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198 results on '"Hu, Wenhuo"'

1. Nav1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis

Author

Fu, Wenyu, Vasylyev, Dmytro, Bi, Yufei, Zhang, Mingshuang, Sun, Guodong, Khleborodova, Asya, Huang, Guiwu, Zhao, Libo, Zhou, Renpeng, Li, Yonggang, Liu, Shujun, Cai, Xianyi, He, Wenjun, Cui, Min, Zhao, Xiangli, Hettinghouse, Aubryanna, Good, Julia, Kim, Ellen, Strauss, Eric, Leucht, Philipp, Schwarzkopf, Ran, Guo, Edward X., Samuels, Jonathan, Hu, Wenhuo, Attur, Mukundan, Waxman, Stephen G., and Liu, Chuan-ju

Published
2024
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3. Author Correction: FOXA1 repression drives lineage plasticity and immune heterogeneity in bladder cancers with squamous differentiation

Author

Warrick, Joshua I., Hu, Wenhuo, Yamashita, Hironobu, Walter, Vonn, Shuman, Lauren, Craig, Jenna M., Gellert, Lan L., Castro, Mauro A. A., Robertson, A. Gordon, Kuo, Fengshen, Ostrovnaya, Irina, Sarungbam, Judy, Chen, Ying-bei, Gopalan, Anuradha, Sirintrapun, Sahussapont J., Fine, Samson W., Tickoo, Satish K., Kim, Kwanghee, Thomas, Jasmine, Karan, Nagar, Gao, Sizhi Paul, Clinton, Timothy N., Lenis, Andrew T., Chan, Timothy A., Chen, Ziyu, Rao, Manisha, Hollman, Travis J., Li, Yanyun, Socci, Nicholas D., Chavan, Shweta, Viale, Agnes, Mohibullah, Neeman, Bochner, Bernard H., Pietzak, Eugene J., Teo, Min Yuen, Iyer, Gopa, Rosenberg, Jonathan E., Bajorin, Dean F., Kaag, Matthew, Merrill, Suzanne B., Joshi, Monika, Adam, Rosalyn, Taylor, III, John A., Clark, Peter E., Raman, Jay D., Reuter, Victor E., Chen, Yu, Funt, Samuel A., Solit, David B., DeGraff, David J., and Al-Ahmadie, Hikmat A.

Published
2022
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4. FOXA1 repression drives lineage plasticity and immune heterogeneity in bladder cancers with squamous differentiation

Author

Warrick, Joshua I., Hu, Wenhuo, Yamashita, Hironobu, Walter, Vonn, Shuman, Lauren, Craig, Jenna M., Gellert, Lan L., Castro, Mauro A. A., Robertson, A. Gordon, Kuo, Fengshen, Ostrovnaya, Irina, Sarungbam, Judy, Chen, Ying-bei, Gopalan, Anuradha, Sirintrapun, Sahussapont J., Fine, Samson W., Tickoo, Satish K., Kim, Kwanghee, Thomas, Jasmine, Karan, Nagar, Gao, Sizhi Paul, Clinton, Timothy N., Lenis, Andrew T., Chan, Timothy A., Chen, Ziyu, Rao, Manisha, Hollman, Travis J., Li, Yanyun, Socci, Nicholas D., Chavan, Shweta, Viale, Agnes, Mohibullah, Neeman, Bochner, Bernard H., Pietzak, Eugene J., Teo, Min Yuen, Iyer, Gopa, Rosenberg, Jonathan E., Bajorin, Dean F., Kaag, Matthew, Merrill, Suzanne B., Joshi, Monika, Adam, Rosalyn, Taylor, III, John A., Clark, Peter E., Raman, Jay D., Reuter, Victor E., Chen, Yu, Funt, Samuel A., Solit, David B., DeGraff, David J., and Al-Ahmadie, Hikmat A.

Published
2022
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9. TNFR2/14-3-3[epsilon] signaling complex instructs macrophage plasticity in inflammation and autoimmunity

Author

Fu, Wenyu, Hu, Wenhuo, Yi, Young-Su, Hettinghouse, Aubryanna, Sun, Guodong, Bi, Yufei, He, Wenjun, Zhang, Lei, Gao, Guanmin, Liu, Jody, Toyo-oka, Kazuhito, Xiao, Guozhi, Solit, David B., Loke, Png, and Liu, Chuan-ju

Subjects
Autoimmunity -- Genetic aspects -- Health aspects, Cytokine receptors -- Genetic aspects -- Health aspects, Tumor necrosis factor -- Health aspects -- Genetic aspects, Cellular signal transduction -- Genetic aspects -- Health aspects, Macrophages -- Genetic aspects -- Physiological aspects, Rheumatoid arthritis -- Development and progression -- Genetic aspects, Health care industry
Abstract

TNFR1 and TNFR2 have received prominent attention because of their dominance in the pathogenesis of inflammation and autoimmunity. TNFR1 has been extensively studied and primarily mediates inflammation. TNFR2 remains far less studied, although emerging evidence demonstrates that TNFR2 plays an antiinflammatory and immunoregulatory role in various conditions and diseases. Herein, we report that TNFR2 regulates macrophage polarization, a highly dynamic process controlled by largely unidentified intracellular regulators. Using biochemical copurification and mass spectrometry approaches, we isolated the signaling molecule 14-3-3[epsilon] as a component of TNFR2 complexes in response to progranulin stimulation in macrophages. In addition, 14-3-3[epsilon] was essential for TNFR2 signaling-mediated regulation of macrophage polarization and switch. Both global and myeloid-specific deletion of 14-3-3[epsilon] resulted in exacerbated inflammatory arthritis and counteracted the protective effects of progranulin-mediated TNFR2 activation against inflammation and autoimmunity. TNFR2/14-3-3[epsilon] signaled through PI3K/Akt/mTOR to restrict NF-[kappa]B activation while simultaneously stimulating C/EBP[beta] activation, thereby instructing macrophage plasticity. Collectively, this study identifies 14-3-3[epsilon] as a previously unrecognized vital component of the TNFR2 receptor complex and provides new insights into the TNFR2 signaling, particularly its role in macrophage polarization with therapeutic implications for various inflammatory and autoimmune diseases with activation of the TNFR2/14-3-3[epsilon] antiinflammatory pathway., Introduction Rheumatoid arthritis (RA) is a common chronic autoimmune condition characterized by inflammatory joint disease (1), resulting from protracted inflammation of the synovial membrane. Macrophages are a major subset of [...]

Published
2021
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10. Abstract 2: Vertical MAPK pathway targeting in novel genetically engineered mouse and cell line models of NF1-altered melanoma: the mSK-Mel murine cohort

Author

Jones, Alexis M., primary, Hanrahan, Aphrothiti J., additional, Nissan, Moriah H., additional, Monette, Sebastien, additional, Chen, Ziyu, additional, Hu, Wenhuo, additional, Misale, Sandra, additional, Schulze, Isabell, additional, Vasani, Naresh, additional, Liu, Cailian, additional, Yang, Xia, additional, Abu-Akeel, Mohsen, additional, de Stanchina, Elisa, additional, Schultz, Nikolaus, additional, Berger, Michael F., additional, Rosen, Neal, additional, Merghoub, Taha, additional, and Solit, David B., additional

Published
2023
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11. Data from AKT1 E17K Inhibits Cancer Cell Migration by Abrogating β-Catenin Signaling

Author

Gao, Sizhi Paul, primary, Kiliti, Amber J., primary, Zhang, Kai, primary, Vasani, Naresh, primary, Mao, Ninghui, primary, Jordan, Emmet, primary, Wise, Hannah C., primary, Shrestha Bhattarai, Tripti, primary, Hu, Wenhuo, primary, Dorso, Madeline, primary, Rodrigues, James A., primary, Kim, Kwanghee, primary, Hanrahan, Aphrothiti J., primary, Razavi, Pedram, primary, Carver, Brett, primary, Chandarlapaty, Sarat, primary, Reis-Filho, Jorge S., primary, Taylor, Barry S., primary, and Solit, David B., primary

Published
2023
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12. Supplementary Figures 1-12, Supplementary Tables 1-3 from AKT1 E17K Inhibits Cancer Cell Migration by Abrogating β-Catenin Signaling

Author

Gao, Sizhi Paul, primary, Kiliti, Amber J., primary, Zhang, Kai, primary, Vasani, Naresh, primary, Mao, Ninghui, primary, Jordan, Emmet, primary, Wise, Hannah C., primary, Shrestha Bhattarai, Tripti, primary, Hu, Wenhuo, primary, Dorso, Madeline, primary, Rodrigues, James A., primary, Kim, Kwanghee, primary, Hanrahan, Aphrothiti J., primary, Razavi, Pedram, primary, Carver, Brett, primary, Chandarlapaty, Sarat, primary, Reis-Filho, Jorge S., primary, Taylor, Barry S., primary, and Solit, David B., primary

Published
2023
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13. Supplementary Table 1 from Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, primary, Hu, Wenhuo, primary, Gadal, Sunyana, primary, Hieronymus, Haley, primary, Wang, Shangqian, primary, Lee, Young Sun, primary, Sullivan, Patrick, primary, Zhang, Zeda, primary, Choi, Danielle, primary, Rosen, Neal, primary, Sawyers, Charles L., primary, Gopalan, Anuradha, primary, Chen, Yu, primary, and Carver, Brett S., primary

Published
2023
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14. Supplementary Data from Leveraging Systematic Functional Analysis to Benchmark an In Silico Framework Distinguishes Driver from Passenger MEK Mutants in Cancer

Author

Hanrahan, Aphrothiti J., primary, Sylvester, Brooke E., primary, Chang, Matthew T., primary, Elzein, Arijh, primary, Gao, Jianjiong, primary, Han, Weiwei, primary, Liu, Ye, primary, Xu, Dong, primary, Gao, Sizhi P., primary, Gorelick, Alexander N., primary, Jones, Alexis M., primary, Kiliti, Amber J., primary, Nissan, Moriah H., primary, Nimura, Clare A., primary, Poteshman, Abigail N., primary, Yao, Zhan, primary, Gao, Yijun, primary, Hu, Wenhuo, primary, Wise, Hannah C., primary, Gavrila, Elena I., primary, Shoushtari, Alexander N., primary, Tiwari, Shakuntala, primary, Viale, Agnes, primary, Abdel-Wahab, Omar, primary, Merghoub, Taha, primary, Berger, Michael F., primary, Rosen, Neal, primary, Taylor, Barry S., primary, and Solit, David B., primary

Published
2023
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15. Data from Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, primary, Hu, Wenhuo, primary, Gadal, Sunyana, primary, Hieronymus, Haley, primary, Wang, Shangqian, primary, Lee, Young Sun, primary, Sullivan, Patrick, primary, Zhang, Zeda, primary, Choi, Danielle, primary, Rosen, Neal, primary, Sawyers, Charles L., primary, Gopalan, Anuradha, primary, Chen, Yu, primary, and Carver, Brett S., primary

Published
2023
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16. Supplementary Figure Legend from Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, primary, Hu, Wenhuo, primary, Gadal, Sunyana, primary, Hieronymus, Haley, primary, Wang, Shangqian, primary, Lee, Young Sun, primary, Sullivan, Patrick, primary, Zhang, Zeda, primary, Choi, Danielle, primary, Rosen, Neal, primary, Sawyers, Charles L., primary, Gopalan, Anuradha, primary, Chen, Yu, primary, and Carver, Brett S., primary

Published
2023
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17. Supplementary Figures from Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, primary, Hu, Wenhuo, primary, Gadal, Sunyana, primary, Hieronymus, Haley, primary, Wang, Shangqian, primary, Lee, Young Sun, primary, Sullivan, Patrick, primary, Zhang, Zeda, primary, Choi, Danielle, primary, Rosen, Neal, primary, Sawyers, Charles L., primary, Gopalan, Anuradha, primary, Chen, Yu, primary, and Carver, Brett S., primary

Published
2023
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19. Supplementary Methods and Supplementary Figures 1 through 14 from Oligodendrocyte Progenitor Cells Promote Neovascularization in Glioma by Disrupting the Blood–Brain Barrier

Author

Huang, Yujie, primary, Hoffman, Caitlin, primary, Rajappa, Prajwal, primary, Kim, Joon-Hyung, primary, Hu, Wenhuo, primary, Huse, Jason, primary, Tang, Zhongshu, primary, Li, Xuri, primary, Weksler, Babette, primary, Bromberg, Jacqueline, primary, Lyden, David C., primary, and Greenfield, Jeffrey P., primary

Published
2023
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20. Supplementary Table 1 from Oligodendrocyte Progenitor Cells Promote Neovascularization in Glioma by Disrupting the Blood–Brain Barrier

Author

Huang, Yujie, primary, Hoffman, Caitlin, primary, Rajappa, Prajwal, primary, Kim, Joon-Hyung, primary, Hu, Wenhuo, primary, Huse, Jason, primary, Tang, Zhongshu, primary, Li, Xuri, primary, Weksler, Babette, primary, Bromberg, Jacqueline, primary, Lyden, David C., primary, and Greenfield, Jeffrey P., primary

Published
2023
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23. Abstract B003: Inactivation mutations of Kmt2c/d license a molecular “field effect” and prime the urothelium for tumorigenesis

Author

Wang, Naitao, primary, Pachai, Mohini R., additional, Li, Dan, additional, Lee, Cindy, additional, Warda, Sarah, additional, Xie, Guojia, additional, Qian, Cheng, additional, Wong, Wai Pung E., additional, Yan, Juan, additional, Hu, Wenhuo, additional, Smith, Alison, additional, Ge, Kai, additional, Chandarlapaty, Sarat, additional, Iyer, Gopakumar V., additional, Rosenberg, Jonathan E., additional, Solit, David B., additional, AI-Ahmadie, Hikmat A., additional, Chi, Ping, additional, and Chen, Yu, additional

Published
2022
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24. Genomic heterogeneity as a barrier to precision oncology in urothelial cancer

Author

Clinton, Timothy N., primary, Chen, Ziyu, additional, Wise, Hannah, additional, Lenis, Andrew T., additional, Chavan, Shweta, additional, Donoghue, Mark T.A., additional, Almassi, Nima, additional, Chu, Carissa E., additional, Dason, Shawn, additional, Rao, Pavitra, additional, Rodrigues, James A., additional, Vasani, Naresh B., additional, Ridouani, Fourat, additional, Rosenberg, Jonathan E., additional, Bajorin, Dean F., additional, Teo, Min Yuen, additional, Bochner, Bernard H., additional, Berger, Michael F., additional, Ostrovnaya, Irina, additional, Pietzak, Eugene J., additional, Iyer, Gopa, additional, Gao, Sizhi Paul, additional, Hu, Wenhuo, additional, Al-Ahmadie, Hikmat A., additional, and Solit, David B., additional

Published
2022
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25. A proangiogenic signaling axis in myeloid cells promotes malignant progression of glioma

Author

Huang, Yujie, Rajappa, Prajwal, Hu, Wenhuo, Hoffman, Caitlin, Cisse, Babacar, Kim, Joon-Hyung, Gorge, Emilie, Yanowitch, Rachel, Cope, William, Vartanian, Emma, Zhang, Raymond Xu, Tuo, Pisapia, David, Xiang, Jenny, Huse, Jason, Matei, Irina, Peinado, Hector, Bromberg, Jacqueline, Holland, Eric, Ding, Bi-sen, Rafii, Shahin, Lyden, David, and Greenfield, Jeffrey

Subjects
Gliomas -- Genetic aspects -- Development and progression -- Research, Hematopoietic stem cells -- Research, Cellular signal transduction -- Research, Health care industry
Abstract

Tumors are capable of coopting hematopoietic cells to create a suitable microenvironment to support malignant growth. Here, we have demonstrated that upregulation of kinase insert domain receptor (KDR), also known as VEGFR2, in a myeloid cell sublineage is necessary for malignant progression of gliomas in transgenic murine models and is associated with high-grade tumors in patients. KDR expression increased in myeloid cells as myeloid-derived suppressor cells (MDSCs) accumulated, which was associated with the transformation and progression of low-grade fibrillary astrocytoma to high-grade anaplastic gliomas. KDR deficiency in murine BM-derived cells (BMDCs) suppressed the differentiation of myeloid lineages and reduced granulocytic/monocytic populations. The depletion of myeloid-derived KDR compromised its proangiogenic function, which inhibited the angiogenic switch necessary for malignant progression of low-grade to high-grade tumors. We also identified inhibitor of DNA binding protein 2 (ID2) as a key upstream regulator of KDR activation during myeloid differentiation. Deficiency of ID2 in BMDCs led to downregulation of KDR, suppression of proangiogenic myeloid cells, and prevention of low-grade to high-grade transition. Tumor-secreted TGF-[beta]and granulocyte-macrophage CSF (GM-CSF) enhanced the KDR/ ID2 signaling axis in BMDCs. Our results suggest that modulation of KDR/ID2 signaling may restrict tumor-associated myeloid cells and could potentially be a therapeutic strategy for preventing transformation of premalignant gliomas., Introduction The emerging role of BM-derived cells (BMDCs), including myeloid-derived suppressor cells (MDSCs), dendritic cells, neutrophils, and macrophages (1-6), has become a focus of recent research in malignant progression. Numerous [...]

Published
2017
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27. Abstract 1596: Genomic heterogeneity as a barrier to precision oncology in urothelial cancer

Author

Chen, Ziyu, primary, Clinton, Timothy N., additional, Park, Soonbum, additional, Lenis, Andrew T., additional, Donoghue, Mark, additional, Rosenberg, Jonathan E., additional, Dean, Bajorin F., additional, Teo, Min Y., additional, Bochner, Bernard H., additional, Ostrovnaya, Irina, additional, Pietzak, Eugene J., additional, Iyer, Gopakumar V., additional, Gao, Sizhi, additional, Hu, Wenhuo, additional, Shen, Michael M., additional, Berger, Michael F., additional, Al-Ahmadie, Hikmat A., additional, Abate-Shen, Corinne T., additional, and Solit, David B., additional

Published
2022
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28. Alternative transcription initiation leads to expression of a novel ALK isoform in cancer

Author

Wiesner, Thomas, Lee, William, Obenauf, Anna C., Ran, Leili, Murali, Rajmohan, Zhang, Qi Fan, Wong, Elissa W.P., Hu, Wenhuo, Scott, Sasinya N., Shah, Ronak H., Landa, Inigo, Button, Julia, Lailler, Nathalie, Sboner, Andrea, Gao, Dong, Murphy, Devan A., Cao, Zhen, Shukla, Shipra, Hollmann, Travis J., Wang, Lu, Borsu, Laetitia, Merghoub, Taha, Schwartz, Gary K., Postow, Michael A., Ariyan, Charlotte E., Fagin, James A., Zheng, Deyou, Ladanyi, Marc, Busam, Klaus J., Berger, Michael F., Chen, Yu, and Chi, Ping

Subjects
Cancer -- Development and progression -- Health aspects -- Genetic aspects, Genetic transcription -- Health aspects, Oncogenes -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Activation of oncogenes by mechanisms other than genetic aberrations such as mutations, translocations, or amplifications is largely undefined. Here we report a novel isoform of the anaplastic lymphoma kinase (ALK) that is expressed in ~11% of melanomas and sporadically in other human cancer types, but not in normal tissues. The novel ALK transcript initiates from a de novo alternative transcription initiation (ATI) site in ALK intron 19, and was termed [ALK.sup.ATI]. In [ALK.sup.ATI]-expressing tumours, the ATI site is enriched for H3K4me3 and RNA polymerase II, chromatin marks characteristic of active transcription initiation sites (1). [ALK.sup.ATI] is expressed from both ALK alleles, and no recurrent genetic aberrations are found at the ALK locus, indicating that the transcriptional activation is independent of genetic aberrations at the ALK locus. The [ALK.sup.ATI] transcript encodes three proteins with molecular weights of 61.1, 60.8 and 58.7 kilodaltons, consisting primarily of the intracellular tyrosine kinase domain. [ALK.sup.ATI] stimulates multiple oncogenic signalling pathways, drives growth-factor-independent cell proliferation in vitro, and promotes tumorigenesis in vivo in mouse models. ALK inhibitors can suppress the kinase activity of [ALK.sup.ATI], suggesting that patients with [ALK.sup.ATI]-expressing tumours may benefit from ALK inhibitors. Our findings suggest a novel mechanism of oncogene activation in cancer through de novo alternative transcription initiation., To identify novel mechanisms of oncogene activation, we performed transcriptome analyses (RNA sequencing (RNA-seq)) of metastatic melanoma and thyroid carcinoma. We used an algorithm (2) to investigate the differential expression [...]

Published
2015

29. Additional file 2 of The immune subtypes and landscape of sarcomas

Author

Weng, Weiwei, Yu, Lin, Li, Zhang, Tan, Cong, Lv, Jiaojie, Lao, I. Weng, Hu, Wenhuo, Deng, Zhenzhong, Liu, Zebing, Wang, Jian, and Xu, Midie

Abstract

Additional file2. Figure S2: A Sample clustering. B Scale-free fit index for various soft-thresholding powers (β). C Mean connectivity for various soft-thresholding powers.

Published
2022
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30. Additional file 3 of The immune subtypes and landscape of sarcomas

Author

Weng, Weiwei, Yu, Lin, Li, Zhang, Tan, Cong, Lv, Jiaojie, Lao, I. Weng, Hu, Wenhuo, Deng, Zhenzhong, Liu, Zebing, Wang, Jian, and Xu, Midie

Abstract

Additional file3. Figure S3: The estimated proportion of significant immune-related features among IMS subgroups with FDR < 0.05. The top and bottom of the box are the upper quartile (Q3) and the lower quartile (Q1) of the data, respectively. The solid black line in the box represents the median. The whiskers represent the maximum and minimum values of this group of data. The Kruskal-Wallis test was used to assess significant differences. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Published
2022
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31. Additional file 1 of The immune subtypes and landscape of sarcomas

Author

Weng, Weiwei, Yu, Lin, Li, Zhang, Tan, Cong, Lv, Jiaojie, Lao, I. Weng, Hu, Wenhuo, Deng, Zhenzhong, Liu, Zebing, Wang, Jian, and Xu, Midie

Abstract

Additional file1. Figure S1: A-B Cumulative distribution function curve (A) and (B) delta area of immune-related genes in the cohort from TCGA.

Published
2022
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32. Upper tract urothelial carcinoma transcriptome profiling and immune microenvironment characterization.

Author

Yip, Wesley, primary, Kim, Kwanghee, additional, Kuo, Fengshen, additional, Lenis, Andrew Thomas, additional, Chen, Jie-Fu, additional, Hu, Wenhuo, additional, Clinton, Timothy Nguyen, additional, Chu, Carissa Ellen, additional, Almassi, Nima, additional, Tracey, Andrew, additional, Reisz, Peter, additional, Thomas, Jasmine, additional, Nogueira, Lucas, additional, Fujii, Yoichi, additional, Iyer, Gopa, additional, Al-Ahmadie, Hikmat A., additional, Hakimi, A. Ari, additional, Merghoub, Taha, additional, Solit, David B., additional, and Coleman, Jonathan, additional

Published
2022
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33. PD43-06 TUMOR STRATIFICATION OF UPPER TRACT UROTHELIAL CARCINOMA BY GENE EXPRESSION PROFILING AND GENETIC VARIATION

Author

Clinton, Timothy, primary, Kim, Kwanghee, additional, Hu, Wenhuo, additional, Almassi, Nima, additional, Tracey, Andrew, additional, Lenis, Andrew, additional, Reisz, Peter, additional, Durdin, Trey, additional, Wong, Nathan, additional, Iyer, Gopa, additional, Bochner, Bernard, additional, Pietzak, Eugene, additional, Al-Ahmadie, Hikmat, additional, Solit, David, additional, and Coleman, Jonathan, additional

Published
2021
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37. 14-3-3 epsilon is an intracellular component of TNFR2 receptor complex and its activation protects against osteoarthritis

Author

Fu, Wenyu, primary, Hettinghouse, Aubryanna, additional, Chen, Yujianan, additional, Hu, Wenhuo, additional, Ding, Xiang, additional, Chen, Meng, additional, Ding, Yuanjing, additional, Mundra, Jyoti, additional, Song, Wenhao, additional, Liu, Ronghan, additional, Yi, Young-Su, additional, Attur, Mukundan, additional, Samuels, Jonathan, additional, Strauss, Eric, additional, Leucht, Philipp, additional, Schwarzkopf, Ran, additional, and Liu, Chuan-ju, additional

Published
2021
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38. Genomic characterization of bladder cancer with variant histology.

Author

Lenis, Andrew Thomas, primary, Clinton, Timothy Nguyen, additional, Hu, Wenhuo, additional, Almassi, Nima, additional, Reisz, Peter, additional, Truong, Hong, additional, Thomas, Jasmine, additional, Nagar, Karan, additional, Goh, Alvin, additional, Cha, Eugene K., additional, Donahue, Timothy F., additional, Bochner, Bernard H., additional, Pietzak, Eugene J., additional, Kim, Kwanghee, additional, Iyer, Gopa, additional, Solit, David B., additional, and Al-Ahmadie, Hikmat A, additional

Published
2021
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39. Bach2 Deficiency Promotes Intestinal Epithelial Regeneration by Accelerating DNA Repair in Intestinal Stem Cells

Author

Li, Yuanchuang, primary, Rao, Xinxin, additional, Tang, Peiyuan, additional, Chen, Shengzhi, additional, Guo, Qiang, additional, Fu, Guoxiang, additional, Pan, Mengxue, additional, Liang, Liping, additional, Yao, Ye, additional, Gao, Xiaoxue, additional, Zhou, Yi, additional, Zhang, Zhen, additional, Xu, Xiaoya, additional, Hu, Wenhuo, additional, Gao, Jianjun, additional, and Hua, Guoqiang, additional

Published
2021
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40. AKT1 E17K Inhibits Cancer Cell Migration by Abrogating β-Catenin Signaling

Author

Gao, Sizhi Paul, primary, Kiliti, Amber J., additional, Zhang, Kai, additional, Vasani, Naresh, additional, Mao, Ninghui, additional, Jordan, Emmet, additional, Wise, Hannah C., additional, Shrestha Bhattarai, Tripti, additional, Hu, Wenhuo, additional, Dorso, Madeline, additional, Rodrigues, James A., additional, Kim, Kwanghee, additional, Hanrahan, Aphrothiti J., additional, Razavi, Pedram, additional, Carver, Brett, additional, Chandarlapaty, Sarat, additional, Reis-Filho, Jorge S., additional, Taylor, Barry S., additional, and Solit, David B., additional

Published
2020
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42. Leveraging Systematic Functional Analysis to Benchmark an In Silico Framework Distinguishes Driver from Passenger MEK Mutants in Cancer

Author

Hanrahan, Aphrothiti J., primary, Sylvester, Brooke E., additional, Chang, Matthew T., additional, Elzein, Arijh, additional, Gao, Jianjiong, additional, Han, Weiwei, additional, Liu, Ye, additional, Xu, Dong, additional, Gao, Sizhi P., additional, Gorelick, Alexander N., additional, Jones, Alexis M., additional, Kiliti, Amber J., additional, Nissan, Moriah H., additional, Nimura, Clare A., additional, Poteshman, Abigail N., additional, Yao, Zhan, additional, Gao, Yijun, additional, Hu, Wenhuo, additional, Wise, Hannah C., additional, Gavrila, Elena I., additional, Shoushtari, Alexander N., additional, Tiwari, Shakuntala, additional, Viale, Agnes, additional, Abdel-Wahab, Omar, additional, Merghoub, Taha, additional, Berger, Michael F., additional, Rosen, Neal, additional, Taylor, Barry S., additional, and Solit, David B., additional

Published
2020
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44. Modeling biological and genetic diversity in upper tract urothelial carcinoma with patient derived xenografts

Author

Kim, Kwanghee, primary, Hu, Wenhuo, additional, Audenet, François, additional, Almassi, Nima, additional, Hanrahan, Aphrothiti J., additional, Murray, Katie, additional, Bagrodia, Aditya, additional, Wong, Nathan, additional, Clinton, Timothy N., additional, Dason, Shawn, additional, Mohan, Vishnu, additional, Jebiwott, Sylvia, additional, Nagar, Karan, additional, Gao, Jianjiong, additional, Penson, Alex, additional, Hughes, Chris, additional, Gordon, Benjamin, additional, Chen, Ziyu, additional, Dong, Yiyu, additional, Watson, Philip A., additional, Alvim, Ricardo, additional, Elzein, Arijh, additional, Gao, Sizhi P., additional, Cocco, Emiliano, additional, Santin, Alessandro D., additional, Ostrovnaya, Irina, additional, Hsieh, James J., additional, Sagi, Irit, additional, Pietzak, Eugene J., additional, Hakimi, A. Ari, additional, Rosenberg, Jonathan E., additional, Iyer, Gopa, additional, Vargas, Herbert A., additional, Scaltriti, Maurizio, additional, Al-Ahmadie, Hikmat, additional, Solit, David B., additional, and Coleman, Jonathan A., additional

Published
2020
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45. PD42-06 DEFINING THE GENETIC EVOLUTION OF EPIGENETIC ALTERATIONS IN BLADDER CANCER

Author

Clinton*, Timothy, primary, Wise, Hannah, additional, Almassi, Nima, additional, Chavan, Shweta, additional, Hu, Wenhuo, additional, Dason, Shawn, additional, Pietzak, Eugene, additional, Cha, Eugene, additional, Dalbagni, Guido, additional, Iyer, Gopa, additional, Bochner, Bernard, additional, Rosenberg, Jonathan, additional, Bajorin, Dean, additional, Arcila, Maria, additional, Al-Ahmadie, Hikmat, additional, Taylor, Barry, additional, and Solit, David, additional

Published
2020
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46. Oncogenic ERG Represses PI3K Signaling through Downregulation of IRS2

Author

Mao, Ninghui, primary, Gao, Dong, additional, Hu, Wenhuo, additional, Gadal, Sunyana, additional, Hieronymus, Haley, additional, Wang, Shangqian, additional, Lee, Young Sun, additional, Sullivan, Patrick, additional, Zhang, Zeda, additional, Choi, Danielle, additional, Rosen, Neal, additional, Sawyers, Charles L., additional, Gopalan, Anuradha, additional, Chen, Yu, additional, and Carver, Brett S., additional

Published
2020
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47. Defining the genetic evolution of epigenetic alterations in bladder cancer.

Author

Clinton, Timothy Nguyen, primary, Wise, Hannah, additional, Almassi, Nima, additional, Chavan, Shweta S., additional, Hu, Wenhuo, additional, Gao, Sizhi Paul, additional, Hanrahan, Aphrothiti, additional, Dason, Shawn, additional, Pietzak, Eugene J., additional, Carlo, Maria Isabel, additional, Funt, Samuel Aaron, additional, Teo, Min Yuen, additional, Iyer, Gopa, additional, Bochner, Bernard H., additional, Rosenberg, Jonathan E., additional, Bajorin, Dean F., additional, Arcila, Maria E., additional, Al-Ahmadie, Hikmat, additional, Taylor, Barry S., additional, and Solit, David B., additional

Published
2020
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48. 14-3-3 epsilon is an intracellular component of TNFR2 receptor complex and its activation protects against osteoarthritis.

Author

Wenyu Fu, Hettinghouse, Aubryanna, Yujianan Chen, Wenhuo Hu, Xiang Ding, Meng Chen, Yuanjing Ding, Mundra, Jyoti, Wenhao Song, Ronghan Liu, Young-Su Yi, Attur, Mukundan, Samuels, Jonathan, Strauss, Eric, Leucht, Philipp, Schwarzkopf, Ran, Chuan-ju Liu, Fu, Wenyu, Chen, Yujianan, and Hu, Wenhuo

Subjects
PROTEIN metabolism, CARTILAGE cells, RESEARCH, ANIMAL experimentation, RESEARCH methodology, CELL receptors, MEDICAL cooperation, EVALUATION research, CELLULAR signal transduction, COMPARATIVE studies, OSTEOARTHRITIS, DNA-binding proteins, RESEARCH funding, ARTICULAR cartilage, CARRIER proteins, MICE
Abstract

Objectives: Osteoarthritis (OA) is the most common joint disease; however, the indeterminate nature of mechanisms by which OA develops has restrained advancement of therapeutic targets. TNF signalling has been implicated in the pathogenesis of OA. TNFR1 primarily mediates inflammation, whereas emerging evidences demonstrate that TNFR2 plays an anti-inflammatory and protective role in several diseases and conditions. This study aims to decipher TNFR2 signalling in chondrocytes and OA.Methods: Biochemical copurification and proteomics screen were performed to isolate the intracellular cofactors of TNFR2 complex. Bulk and single cell RNA-seq were employed to determine 14-3-3 epsilon (14-3-3ε) expression in human normal and OA cartilage. Transcription factor activity screen was used to isolate the transcription factors downstream of TNFR2/14-3-3ε. Various cell-based assays and genetically modified mice with naturally occurring and surgically induced OA were performed to examine the importance of this pathway in chondrocytes and OA.Results: Signalling molecule 14-3-3ε was identified as an intracellular component of TNFR2 complexes in chondrocytes in response to progranulin (PGRN), a growth factor known to protect against OA primarily through activating TNFR2. 14-3-3ε was downregulated in OA and its deficiency deteriorated OA. 14-3-3ε was required for PGRN regulation of chondrocyte metabolism. In addition, both global and chondrocyte-specific deletion of 14-3-3ε largely abolished PGRN's therapeutic effects against OA. Furthermore, PGRN/TNFR2/14-3-3ε signalled through activating extracellular signal-regulated kinase (ERK)-dependent Elk-1 while suppressing nuclear factor kappa B (NF-κB) in chondrocytes.Conclusions: This study identifies 14-3-3ε as an inducible component of TNFR2 receptor complex in response to PGRN in chondrocytes and presents a previously unrecognised TNFR2 pathway in the pathogenesis of OA. [ABSTRACT FROM AUTHOR]

Published
2021
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