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297 results on '"Choi, Kwangmin"'

6. RUNX represses Pmp22 to drive neurofibromagenesis.

Author

Hall, Ashley, Choi, Kwangmin, Liu, Wei, Rose, Jonathan, Zhao, Chuntao, Yu, Yanan, Na, Youjin, Cai, Yuqi, Coover, Robert, Lin, Yi, Dombi, Eva, Kim, MiOk, Levanon, Ditsa, Groner, Yoram, Boscolo, Elisa, Pan, Dao, Liu, P, Lu, Q, Ratner, Nancy, Huang, Gang, and Wu, Jianqiang

Subjects
Alleles, Animals, Base Sequence, Cell Proliferation, Cell Survival, Core Binding Factor Alpha 2 Subunit, Core Binding Factor Alpha 3 Subunit, Core Binding Factor beta Subunit, Female, Gene Deletion, Gene Expression Regulation, Neoplastic, Humans, Male, Mice, Mice, Nude, Myelin Proteins, Neurofibroma, Promoter Regions, Genetic, RNA, Small Interfering, Schwann Cells, Signal Transduction, Transcriptome
Abstract

Patients with neurofibromatosis type 1 (NF1) are predisposed to develop neurofibromas, but the underlying molecular mechanisms of neurofibromagenesis are not fully understood. We showed dual genetic deletion of Runx1 and Runx3 in Schwann cells (SCs) and SC precursors delayed neurofibromagenesis and prolonged mouse survival. We identified peripheral myelin protein 22 (Pmp22/Gas3) related to neurofibroma initiation. Knockdown of Pmp22 with short hairpin RNAs increased Runx1fl/fl;Runx3fl/fl;Nf1fl/fl;DhhCre tumor-derived sphere numbers and enabled significantly more neurofibroma-like microlesions on transplantation. Conversely, overexpression of Pmp22 in mouse neurofibroma SCs decreased cell proliferation. Mechanistically, RUNX1/3 regulated alternative promoter usage and induced levels of protein expression of Pmp22 to control SC growth. Last, pharmacological inhibition of RUNX/core-binding factor β (CBFB) activity significantly reduced neurofibroma volume in vivo. Thus, we identified a signaling pathway involving RUNX1/3 suppression of Pmp22 in neurofibroma initiation and/or maintenance. Targeting disruption of RUNX/CBFB interaction might provide a novel therapy for patients with neurofibroma.

Published
2019

7. Chemotherapy resistance in acute myeloid leukemia is mediated by A20 suppression of spontaneous necroptosis.

Author

Culver-Cochran, Ashley E., Hassan, Aishlin, Hueneman, Kathleen, Choi, Kwangmin, Ma, Averil, VanCauwenbergh, Brett, O'Brien, Eric, Wunderlich, Mark, Perentesis, John P., and Starczynowski, Daniel T.

Subjects
ACUTE myeloid leukemia, TUMOR necrosis factors, HEMATOLOGIC malignancies, STEM cell transplantation, REMISSION induction
Abstract

Acute myeloid leukemia (AML) is a deadly hematopoietic malignancy. Although many patients achieve complete remission with standard induction therapy, a combination of cytarabine and anthracycline, ~40% of patients have induction failure. These refractory patients pose a treatment challenge, as they do not respond to salvage therapy or allogeneic stem cell transplant. Herein, we show that AML patients who experience induction failure have elevated expression of the NF-κB target gene tumor necrosis factor alpha-induced protein-3 (TNFAIP3/A20) and impaired necroptotic cell death. A20High AML are resistant to anthracyclines, while A20Low AML are sensitive. Loss of A20 in AML restores sensitivity to anthracycline treatment by inducing necroptosis. Moreover, A20 prevents necroptosis in AML by targeting the necroptosis effector RIPK1, and anthracycline-induced necroptosis is abrogated in A20High AML. These findings suggest that NF-κB-driven A20 overexpression plays a role in failed chemotherapy induction and highlights the potential of targeting an alternative cell death pathway in AML. Patients with Acute myeloid leukemia (AML) who do not respond to standard chemotherapy have limited treatment options. Here, the authors show that high expression of the gene TNFAIP3/A20 in AML cells contributes to chemotherapy resistance by blocking a type of cell death called necroptosis. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Natural and Artificial Aging Effects on the Deformation Behaviors of Al–Mg–Zn Alloy Sheets.

Author

Choi, Kwangmin, Lee, Sangjun, and Bae, Donghyun

Subjects
*STRAINS & stresses (Mechanics), *ALUMINUM alloys, *TRANSMISSION electron microscopy, *PRECIPITATION (Chemistry), *DISLOCATION density
Abstract

This study investigated the effects of aging profiles on the precipitate formation and the corresponding strengthening and deformation behaviors of Al–Mg–Zn alloys. The alloys subjected to natural aging (NA) demonstrated significantly enhanced ductility at equivalent stress levels compared to those subjected to artificial aging (AA). In AA-treated alloys, η′ and η-phases with incoherent interfaces were formed, while GP zones and solute clusters were dominantly exhibited in the NA-treated alloy with a coherent interface with the matrix. Due to the change in interface bonding, the dislocation movement and pinning behavior after deformation are varied depending on the aging conditions of Al–Mg–Zn alloy sheet. Thus, the elongation to fracture of the NA alloy sheet was improved compared to that of the AA alloy sheet because of the enhanced work-hardening capacity and the thin precipitate-free zone (PFZ). Deformation textures and dislocation densities varied between NA and AA treatments, as revealed by electron backscatter diffraction (EBSD) and kernel average misorientation (KAM) analysis. The interactions between the precipitates, dislocations, and the PFZ in the AA- and NA-treated alloys were analyzed via transmission electron microscopy (TEM). The insights gained from this research provide a valuable foundation for industrial applications, particularly in sectors demanding lightweight, high-strength materials, where optimizing the aging process can lead to significant performance improvement and cost savings. [ABSTRACT FROM AUTHOR]

Published
2024
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10. Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes.

Author

Hayashi, Yoshihiro, Zhang, Yue, Yokota, Asumi, Yan, Xiaomei, Liu, Jinqin, Choi, Kwangmin, Li, Bing, Sashida, Goro, Peng, Yanyan, Xu, Zefeng, Huang, Rui, Zhang, Lulu, Freudiger, George M, Wang, Jingya, Dong, Yunzhu, Zhou, Yile, Wang, Jieyu, Wu, Lingyun, Bu, Jiachen, Chen, Aili, Zhao, Xinghui, Sun, Xiujuan, Chetal, Kashish, Olsson, Andre, Watanabe, Miki, Romick-Rosendale, Lindsey E, Harada, Hironori, Shih, Lee-Yung, Tse, William, Bridges, James P, Caligiuri, Michael A, Huang, Taosheng, Zheng, Yi, Witte, David P, Wang, Qian-Fei, Qu, Cheng-Kui, Salomonis, Nathan, Grimes, H Leighton, Nimer, Stephen D, Xiao, Zhijian, and Huang, Gang

Subjects
Animals, Mice, Knockout, Humans, Mice, Myelodysplastic Syndromes, Histone-Lysine N-Methyltransferase, Gene Expression Regulation, Neoplastic, Core Binding Factor Alpha 2 Subunit, Myeloid-Lymphoid Leukemia Protein, Hypoxia-Inducible Factor 1, alpha Subunit, Metabolome, Hypoxia, Rare Diseases, Hematology, Genetics, Cancer, Stem Cell Research, Aging, 2.1 Biological and endogenous factors, Aetiology, Oncology and Carcinogenesis
Abstract

Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic disorders that are incurable with conventional therapy. Their incidence is increasing with global population aging. Although many genetic, epigenetic, splicing, and metabolic aberrations have been identified in patients with MDS, their clinical features are quite similar. Here, we show that hypoxia-independent activation of hypoxia-inducible factor 1α (HIF1A) signaling is both necessary and sufficient to induce dysplastic and cytopenic MDS phenotypes. The HIF1A transcriptional signature is generally activated in MDS patient bone marrow stem/progenitors. Major MDS-associated mutations (Dnmt3a, Tet2, Asxl1, Runx1, and Mll1) activate the HIF1A signature. Although inducible activation of HIF1A signaling in hematopoietic cells is sufficient to induce MDS phenotypes, both genetic and chemical inhibition of HIF1A signaling rescues MDS phenotypes in a mouse model of MDS. These findings reveal HIF1A as a central pathobiologic mediator of MDS and as an effective therapeutic target for a broad spectrum of patients with MDS.Significance: We showed that dysregulation of HIF1A signaling could generate the clinically relevant diversity of MDS phenotypes by functioning as a signaling funnel for MDS driver mutations. This could resolve the disconnection between genotypes and phenotypes and provide a new clue as to how a variety of driver mutations cause common MDS phenotypes. Cancer Discov; 8(11); 1438-57. ©2018 AACR. See related commentary by Chen and Steidl, p. 1355 This article is highlighted in the In This Issue feature, p. 1333.

Published
2018

11. Hepatic Ago2-mediated RNA silencing controls energy metabolism linked to AMPK activation and obesity-associated pathophysiology.

Author

Zhang, Cai, Seo, Joonbae, Murakami, Kazutoshi, Salem, Esam SB, Bernhard, Elise, Borra, Vishnupriya J, Choi, Kwangmin, Yuan, Celvie L, Chan, Calvin C, Chen, Xiaoting, Huang, Taosheng, Weirauch, Matthew T, Divanovic, Senad, Qi, Nathan R, Thomas, Hala Einakat, Mercer, Carol A, Siomi, Haruhiko, and Nakamura, Takahisa

Subjects
Liver, Mitochondria, Animals, Mice, Inbred C57BL, Mice, Knockout, Humans, Mice, Hyperglycemia, Obesity, Oxygen, Pyruvic Acid, Glucose, Eukaryotic Initiation Factors, MicroRNAs, Glucose Tolerance Test, RNA Interference, Gene Deletion, Glycolysis, Genotype, AMP-Activated Protein Kinases, Argonaute Proteins, Diet, High-Fat, Diabetes, Digestive Diseases, Liver Disease, Nutrition, Genetics, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Metabolic and endocrine
Abstract

RNA silencing inhibits mRNA translation. While mRNA translation accounts for the majority of cellular energy expenditure, it is unclear if RNA silencing regulates energy homeostasis. Here, we report that hepatic Argonaute 2 (Ago2)-mediated RNA silencing regulates both intrinsic energy production and consumption and disturbs energy metabolism in the pathogenesis of obesity. Ago2 regulates expression of specific miRNAs including miR-802, miR-103/107, and miR-148a/152, causing metabolic disruption, while simultaneously suppressing the expression of genes regulating glucose and lipid metabolism, including Hnf1β, Cav1, and Ampka1. Liver-specific Ago2-deletion enhances mitochondrial oxidation and ATP consumption associated with mRNA translation, which results in AMPK activation, and improves obesity-associated pathophysiology. Notably, hepatic Ago2-deficiency improves glucose metabolism in conditions of insulin receptor antagonist treatment, high-fat diet challenge, and hepatic AMPKα1-deletion. The regulation of energy metabolism by Ago2 provides a novel paradigm in which RNA silencing plays an integral role in determining basal metabolic activity in obesity-associated sequelae.

Published
2018

13. Schwann cells modulate nociception in neurofibromatosis 1

Author

Raut, Namrata G.R., primary, Maile, Laura A., additional, Oswalt, Leila M., additional, Mitxelena, Irati, additional, Adlakha, Aaditya, additional, Sprague, Kourtney L., additional, Rupert, Ashley R., additional, Bokros, Lane, additional, Hofmann, Megan C., additional, Patritti-Cram, Jennifer, additional, Rizvi, Tilat A., additional, Queme, Luis F., additional, Choi, Kwangmin, additional, Ratner, Nancy, additional, and Jankowski, Michael P., additional

Published
2024
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15. Insertional Mutagenesis Identifies a STAT3/Arid1b/β-catenin Pathway Driving Neurofibroma Initiation.

Author

Wu, Jianqiang, Keng, Vincent, Patmore, Deanna, Kendall, Jed, Patel, Ami, Jousma, Edwin, Jessen, Walter, Choi, Kwangmin, Tschida, Barbara, Silverstein, Kevin, Fan, Danhua, Schwartz, Eric, Fuchs, James, Zou, Yuanshu, Kim, Mi-Ok, Dombi, Eva, Levy, David, Huang, Gang, Cancelas, Jose, Stemmer-Rachamimov, Anat, Spinner, Robert, Largaespada, David, and Ratner, Nancy

Subjects
Animals, Carcinogenesis, DNA Helicases, DNA-Binding Proteins, Disease Models, Animal, Female, Gene Expression Regulation, Neoplastic, Glycogen Synthase Kinase 3 beta, Histones, Humans, Mice, Mice, Nude, Mutagenesis, Insertional, N-Terminal Acetyltransferase A, Neoplasm Transplantation, Neural Stem Cells, Neurofibromatosis 1, Neurofibromin 1, Nuclear Proteins, Peripheral Nervous System Neoplasms, Phosphorylation, RNA, Small Interfering, STAT3 Transcription Factor, Schwann Cells, Signal Transduction, Transcription Factors, beta Catenin
Abstract

To identify genes and signaling pathways that initiate Neurofibromatosis type 1 (NF1) neurofibromas, we used unbiased insertional mutagenesis screening, mouse models, and molecular analyses. We mapped an Nf1-Stat3-Arid1b/β-catenin pathway that becomes active in the context of Nf1 loss. Genetic deletion of Stat3 in Schwann cell progenitors (SCPs) and Schwann cells (SCs) prevents neurofibroma formation, decreasing SCP self-renewal and β-catenin activity. β-catenin expression rescues effects of Stat3 loss in SCPs. Importantly, P-STAT3 and β-catenin expression correlate in human neurofibromas. Mechanistically, P-Stat3 represses Gsk3β and the SWI/SNF gene Arid1b to increase β-catenin. Knockdown of Arid1b or Gsk3β in Stat3(fl/fl);Nf1(fl/fl);DhhCre SCPs rescues neurofibroma formation after in vivo transplantation. Stat3 represses Arid1b through histone modification in a Brg1-dependent manner, indicating that epigenetic modification plays a role in early tumorigenesis. Our data map a neural tumorigenesis pathway and support testing JAK/STAT and Wnt/β-catenin pathway inhibitors in neurofibroma therapeutic trials.

Published
2016

19. U2AF1 mutations induce oncogenic IRAK4 isoforms and activate innate immune pathways in myeloid malignancies

Author

Smith, Molly A., Choudhary, Gaurav S., Pellagatti, Andrea, Choi, Kwangmin, Bolanos, Lyndsey C., Bhagat, Tushar D., Gordon-Mitchell, Shanisha, Von Ahrens, Dagny, Pradhan, Kith, Steeples, Violetta, Kim, Sanghyun, Steidl, Ulrich, Walter, Matthew, Fraser, Iain D. C., Kulkarni, Aishwarya, Salomonis, Nathan, Komurov, Kakajan, Boultwood, Jacqueline, Verma, Amit, and Starczynowski, Daniel T.

Published
2019
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23. Inactivation of p53 provides a competitive advantage to del(5q) myelodysplastic syndrome hematopoietic stem cells during inflammation

Author

Muto, Tomoya, primary, Walker, Callum S., additional, Agarwal, Puneet, additional, Vick, Eric, additional, Sampson, Avery, additional, Choi, Kwangmin, additional, Niederkorn, Madeline, additional, Ishikawa, Chiharu, additional, Hueneman, Kathleen, additional, Varney, Melinda, additional, and Starczynowski, Daniel T., additional

Published
2023
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24. Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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26. Supplementary Figure 1 from Canonical Wnt/β-catenin Signaling Drives Human Schwann Cell Transformation, Progression, and Tumor Maintenance

Author

Watson, Adrienne L., primary, Rahrmann, Eric P., primary, Moriarity, Branden S., primary, Choi, Kwangmin, primary, Conboy, Caitlin B., primary, Greeley, Andrew D., primary, Halfond, Amanda L., primary, Anderson, Leah K., primary, Wahl, Brian R., primary, Keng, Vincent W., primary, Rizzardi, Anthony E., primary, Forster, Colleen L., primary, Collins, Margaret H., primary, Sarver, Aaron L., primary, Wallace, Margaret R., primary, Schmechel, Stephen C., primary, Ratner, Nancy, primary, and Largaespada, David A., primary

Published
2023
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27. Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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28. Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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30. Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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31. Data from Canonical Wnt/β-catenin Signaling Drives Human Schwann Cell Transformation, Progression, and Tumor Maintenance

Author

Watson, Adrienne L., primary, Rahrmann, Eric P., primary, Moriarity, Branden S., primary, Choi, Kwangmin, primary, Conboy, Caitlin B., primary, Greeley, Andrew D., primary, Halfond, Amanda L., primary, Anderson, Leah K., primary, Wahl, Brian R., primary, Keng, Vincent W., primary, Rizzardi, Anthony E., primary, Forster, Colleen L., primary, Collins, Margaret H., primary, Sarver, Aaron L., primary, Wallace, Margaret R., primary, Schmechel, Stephen C., primary, Ratner, Nancy, primary, and Largaespada, David A., primary

Published
2023
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33. Supplementary Figure 4 from Canonical Wnt/β-catenin Signaling Drives Human Schwann Cell Transformation, Progression, and Tumor Maintenance

Author

Watson, Adrienne L., primary, Rahrmann, Eric P., primary, Moriarity, Branden S., primary, Choi, Kwangmin, primary, Conboy, Caitlin B., primary, Greeley, Andrew D., primary, Halfond, Amanda L., primary, Anderson, Leah K., primary, Wahl, Brian R., primary, Keng, Vincent W., primary, Rizzardi, Anthony E., primary, Forster, Colleen L., primary, Collins, Margaret H., primary, Sarver, Aaron L., primary, Wallace, Margaret R., primary, Schmechel, Stephen C., primary, Ratner, Nancy, primary, and Largaespada, David A., primary

Published
2023
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34. Supplementary Table 1 from Canonical Wnt/β-catenin Signaling Drives Human Schwann Cell Transformation, Progression, and Tumor Maintenance

Author

Watson, Adrienne L., primary, Rahrmann, Eric P., primary, Moriarity, Branden S., primary, Choi, Kwangmin, primary, Conboy, Caitlin B., primary, Greeley, Andrew D., primary, Halfond, Amanda L., primary, Anderson, Leah K., primary, Wahl, Brian R., primary, Keng, Vincent W., primary, Rizzardi, Anthony E., primary, Forster, Colleen L., primary, Collins, Margaret H., primary, Sarver, Aaron L., primary, Wallace, Margaret R., primary, Schmechel, Stephen C., primary, Ratner, Nancy, primary, and Largaespada, David A., primary

Published
2023
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35. Supplementary Table 2 from Canonical Wnt/β-catenin Signaling Drives Human Schwann Cell Transformation, Progression, and Tumor Maintenance

Author

Watson, Adrienne L., primary, Rahrmann, Eric P., primary, Moriarity, Branden S., primary, Choi, Kwangmin, primary, Conboy, Caitlin B., primary, Greeley, Andrew D., primary, Halfond, Amanda L., primary, Anderson, Leah K., primary, Wahl, Brian R., primary, Keng, Vincent W., primary, Rizzardi, Anthony E., primary, Forster, Colleen L., primary, Collins, Margaret H., primary, Sarver, Aaron L., primary, Wallace, Margaret R., primary, Schmechel, Stephen C., primary, Ratner, Nancy, primary, and Largaespada, David A., primary

Published
2023
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36. Supplementary Table and Figure Legends from Canonical Wnt/β-catenin Signaling Drives Human Schwann Cell Transformation, Progression, and Tumor Maintenance

Author

Watson, Adrienne L., primary, Rahrmann, Eric P., primary, Moriarity, Branden S., primary, Choi, Kwangmin, primary, Conboy, Caitlin B., primary, Greeley, Andrew D., primary, Halfond, Amanda L., primary, Anderson, Leah K., primary, Wahl, Brian R., primary, Keng, Vincent W., primary, Rizzardi, Anthony E., primary, Forster, Colleen L., primary, Collins, Margaret H., primary, Sarver, Aaron L., primary, Wallace, Margaret R., primary, Schmechel, Stephen C., primary, Ratner, Nancy, primary, and Largaespada, David A., primary

Published
2023
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37. Supplementary Figure 2 from Canonical Wnt/β-catenin Signaling Drives Human Schwann Cell Transformation, Progression, and Tumor Maintenance

Author

Watson, Adrienne L., primary, Rahrmann, Eric P., primary, Moriarity, Branden S., primary, Choi, Kwangmin, primary, Conboy, Caitlin B., primary, Greeley, Andrew D., primary, Halfond, Amanda L., primary, Anderson, Leah K., primary, Wahl, Brian R., primary, Keng, Vincent W., primary, Rizzardi, Anthony E., primary, Forster, Colleen L., primary, Collins, Margaret H., primary, Sarver, Aaron L., primary, Wallace, Margaret R., primary, Schmechel, Stephen C., primary, Ratner, Nancy, primary, and Largaespada, David A., primary

Published
2023
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38. Supplementary Figure 3 from Canonical Wnt/β-catenin Signaling Drives Human Schwann Cell Transformation, Progression, and Tumor Maintenance

Author

Watson, Adrienne L., primary, Rahrmann, Eric P., primary, Moriarity, Branden S., primary, Choi, Kwangmin, primary, Conboy, Caitlin B., primary, Greeley, Andrew D., primary, Halfond, Amanda L., primary, Anderson, Leah K., primary, Wahl, Brian R., primary, Keng, Vincent W., primary, Rizzardi, Anthony E., primary, Forster, Colleen L., primary, Collins, Margaret H., primary, Sarver, Aaron L., primary, Wallace, Margaret R., primary, Schmechel, Stephen C., primary, Ratner, Nancy, primary, and Largaespada, David A., primary

Published
2023
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43. Schwann cells modulate nociception in neurofibromatosis 1

Author

Raut, Namrata GR, primary, Maile, Laura A, additional, Oswalt, Leila M, additional, Mitxelena, Irati, additional, Adlakha, Aaditya, additional, Sprague, Kourtney L, additional, Rupert, Ashley R, additional, Bokros, Lane, additional, Hofmann, Megan C, additional, Patritti-Cram, Jennifer, additional, Rizvi, Tilat A, additional, Queme, Luis F, additional, Choi, Kwangmin, additional, Ratner, Nancy, additional, and Jankowski, Michael P, additional

Published
2023
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44. Possible role of intragenic DNA hypermethylation in gene silencing of the tumor suppressor gene NR4A3 in acute myeloid leukemia

Author

Shimizu, Ryo, Muto, Tomoya, Aoyama, Kazumasa, Choi, Kwangmin, Takeuchi, Masahiro, Koide, Shuhei, Hasegawa, Nagisa, Isshiki, Yusuke, Togasaki, Emi, Kawajiri-Manako, Chika, Nagao, Yuhei, Tsukamoto, Shokichi, Sakai, Shio, Takeda, Yusuke, Mimura, Naoya, Ohwada, Chikako, Sakaida, Emiko, Iseki, Tohru, Starczynowski, Daniel T., Iwama, Atsushi, Yokote, Koutaro, and Nakaseko, Chiaki

Published
2016
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