PTPIP51, a positive modulator of the MAPK/Erk pathway, is upregulated in glioblastoma and interacts with 14-3-3β and PTP1B in situ
Glioblastoma multiforme (GBM) is the most common and most malignant primary brain tumour. Protein tyrosine phosphatase interacting protein 51 (PTPIP51) is an interaction partner of 14-3-3β, which correlates with the grade of malignancy in gliomas. In this study PTPIP51 and its interacting partners 1...
Gespeichert in:
| Hauptverfasser: | , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2011
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| In: |
Histology and histopathology
Year: 2011, Jahrgang: 26, Heft: 12, Pages: 1531-1543 |
| ISSN: | 1699-5848 |
| DOI: | 10.14670/HH-26.1531 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.14670/HH-26.1531 |
| Verfasserangaben: | M. K. Petri, P. Koch, A. Stenzinger, K. Kuchelmeister, U. Nestler, A. Paradowska, K. Steger, A. Brobeil, M. Viard, M. Wimmer |
MARC
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| 245 | 1 | 0 | |a PTPIP51, a positive modulator of the MAPK/Erk pathway, is upregulated in glioblastoma and interacts with 14-3-3β and PTP1B in situ |c M. K. Petri, P. Koch, A. Stenzinger, K. Kuchelmeister, U. Nestler, A. Paradowska, K. Steger, A. Brobeil, M. Viard, M. Wimmer |
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| 520 | |a Glioblastoma multiforme (GBM) is the most common and most malignant primary brain tumour. Protein tyrosine phosphatase interacting protein 51 (PTPIP51) is an interaction partner of 14-3-3β, which correlates with the grade of malignancy in gliomas. In this study PTPIP51 and its interacting partners 14-3-3β, PTP1B, c-Src, Raf-1 as well as EGFR were investigated in human glioblastoma. Twenty glioblastoma samples were analyzed on transcriptional and translational level by immunohistochemistry, in situ hybridization and RT-PCR. To compare PTPIP51 expression in gliomas of different malignancies, quantitative RT-PCR for grade II astrocytoma and GBM samples was employed. Additionally, we analyzed the correlation between PTPIP51 and 14-3-3β transcription, and checked for in situ interaction between PTPIP51 and 14-3-3β and PTP1B, respectively. PTPIP51 and 14-3-3β mRNA showed a tumour grade dependent upregulation in gliomas. Glioblastoma cells displayed a strong immunoreaction of PTPIP51, which co-localized with 14-3-3β and PTP1B. The duolink proximity ligation assay corroborated a direct in situ interaction of PTPIP51 with both proteins, known to interact with PTPIP51 in vitro. The in vitro interacting partners Raf-1 and c-Src showed a partial co-localization. Besides, immune cells located in capillaries or infiltrating the tumour tissue and endothelial cells of pseudoglomerular vessels revealed a high PTPIP51 expression. The upregulation of PTPIP51 and its connection with the EGFR/MAPK pathway by 14-3-3β via Raf-1 and by PTP1B via c-Src, argue for a functional role of PTPIP51 in the pathogenesis of human glioblastoma. | ||
| 650 | 4 | |a 14-3-3 Proteins | |
| 650 | 4 | |a Adult | |
| 650 | 4 | |a Aged | |
| 650 | 4 | |a Brain Neoplasms | |
| 650 | 4 | |a Extracellular Signal-Regulated MAP Kinases | |
| 650 | 4 | |a Female | |
| 650 | 4 | |a Germany | |
| 650 | 4 | |a Glioblastoma | |
| 650 | 4 | |a Humans | |
| 650 | 4 | |a Immunohistochemistry | |
| 650 | 4 | |a In Situ Hybridization | |
| 650 | 4 | |a Male | |
| 650 | 4 | |a MAP Kinase Signaling System | |
| 650 | 4 | |a Middle Aged | |
| 650 | 4 | |a Mitochondrial Proteins | |
| 650 | 4 | |a Neoplasm Grading | |
| 650 | 4 | |a Protein Tyrosine Phosphatase, Non-Receptor Type 1 | |
| 650 | 4 | |a Protein Tyrosine Phosphatases | |
| 650 | 4 | |a Proto-Oncogene Proteins c-raf | |
| 650 | 4 | |a Real-Time Polymerase Chain Reaction | |
| 650 | 4 | |a Reverse Transcriptase Polymerase Chain Reaction | |
| 650 | 4 | |a RNA, Messenger | |
| 650 | 4 | |a src-Family Kinases | |
| 650 | 4 | |a Up-Regulation | |
| 650 | 4 | |a Young Adult | |
| 700 | 1 | |a Koch, P. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Stenzinger, Albrecht |e VerfasserIn |0 (DE-588)139606106 |0 (DE-627)703395238 |0 (DE-576)312432755 |4 aut | |
| 700 | 1 | |a Kuchelmeister, K. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Nestler, U. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Paradowska, A. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Steger, K. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Brobeil, A. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Viard, M. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Wimmer, M. |e VerfasserIn |4 aut | |
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