATF4, and DLX5. For RUNX2, phosphorylation at specific serine residues initiates epigenetic changes in chromatin necessary for decondensation and increased transcription. MAPK also suppresses marrow adipogenesis by phosphorylating and inhibiting PPARγ, which may explain the well-known relationship between reduced skeletal loading and marrow fat accumulation. Summary MAPKs transduce signals from the extracellular environment to the nucleus allowing bone cells to respond to changes in hormonal/growth factor signaling and mechanical loading, thereby optimizing bone structure to meet physiological and mechanical needs of the body. © Springer International Publishing AG 2017 |
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Control of the Osteoblast Lineage by Mitogen-Activated Protein Kinase Signaling |
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https://dx.doi.org/10.1007/s40610-017-0059-5 |
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Ge, Chunxi |
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10.1007/s40610-017-0059-5 |
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2024-07-03T19:26:08.375Z |
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