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6. Data from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

Author

Kazerounian, Shiva, primary, Gerald, Damien, primary, Huang, Minzhou, primary, Chin, Y. Rebecca, primary, Udayakumar, Durga, primary, Zheng, Ningning, primary, O'Donnell, Rebekah K., primary, Perruzzi, Carole, primary, Mangiante, Lee, primary, Pourat, Jacob, primary, Phung, Thuy L., primary, Bravo-Nuevo, Arturo, primary, Shechter, Sharon, primary, McNamara, Stephanie, primary, DuHadaway, James B., primary, Kocher, Olivier N., primary, Brown, Lawrence F., primary, Toker, Alex, primary, Prendergast, George C., primary, and Benjamin, Laura E., primary

Published
2023
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7. Supplementary Figure 6 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

Author

Kazerounian, Shiva, primary, Gerald, Damien, primary, Huang, Minzhou, primary, Chin, Y. Rebecca, primary, Udayakumar, Durga, primary, Zheng, Ningning, primary, O'Donnell, Rebekah K., primary, Perruzzi, Carole, primary, Mangiante, Lee, primary, Pourat, Jacob, primary, Phung, Thuy L., primary, Bravo-Nuevo, Arturo, primary, Shechter, Sharon, primary, McNamara, Stephanie, primary, DuHadaway, James B., primary, Kocher, Olivier N., primary, Brown, Lawrence F., primary, Toker, Alex, primary, Prendergast, George C., primary, and Benjamin, Laura E., primary

Published
2023
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8. Data from Bin3 Deletion Causes Cataracts and Increased Susceptibility to Lymphoma during Aging

Author

Ramalingam, Arivudainambi, primary, Duhadaway, James B., primary, Sutanto-Ward, Erika, primary, Wang, Yan, primary, Dinchuk, Joseph, primary, Huang, Minzhou, primary, Donover, Preston S., primary, Boulden, Janette, primary, McNally, Lois M., primary, Soler, Alejandro P., primary, Muller, Alexander J., primary, Duncan, Melinda K., primary, and Prendergast, George C., primary

Published
2023
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9. Supplementary Table 2, Figure Legend 1 from Bin3 Deletion Causes Cataracts and Increased Susceptibility to Lymphoma during Aging

Author

Ramalingam, Arivudainambi, primary, Duhadaway, James B., primary, Sutanto-Ward, Erika, primary, Wang, Yan, primary, Dinchuk, Joseph, primary, Huang, Minzhou, primary, Donover, Preston S., primary, Boulden, Janette, primary, McNally, Lois M., primary, Soler, Alejandro P., primary, Muller, Alexander J., primary, Duncan, Melinda K., primary, and Prendergast, George C., primary

Published
2023
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10. Supplementary Figure 5 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

Author

Kazerounian, Shiva, primary, Gerald, Damien, primary, Huang, Minzhou, primary, Chin, Y. Rebecca, primary, Udayakumar, Durga, primary, Zheng, Ningning, primary, O'Donnell, Rebekah K., primary, Perruzzi, Carole, primary, Mangiante, Lee, primary, Pourat, Jacob, primary, Phung, Thuy L., primary, Bravo-Nuevo, Arturo, primary, Shechter, Sharon, primary, McNamara, Stephanie, primary, DuHadaway, James B., primary, Kocher, Olivier N., primary, Brown, Lawrence F., primary, Toker, Alex, primary, Prendergast, George C., primary, and Benjamin, Laura E., primary

Published
2023
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11. Supplementary Figure 4 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

Author

Kazerounian, Shiva, primary, Gerald, Damien, primary, Huang, Minzhou, primary, Chin, Y. Rebecca, primary, Udayakumar, Durga, primary, Zheng, Ningning, primary, O'Donnell, Rebekah K., primary, Perruzzi, Carole, primary, Mangiante, Lee, primary, Pourat, Jacob, primary, Phung, Thuy L., primary, Bravo-Nuevo, Arturo, primary, Shechter, Sharon, primary, McNamara, Stephanie, primary, DuHadaway, James B., primary, Kocher, Olivier N., primary, Brown, Lawrence F., primary, Toker, Alex, primary, Prendergast, George C., primary, and Benjamin, Laura E., primary

Published
2023
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12. Supplementary Figure 1 from Bin3 Deletion Causes Cataracts and Increased Susceptibility to Lymphoma during Aging

Author

Ramalingam, Arivudainambi, primary, Duhadaway, James B., primary, Sutanto-Ward, Erika, primary, Wang, Yan, primary, Dinchuk, Joseph, primary, Huang, Minzhou, primary, Donover, Preston S., primary, Boulden, Janette, primary, McNally, Lois M., primary, Soler, Alejandro P., primary, Muller, Alexander J., primary, Duncan, Melinda K., primary, and Prendergast, George C., primary

Published
2023
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13. Supplementary Figure 1 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

Author

Kazerounian, Shiva, primary, Gerald, Damien, primary, Huang, Minzhou, primary, Chin, Y. Rebecca, primary, Udayakumar, Durga, primary, Zheng, Ningning, primary, O'Donnell, Rebekah K., primary, Perruzzi, Carole, primary, Mangiante, Lee, primary, Pourat, Jacob, primary, Phung, Thuy L., primary, Bravo-Nuevo, Arturo, primary, Shechter, Sharon, primary, McNamara, Stephanie, primary, DuHadaway, James B., primary, Kocher, Olivier N., primary, Brown, Lawrence F., primary, Toker, Alex, primary, Prendergast, George C., primary, and Benjamin, Laura E., primary

Published
2023
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14. Supplementary Methods and Materials from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

Author

Kazerounian, Shiva, primary, Gerald, Damien, primary, Huang, Minzhou, primary, Chin, Y. Rebecca, primary, Udayakumar, Durga, primary, Zheng, Ningning, primary, O'Donnell, Rebekah K., primary, Perruzzi, Carole, primary, Mangiante, Lee, primary, Pourat, Jacob, primary, Phung, Thuy L., primary, Bravo-Nuevo, Arturo, primary, Shechter, Sharon, primary, McNamara, Stephanie, primary, DuHadaway, James B., primary, Kocher, Olivier N., primary, Brown, Lawrence F., primary, Toker, Alex, primary, Prendergast, George C., primary, and Benjamin, Laura E., primary

Published
2023
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15. Supplementary Figure 3 from RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

Author

Kazerounian, Shiva, primary, Gerald, Damien, primary, Huang, Minzhou, primary, Chin, Y. Rebecca, primary, Udayakumar, Durga, primary, Zheng, Ningning, primary, O'Donnell, Rebekah K., primary, Perruzzi, Carole, primary, Mangiante, Lee, primary, Pourat, Jacob, primary, Phung, Thuy L., primary, Bravo-Nuevo, Arturo, primary, Shechter, Sharon, primary, McNamara, Stephanie, primary, DuHadaway, James B., primary, Kocher, Olivier N., primary, Brown, Lawrence F., primary, Toker, Alex, primary, Prendergast, George C., primary, and Benjamin, Laura E., primary

Published
2023
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18. Pilot study of a novel nanobody 68Ga-NODGAG-SNA006 for instant PET imaging of CD8+ T cells

Author

Wang, Yan, primary, Wang, Chao, additional, Huang, Minzhou, additional, Qin, Songbin, additional, Zhao, Jun, additional, Sang, Shibiao, additional, Zheng, Meng, additional, Bian, Yicong, additional, Huang, Chenrong, additional, Zhang, Hua, additional, Guo, Linchuan, additional, Jiang, Jiwei, additional, Xu, Chun, additional, Dai, Na, additional, Zheng, Yushuang, additional, Han, Jiajun, additional, Yang, Min, additional, Xu, Tao, additional, and Miao, Liyan, additional

Published
2022
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19. Pilot study of a novel nanobody 68 Ga-NODAGA-SNA006 for instant PET imaging of CD8+ T cells.

Author

Wang, Yan, Wang, Chao, Huang, Minzhou, Qin, Songbing, Zhao, Jun, Sang, Shibiao, Zheng, Meng, Bian, Yicong, Huang, Chenrong, Zhang, Hua, Guo, Lingchuan, Jiang, Jiwei, Xu, Chun, Dai, Na, Zheng, Yushuang, Han, Jiajun, Yang, Min, Xu, Tao, and Miao, Liyan

Subjects
POSITRON emission tomography, CD8 antigen, IMMUNE response, PATIENT monitoring, CANCER immunotherapy
Abstract

Purpose: Positron emission tomography (PET) with specific diagnostic probes for quantifying CD8+ T cells has emerged as a powerful technique for monitoring the immune response. However, most CD8+ T cell radiotracers are based on antibodies or antibody fragments, which are slowly cleared from circulation. Herein, we aimed to develop and assess 68 Ga-NODAGA-SNA006 for instant PET (iPET) imaging of CD8+ T cells. Methods: A novel nanobody without a hexahistidine (His6) tag, SNA006-GSC, was designed, site-specifically conjugated with NODAGA-maleimide and radiolabelled with 68 Ga. The PET imaging profiles of 68 Ga-NODAGA-SNA006 were evaluated in BALB/c MC38-CD8+/CD8− tumour models and cynomolgus monkeys. Three volunteers with lung cancer underwent whole-body PET/CT imaging after 68 Ga-NODAGA-SNA006 administration. The biodistribution, pharmacokinetics and dosimetry of patients were also investigated. In addition, combined with immunohistochemistry (IHC), the quantitative performance of the tracer for monitoring CD8 expression was evaluated in BALB/c MC38-CD8+/CD8− and human subjects. Results: 68 Ga-NODAGA-SNA006 was prepared with RCP > 98% and SA > 100 GBq/μmol. 68 Ga-NODAGA-SNA006 exhibited specific uptake in MC38-CD8+ xenografts tumours, CD8-rich tissues (such as the spleen) in monkeys and CD8+ tumour lesions in patients within 1 h. Fast washout from circulation was observed in three volunteers (t1/2 < 20 min). A preliminary quantitative linear relationship (R2 = 0.9668, p < 0.0001 for xenografts and R2 = 0.7924, p = 0.0013 for lung patients) appeared between 68 Ga-NODAGA-SNA006 uptake and CD8 expression. 68 Ga-NODAGA-SNA006 was well tolerated by all patients. Conclusion: 68 Ga-NODAGA-SNA006 PET imaging can instantly quantify CD8 expression with an ideal safety profile and is expected to be important for dynamically tracking CD8+ T cells and monitoring immune responses for individualised cancer immunotherapy. Trial registration: NCT05126927 (19 November 2021, retrospectively registered). [ABSTRACT FROM AUTHOR]

Published
2022
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20. Additional file 1 of Dose escalation biodistribution, positron emission tomography/computed tomography imaging and dosimetry of a highly specific radionuclide-labeled non-blocking nanobody

Author

Yang, Yanling, Wang, Chao, Wang, Yan, Sun, Yan, Huang, Xing, Huang, Minzhou, Xu, Hui, Fan, Huaying, Chen, Daquan, and Zhao, Feng

Subjects
genetic structures
Abstract

Additional file 1. Additional data on stability, pharmacokinetics and biodistribution analysis of transgetic mice or cynomolgus monkeys.

Published
2021
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23. Role of RhoB in the Regulation of Pulmonary Endothelial and Smooth Muscle Cell Responses to Hypoxia

Author

Wojciak-Stothard, Beata, Zhao, Lan, Oliver, Eduardo, Dubois, Olivier, Wu, Yixing, Kardassis, Dimitris, Vasilaki, Eleftheria, Huang, Minzhou, Mitchell, Jane A., Louise, Harrington, Prendergast, George C., Wilkins, Martin R., Wojciak-Stothard, Beata, Zhao, Lan, Oliver, Eduardo, Dubois, Olivier, Wu, Yixing, Kardassis, Dimitris, Vasilaki, Eleftheria, Huang, Minzhou, Mitchell, Jane A., Louise, Harrington, Prendergast, George C., and Wilkins, Martin R.

Abstract

Rationale: RhoA and Rho kinase contribute to pulmonary vasoconstriction and vascular remodeling in pulmonary hypertension. RhoB, a protein homologous to RhoA and activated by hypoxia, regulates neoplastic growth and vasoconstriction but its role in the regulation of pulmonary vascular function is not known. Objective: To determine the role of RhoB in pulmonary endothelial and smooth muscle cell responses to hypoxia and in pulmonary vascular remodeling in chronic hypoxia-induced pulmonary hypertension. Methods and Results: Hypoxia increased expression and activity of RhoB in human pulmonary artery endothelial and smooth muscle cells, coincidental with activation of RhoA. Hypoxia or adenoviral overexpression of constitutively activated RhoB increased actomyosin contractility, induced endothelial permeability, and promoted cell growth; dominant negative RhoB or manumycin, a farnesyltransferase inhibitor that targets the vascular function of RhoB, inhibited the effects of hypoxia. Coordinated activation of RhoA and RhoB maximized the hypoxia-induced stress fiber formation caused by RhoB/mammalian homolog of Drosophila diaphanous-induced actin polymerization and RhoA/Rho kinase-induced phosphorylation of myosin light chain on Ser19. Notably, RhoB was specifically required for hypoxia-induced factor-1 alpha stabilization and for hypoxia- and platelet-derived growth factor-induced cell proliferation and migration. RhoB deficiency in mice markedly attenuated development of chronic hypoxia-induced pulmonary hypertension, despite compensatory expression of RhoA in the lung. Conclusions: RhoB mediates adaptational changes to acute hypoxia in the vasculature, but its continual activation by chronic hypoxia can accentuate vascular remodeling to promote development of pulmonary hypertension. RhoB is a potential target for novel approaches (eg, farnesyltransferase inhibitors) aimed at regulating pulmonary vascular tone and structure.

Published
2012
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26. RhoB Differentially Controls Akt Function in Tumor Cells and Stromal Endothelial Cells during Breast Tumorigenesis

Author

Kazerounian, Shiva, primary, Gerald, Damien, additional, Huang, Minzhou, additional, Chin, Y. Rebecca, additional, Udayakumar, Durga, additional, Zheng, Ningning, additional, O'Donnell, Rebekah K., additional, Perruzzi, Carole, additional, Mangiante, Lee, additional, Pourat, Jacob, additional, Phung, Thuy L., additional, Bravo-Nuevo, Arturo, additional, Shechter, Sharon, additional, McNamara, Stephanie, additional, DuHadaway, James B., additional, Kocher, Olivier N., additional, Brown, Lawrence F., additional, Toker, Alex, additional, Prendergast, George C., additional, and Benjamin, Laura E., additional

Published
2013
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27. Role of RhoB in the Regulation of Pulmonary Endothelial and Smooth Muscle Cell Responses to Hypoxia

Author

Wojciak-Stothard, Beata, primary, Zhao, Lan, additional, Oliver, Eduardo, additional, Dubois, Olivier, additional, Wu, Yixing, additional, Kardassis, Dimitris, additional, Vasilaki, Eleftheria, additional, Huang, Minzhou, additional, Mitchell, Jane A., additional, Harrington, Louise S., additional, Prendergast, George C., additional, and Wilkins, Martin R., additional

Published
2012
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30. Bin3 Deletion Causes Cataracts and Increased Susceptibility to Lymphoma during Aging

Author

Ramalingam, Arivudainambi, primary, Duhadaway, James B., additional, Sutanto-Ward, Erika, additional, Wang, Yan, additional, Dinchuk, Joseph, additional, Huang, Minzhou, additional, Donover, Preston S., additional, Boulden, Janette, additional, McNally, Lois M., additional, Soler, Alejandro P., additional, Muller, Alexander J., additional, Duncan, Melinda K., additional, and Prendergast, George C., additional

Published
2008
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36. RhoB regulates PDGFR-beta trafficking and signaling in vascular smooth muscle cells.

Author

Huang M, Duhadaway JB, Prendergast GC, and Laury-Kleintop LD

Subjects
Animals, Cell Nucleus metabolism, Cell Proliferation, Cells, Cultured, Endosomes metabolism, Mice, Mice, Knockout, Mice, Transgenic, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinase 3 metabolism, Muscle, Smooth, Vascular enzymology, Myocytes, Smooth Muscle enzymology, Phosphorylation, Protein Transport, Proto-Oncogene Proteins c-akt metabolism, Transport Vesicles metabolism, rhoB GTP-Binding Protein deficiency, rhoB GTP-Binding Protein genetics, src-Family Kinases metabolism, Muscle, Smooth, Vascular metabolism, Myocytes, Smooth Muscle metabolism, Platelet-Derived Growth Factor metabolism, Receptor, Platelet-Derived Growth Factor beta metabolism, Signal Transduction, rhoB GTP-Binding Protein metabolism
Abstract

Objective: RhoB is a small GTPase localized at the plasma membrane and endosomes that participates in the regulation of endocytic trafficking of the epidermal growth factor (EGF) receptor and the nonreceptor kinases Src and Akt. This study was performed to determine whether RhoB plays a critical role in trafficking and signaling by the platelet-derived growth factor receptor-beta (PDGFR-beta) in vascular smooth muscle cells., Methods and Results: Cells derived from RhoB knockout mice failed to proliferate in response to PDGF, and downstream signaling was compromised as reflected by reduced phosphorylation of the effector kinases Akt and ERK1/2. In normal cells, PDGF stimulated trafficking of PDGFR-beta into a perinuclear late endosomal compartment and triggered entry of Src, Akt, extracellular signal-regulated kinase (ERK) into the cell nucleus. In contrast, PDGF treatment of RhoB null cells resulted in neither PDGFR-beta trafficking to late endosomes nor nuclear localization of Src, Akt, or ERK. In support of an essential function in these processes, restoring expression of RhoB in null cells rescued these defects and restored cell proliferation in response to PDGF., Conclusions: Our findings establish RhoB as a critical regulator of PDGFR-beta trafficking and signaling in vascular smooth muscle cells.

Published
2007
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