Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor
Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the S...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Behrendsen, Lena Sophie [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
Lymphoma-associated missense mutation |
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| Anmerkung: |
© The Author(s) 2022 |
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| Übergeordnetes Werk: |
Enthalten in: BMC cell biology - London : BioMed Central, 2000, 23(2022), 1 vom: 25. Juni |
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| Übergeordnetes Werk: |
volume:23 ; year:2022 ; number:1 ; day:25 ; month:06 |
| Links: |
|---|
| DOI / URN: |
10.1186/s12860-022-00422-9 |
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| Katalog-ID: |
SPR050810340 |
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| 100 | 1 | |a Behrendsen, Lena Sophie |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor |
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| 520 | |a Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. | ||
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| 700 | 1 | |a Khan, Muhammad Jawad |4 aut | |
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| 700 | 1 | |a Meyer, Thomas |4 aut | |
| 700 | 1 | |a Staab, Julia |4 aut | |
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10.1186/s12860-022-00422-9 doi (DE-627)SPR050810340 (SPR)s12860-022-00422-9-e DE-627 ger DE-627 rakwb eng Behrendsen, Lena Sophie verfasserin aut Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. Lymphoma-associated missense mutation (dpeaa)DE-He213 Signal transducer and activator of transcription 3 (STAT3) (dpeaa)DE-He213 Interleukin-6 signaling (dpeaa)DE-He213 DNA binding (dpeaa)DE-He213 Gene expression (dpeaa)DE-He213 Menon, Priyanka Rajeev aut Khan, Muhammad Jawad aut Gregus, Anke aut Wirths, Oliver aut Meyer, Thomas aut Staab, Julia aut Enthalten in BMC cell biology London : BioMed Central, 2000 23(2022), 1 vom: 25. Juni (DE-627)326644830 (DE-600)2041486-9 1471-2121 nnns volume:23 year:2022 number:1 day:25 month:06 https://dx.doi.org/10.1186/s12860-022-00422-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_22 GBV_ILN_2003 GBV_ILN_2008 GBV_ILN_2021 GBV_ILN_4305 AR 23 2022 1 25 06 |
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10.1186/s12860-022-00422-9 doi (DE-627)SPR050810340 (SPR)s12860-022-00422-9-e DE-627 ger DE-627 rakwb eng Behrendsen, Lena Sophie verfasserin aut Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. Lymphoma-associated missense mutation (dpeaa)DE-He213 Signal transducer and activator of transcription 3 (STAT3) (dpeaa)DE-He213 Interleukin-6 signaling (dpeaa)DE-He213 DNA binding (dpeaa)DE-He213 Gene expression (dpeaa)DE-He213 Menon, Priyanka Rajeev aut Khan, Muhammad Jawad aut Gregus, Anke aut Wirths, Oliver aut Meyer, Thomas aut Staab, Julia aut Enthalten in BMC cell biology London : BioMed Central, 2000 23(2022), 1 vom: 25. Juni (DE-627)326644830 (DE-600)2041486-9 1471-2121 nnns volume:23 year:2022 number:1 day:25 month:06 https://dx.doi.org/10.1186/s12860-022-00422-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_22 GBV_ILN_2003 GBV_ILN_2008 GBV_ILN_2021 GBV_ILN_4305 AR 23 2022 1 25 06 |
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10.1186/s12860-022-00422-9 doi (DE-627)SPR050810340 (SPR)s12860-022-00422-9-e DE-627 ger DE-627 rakwb eng Behrendsen, Lena Sophie verfasserin aut Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. Lymphoma-associated missense mutation (dpeaa)DE-He213 Signal transducer and activator of transcription 3 (STAT3) (dpeaa)DE-He213 Interleukin-6 signaling (dpeaa)DE-He213 DNA binding (dpeaa)DE-He213 Gene expression (dpeaa)DE-He213 Menon, Priyanka Rajeev aut Khan, Muhammad Jawad aut Gregus, Anke aut Wirths, Oliver aut Meyer, Thomas aut Staab, Julia aut Enthalten in BMC cell biology London : BioMed Central, 2000 23(2022), 1 vom: 25. Juni (DE-627)326644830 (DE-600)2041486-9 1471-2121 nnns volume:23 year:2022 number:1 day:25 month:06 https://dx.doi.org/10.1186/s12860-022-00422-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_22 GBV_ILN_2003 GBV_ILN_2008 GBV_ILN_2021 GBV_ILN_4305 AR 23 2022 1 25 06 |
| allfieldsGer |
10.1186/s12860-022-00422-9 doi (DE-627)SPR050810340 (SPR)s12860-022-00422-9-e DE-627 ger DE-627 rakwb eng Behrendsen, Lena Sophie verfasserin aut Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. Lymphoma-associated missense mutation (dpeaa)DE-He213 Signal transducer and activator of transcription 3 (STAT3) (dpeaa)DE-He213 Interleukin-6 signaling (dpeaa)DE-He213 DNA binding (dpeaa)DE-He213 Gene expression (dpeaa)DE-He213 Menon, Priyanka Rajeev aut Khan, Muhammad Jawad aut Gregus, Anke aut Wirths, Oliver aut Meyer, Thomas aut Staab, Julia aut Enthalten in BMC cell biology London : BioMed Central, 2000 23(2022), 1 vom: 25. Juni (DE-627)326644830 (DE-600)2041486-9 1471-2121 nnns volume:23 year:2022 number:1 day:25 month:06 https://dx.doi.org/10.1186/s12860-022-00422-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_22 GBV_ILN_2003 GBV_ILN_2008 GBV_ILN_2021 GBV_ILN_4305 AR 23 2022 1 25 06 |
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10.1186/s12860-022-00422-9 doi (DE-627)SPR050810340 (SPR)s12860-022-00422-9-e DE-627 ger DE-627 rakwb eng Behrendsen, Lena Sophie verfasserin aut Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. Lymphoma-associated missense mutation (dpeaa)DE-He213 Signal transducer and activator of transcription 3 (STAT3) (dpeaa)DE-He213 Interleukin-6 signaling (dpeaa)DE-He213 DNA binding (dpeaa)DE-He213 Gene expression (dpeaa)DE-He213 Menon, Priyanka Rajeev aut Khan, Muhammad Jawad aut Gregus, Anke aut Wirths, Oliver aut Meyer, Thomas aut Staab, Julia aut Enthalten in BMC cell biology London : BioMed Central, 2000 23(2022), 1 vom: 25. Juni (DE-627)326644830 (DE-600)2041486-9 1471-2121 nnns volume:23 year:2022 number:1 day:25 month:06 https://dx.doi.org/10.1186/s12860-022-00422-9 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_22 GBV_ILN_2003 GBV_ILN_2008 GBV_ILN_2021 GBV_ILN_4305 AR 23 2022 1 25 06 |
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Behrendsen, Lena Sophie misc Lymphoma-associated missense mutation misc Signal transducer and activator of transcription 3 (STAT3) misc Interleukin-6 signaling misc DNA binding misc Gene expression Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor |
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Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor Lymphoma-associated missense mutation (dpeaa)DE-He213 Signal transducer and activator of transcription 3 (STAT3) (dpeaa)DE-He213 Interleukin-6 signaling (dpeaa)DE-He213 DNA binding (dpeaa)DE-He213 Gene expression (dpeaa)DE-He213 |
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Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor |
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Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor |
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Behrendsen, Lena Sophie |
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BMC cell biology |
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2022 |
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Behrendsen, Lena Sophie Menon, Priyanka Rajeev Khan, Muhammad Jawad Gregus, Anke Wirths, Oliver Meyer, Thomas Staab, Julia |
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Behrendsen, Lena Sophie |
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10.1186/s12860-022-00422-9 |
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evaluation of the putative lymphoma-associated point mutation d427h in the stat3 transcription factor |
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Evaluation of the putative lymphoma-associated point mutation D427H in the STAT3 transcription factor |
| abstract |
Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. © The Author(s) 2022 |
| abstractGer |
Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. © The Author(s) 2022 |
| abstract_unstemmed |
Background Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor that promotes cell proliferation and immunomodulation in untransformed cells and maintains stemness of transformed cells, facilitating invasion and metastasis. Numerous point mutations in the STAT3 protein have been identified that drive malignancy in various tumor entities. The missense mutation D427H localized in the STAT3 DNA-binding domain has been previously reported in patients with NK/T cell lymphomas. To assess the biological activity of this missense mutation, we compared the STAT3-D427H mutant to wild-type (WT) protein as well as the known hyper-active mutant F174A. Results Although previously reported as an activating mutation, the STAT3-D427H mutant neither showed elevated cytokine-induced tyrosine phosphorylation nor altered nuclear accumulation, as compared to the WT protein. However, the D427H mutant displayed enhanced binding to STAT-specific DNA-binding sites but a reduced sequence specificity and dissociation rate from DNA, which was demonstrated by electrophoretic mobility shift assays. This observation is consistent with the phenotype of the homologous E421K mutation in the STAT1 protein, which also displayed enhanced binding to DNA but lacked a corresponding increase in transcriptional activity. Conclusions Based on our data, it is unlikely that the D427H missense mutation in the STAT3 protein possesses an oncogenic potential beyond the WT molecule. © The Author(s) 2022 |
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