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1,135 results on '"Johnson, Gary L."'

3. High-content image-based analysis and proteomic profiling identifies Tau phosphorylation inhibitors in a human iPSC-derived glutamatergic neuronal model of tauopathy

Author

Cheng, Chialin, Reis, Surya A, Adams, Emily T, Fass, Daniel M, Angus, Steven P, Stuhlmiller, Timothy J, Richardson, Jared, Olafson, Hailey, Wang, Eric T, Patnaik, Debasis, Beauchamp, Roberta L, Feldman, Danielle A, Silva, M Catarina, Sur, Mriganka, Johnson, Gary L, Ramesh, Vijaya, Miller, Bruce L, Temple, Sally, Kosik, Kenneth S, Dickerson, Bradford C, and Haggarty, Stephen J

Subjects
Biochemistry and Cell Biology, Biological Sciences, Brain Disorders, Stem Cell Research - Induced Pluripotent Stem Cell - Human, Frontotemporal Dementia (FTD), Alzheimer's Disease, Neurosciences, Acquired Cognitive Impairment, Stem Cell Research - Nonembryonic - Human, Stem Cell Research - Induced Pluripotent Stem Cell, Stem Cell Research, Alzheimer's Disease Related Dementias (ADRD), Dementia, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, Aetiology, Neurological, Basic Helix-Loop-Helix Transcription Factors, Biomarkers, Cell Line, Glutamates, Humans, Image Processing, Computer-Assisted, Induced Pluripotent Stem Cells, Models, Biological, Nerve Tissue Proteins, Neurons, Phosphorylation, Protein Kinases, Proteomics, Pyridines, Pyrimidines, Small Molecule Libraries, Tauopathies, tau Proteins
Abstract

Mutations in MAPT (microtubule-associated protein tau) cause frontotemporal dementia (FTD). MAPT mutations are associated with abnormal tau phosphorylation levels and accumulation of misfolded tau protein that can propagate between neurons ultimately leading to cell death (tauopathy). Recently, a p.A152T tau variant was identified as a risk factor for FTD, Alzheimer's disease, and synucleinopathies. Here we used induced pluripotent stem cells (iPSC) from a patient carrying this p.A152T variant to create a robust, functional cellular assay system for probing pathophysiological tau accumulation and phosphorylation. Using stably transduced iPSC-derived neural progenitor cells engineered to enable inducible expression of the pro-neural transcription factor Neurogenin 2 (Ngn2), we generated disease-relevant, cortical-like glutamatergic neurons in a scalable, high-throughput screening compatible format. Utilizing automated confocal microscopy, and an advanced image-processing pipeline optimized for analysis of morphologically complex human neuronal cultures, we report quantitative, subcellular localization-specific effects of multiple kinase inhibitors on tau, including ones under clinical investigation not previously reported to affect tau phosphorylation. These results demonstrate the potential for using patient iPSC-derived ex vivo models of tauopathy as genetically accurate, disease-relevant systems to probe tau biochemistry and support the discovery of novel therapeutics for tauopathies.

Published
2021

5. Nf1-Mutant Tumors Undergo Transcriptome and Kinome Remodeling after Inhibition of either mTOR or MEK

Author

Pucciarelli, Daniela, Angus, Steven P, Huang, Benjamin, Zhang, Chi, Nakaoka, Hiroki J, Krishnamurthi, Ganesh, Bandyopadhyay, Sourav, Clapp, D Wade, Shannon, Kevin, Johnson, Gary L, and Nakamura, Jean L

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Orphan Drug, Rare Diseases, Neurofibromatosis, Cancer, Neurosciences, Genetics, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Good Health and Well Being, Animals, Cell Line, Tumor, Computational Biology, Disease Models, Animal, Drug Resistance, Neoplasm, Gene Expression Profiling, High-Throughput Nucleotide Sequencing, Humans, Mice, Models, Biological, Mutation, Neurofibromatosis 1, Neurofibromin 1, Protein Kinase Inhibitors, Protein Kinases, Signal Transduction, Transcriptome, Pharmacology and Pharmaceutical Sciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Loss of the tumor suppressor NF1 leads to activation of RAS effector pathways, which are therapeutically targeted by inhibition of mTOR (mTORi) or MEK (MEKi). However, therapeutic inhibition of RAS effectors leads to the development of drug resistance and ultimately disease progression. To investigate molecular signatures in the context of NF1 loss and subsequent acquired drug resistance, we analyzed the exomes, transcriptomes, and kinomes of Nf1-mutant mouse tumor cell lines and derivatives of these lines that acquired resistance to either MEKi or mTORi. Biochemical comparisons of this unique panel of tumor cells, all of which arose in Nf1+/- mice, indicate that loss of heterozygosity of Nf1 as an initial genetic event does not confer a common biochemical signature or response to kinase inhibition. Although acquired drug resistance by Nf1-mutant tumor cells was accompanied by altered kinomes and irreversibly altered transcriptomes, functionally in multiple Nf1-mutant tumor cell lines, MEKi resistance was a stable phenotype, in contrast to mTORi resistance, which was reversible. Collectively, these findings demonstrate that Nf1-mutant tumors represent a heterogeneous group biochemically and undergo broader remodeling of kinome activity and gene expression in response to targeted kinase inhibition.

Published
2020

6. FDA Approaches in Monitoring Drug Quality, Forces Impacting the Drug Quality, and Recent Alternative Strategies to Assess Quality in the US Drug Supply

Author

Almeter, Philip J., Isaacs, James T., Hunter, Aaron N., Henderson, Bradley S., Platt, Thomas, Mitchell, Billie J., Do, David, Brainard, Alyssa B., Brown, Joshua E., Stone, Rachael M., Nguyen, Bao-Han, Warren, Matthew F., Bhaktawara, Smaran A., Bossle, Megan N., Long, Lindsey M., Zapata, Stephanie P., Larkin, Cinnamon R., Lyman, Thomas A., Larkin, Seth A., Labuhn, Jonathan A., Reynolds, Jeffrey W., Schuler, Erin E., Naseman, Ryan W., Johnson, Gary L., and Lodder, Robert A.

Published
2022
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7. Far away from the lamppost.

Author

Oprea, Tudor I, Jan, Lily, Johnson, Gary L, Roth, Bryan L, Ma'ayan, Avi, Schürer, Stephan, Shoichet, Brian K, Sklar, Larry A, and McManus, Michael T

Subjects
Genome, Research, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Developmental Biology
Abstract

This Formal Comment responds to a recent Meta-Research Article by identifying initiatives that are already in place for funding risky exploratory research that illuminate mysteries of the dark genome.

Published
2018

8. Kinome state is predictive of cell viability in pancreatic cancer tumor and cancer-associated fibroblast cell lines.

Author

Berginski, Matthew E., Jenner, Madison R., Joisa, Chinmaya U., Herrera Loeza, Gabriela, Golitz, Brian T., Lipner, Matthew B., Leary, Jack R., Rashid, Naim, Johnson, Gary L., Yeh, Jen Jen, and Gomez, Shawn M.

Subjects
PROTEIN kinases, PANCREATIC duct, CELL communication, CALCIUM-dependent protein kinase, CELL survival
Abstract

Numerous aspects of cellular signaling are regulated by the kinome—the network of over 500 protein kinases that guides and modulates information transfer throughout the cell. The key role played by both individual kinases and assemblies of kinases organized into functional subnetworks leads to kinome dysregulation driving many diseases, particularly cancer. In the case of pancreatic ductal adenocarcinoma (PDAC), a variety of kinases and associated signaling pathways have been identified for their key role in the establishment of disease as well as its progression. However, the identification of additional relevant therapeutic targets has been slow and is further confounded by interactions between the tumor and the surrounding tumor microenvironment. In this work, we attempt to link the state of the human kinome, or kinotype, with cell viability in treated, patient-derived PDAC tumor and cancer-associated fibroblast cell lines. We applied classification models to independent kinome perturbation and kinase inhibitor cell screen data, and found that the inferred kinotype of a cell has a significant and predictive relationship with cell viability. We further find that models are able to identify a set of kinases whose behavior in response to perturbation drive the majority of viability responses in these cell lines, including the understudied kinases CSNK2A1/3, CAMKK2, and PIP4K2C. We next utilized these models to predict the response of new, clinical kinase inhibitors that were not present in the initial dataset for model devlopment and conducted a validation screen that confirmed the accuracy of the models. These results suggest that characterizing the perturbed state of the human protein kinome provides significant opportunity for better understanding of signaling behavior and downstream cell phenotypes, as well as providing insight into the broader design of potential therapeutic strategies for PDAC. [ABSTRACT FROM AUTHOR]

Published
2024
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9. Table S4 from Combined CDK4/6 and ERK1/2 Inhibition Enhances Antitumor Activity in NF1-Associated Plexiform Neurofibroma

Author

Flint, Alyssa C., primary, Mitchell, Dana K., primary, Angus, Steven P., primary, Smith, Abbi E., primary, Bessler, Waylan, primary, Jiang, Li, primary, Mang, Henry, primary, Li, Xiaohong, primary, Lu, Qingbo, primary, Rodriguez, Brooke, primary, Sandusky, George E., primary, Masters, Andi R., primary, Zhang, Chi, primary, Dang, Pengtao, primary, Koenig, Jenna, primary, Johnson, Gary L., primary, Shen, Weihua, primary, Liu, Jiangang, primary, Aggarwal, Amit, primary, Donoho, Gregory P., primary, Willard, Melinda D., primary, Bhagwat, Shripad V., primary, Clapp, D. Wade, primary, and Rhodes, Steven D., primary

Published
2024
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10. Figure S8 from Combined CDK4/6 and ERK1/2 Inhibition Enhances Antitumor Activity in NF1-Associated Plexiform Neurofibroma

Author

Flint, Alyssa C., primary, Mitchell, Dana K., primary, Angus, Steven P., primary, Smith, Abbi E., primary, Bessler, Waylan, primary, Jiang, Li, primary, Mang, Henry, primary, Li, Xiaohong, primary, Lu, Qingbo, primary, Rodriguez, Brooke, primary, Sandusky, George E., primary, Masters, Andi R., primary, Zhang, Chi, primary, Dang, Pengtao, primary, Koenig, Jenna, primary, Johnson, Gary L., primary, Shen, Weihua, primary, Liu, Jiangang, primary, Aggarwal, Amit, primary, Donoho, Gregory P., primary, Willard, Melinda D., primary, Bhagwat, Shripad V., primary, Clapp, D. Wade, primary, and Rhodes, Steven D., primary

Published
2024
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11. Cabozantinib for neurofibromatosis type 1–related plexiform neurofibromas: a phase 2 trial

Author

Fisher, Michael J., Shih, Chie-Schin, Rhodes, Steven D., Armstrong, Amy E., Wolters, Pamela L., Dombi, Eva, Zhang, Chi, Angus, Steven P., Johnson, Gary L., Packer, Roger J., Allen, Jeffrey C., Ullrich, Nicole J., Goldman, Stewart, Gutmann, David H., Plotkin, Scott R., Rosser, Tena, Robertson, Kent A., Widemann, Brigitte C., Smith, Abbi E., Bessler, Waylan K., He, Yongzheng, Park, Su-Jung, Mund, Julie A., Jiang, Li, Bijangi-Vishehsaraei, Khadijeh, Robinson, Coretta Thomas, Cutter, Gary R., Korf, Bruce R., Blakeley, Jaishri O., and Clapp, D. Wade

Published
2021
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13. FGFR4 regulates tumor subtype differentiation in luminal breast cancer and metastatic disease

Author

Garcia-Recio, Susana, Thennavan, Aatish, East, Michael P., Parker, Joel S., Cejalvo, Juan M., Garay, Joseph P., Hollern, Daniel P., He, Xiaping, Mott, Kevin R., Galvan, Patricia, Fan, Cheng, Selitsky, Sara R., Coffey, Alisha R., Marron, David, Braso-Maristany, Fara, Burgues, Octavio, Albanell, Joan, Rojo, Federico, Lluch, Ana, de Duenas, Eduardo Martinez, Rosen, Jeffery M., Johnson, Gary L., Carey, Lisa A., Prat, Aleix, and Perou, Charles M.

Subjects
Lapatinib -- Analysis, Genes -- Analysis, RNA sequencing -- Analysis, Breast cancer -- Development and progression, Cancer metastasis -- Development and progression, Gene expression -- Analysis, RNA -- Analysis, Health care industry
Abstract

Mechanisms driving tumor progression from less aggressive subtypes to more aggressive states represent key targets for therapy. We identified a subset of luminal A primary breast tumors that give rise to HER2-enriched (HER2E) subtype metastases, but remain clinically HER2 negative (cHER2). By testing the unique genetic and transcriptomic features of these cases, we developed the hypothesis that FGFR4 likely participates in this subtype switching. To evaluate this, we developed 2 FGFR4 genomic signatures using a patient-derived xenograft (PDX) model treated with an FGFR4 inhibitor, which inhibited PDX growth in vivo. Bulk tumor gene expression analysis and single-cell RNA sequencing demonstrated that the inhibition of FGFR4 signaling caused molecular switching. In the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) breast cancer cohort, FGFR4-induced and FGFR4-repressed signatures each predicted overall survival. Additionally, the FGFR4-induced signature was an independent prognostic factor beyond subtype and stage. Supervised analysis of 77 primary tumors with paired metastases revealed that the FGFR4-induced signature was significantly higher in luminal/[ER.sup.+] tumor metastases compared with their primaries. Finally, multivariate analysis demonstrated that the FGFR4-induced signature also predicted site-specific metastasis for lung, liver, and brain, but not for bone or lymph nodes. These data identify a link between FGFR4-regulated genes and metastasis, suggesting treatment options for FGFR4-positive patients, whose high expression is not caused by mutation or amplification., Introduction Treating metastatic breast cancer patients has become increasingly complex, in part due to the large number of therapeutic options in the second- and third-line settings. Tumor heterogeneity imparts another [...]

Published
2020
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15. FOXA1 and adaptive response determinants to HER2 targeted therapy in TBCRC 036

Author

Angus, Steven P., Stuhlmiller, Timothy J., Mehta, Gaurav, Bevill, Samantha M., Goulet, Daniel R., Olivares-Quintero, J. Felix, East, Michael P., Tanioka, Maki, Zawistowski, Jon S., Singh, Darshan, Sciaky, Noah, Chen, Xin, He, Xiaping, Rashid, Naim U., Chollet-Hinton, Lynn, Fan, Cheng, Soloway, Matthew G., Spears, Patricia A., Jefferys, Stuart, Parker, Joel S., Gallagher, Kristalyn K., Forero-Torres, Andres, Krop, Ian E., Thompson, Alastair M., Murthy, Rashmi, Gatza, Michael L., Perou, Charles M., Earp, H. Shelton, Carey, Lisa A., and Johnson, Gary L.

Published
2021
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16. Neratinib, a pan ERBB/HER inhibitor, restores sensitivity of PTEN-null, BRAFV600E melanoma to BRAF/MEK inhibition.

Author

DuBose, Evan, Bevill, Samantha M., Mitchell, Dana K., Sciaky, Noah, Golitz, Brian T., Dixon, Shelley A. H., Rhodes, Steven D., Bear, James E., Johnson, Gary L., and Angus, Steven P.

Subjects
BRAF genes, GENE expression, MELANOMA, DRUG synergism, RNA sequencing, DACARBAZINE
Abstract

Introduction: Approximately 50% of melanomas harbor an activating BRAFV600E mutation. Standard of care involves a combination of inhibitors targeting mutant BRAF and MEK1/2, the substrate for BRAF in the MAPK pathway. PTEN loss-of-function mutations occur in ~40% of BRAFV600E melanomas, resulting in increased PI3K/AKT activity that enhances resistance to BRAF/MEK combination inhibitor therapy. Methods: To compare the response of PTEN null to PTEN wild-type cells in an isogenic background, CRISPR/Cas9 was used to knock out PTEN in a melanoma cell line that harbors a BRAFV600E mutation. RNA sequencing, functional kinome analysis, and drug synergy screening were employed in the context of BRAF/MEK inhibition. Results: RNA sequencing and functional kinome analysis revealed that the loss of PTEN led to an induction of FOXD3 and an increase in expression of the FOXD3 target gene, ERBB3/HER3. Inhibition of BRAF and MEK1/2 in PTEN null, BRAFV600E cells dramatically induced the expression of ERBB3/HER3 relative to wild-type cells. A synergy screen of epigenetic modifiers and kinase inhibitors in combination with BRAFi/MEKi revealed that the pan ERBB/HER inhibitor, neratinib, could reverse the resistance observed in PTEN null, BRAFV600E cells. Conclusions: The findings indicate that PTEN null BRAFV600E melanoma exhibits increased reliance on ERBB/HER signaling when treated with clinically approved BRAFi/MEKi combinations. Future studies are warranted to test neratinib reversal of BRAFi/MEKi resistance in patient melanomas expressing ERBB3/HER3 in combination with its dimerization partner ERBB2/HER2. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Discovery and Optimization of Narrow Spectrum Inhibitors of Tousled Like Kinase 2 (TLK2) Using Quantitative Structure Activity Relationships

Author

Asquith, Christopher R. M., primary, East, Michael P., additional, Laitinen, Tuomo, additional, Alamillo-Ferrer, Carla, additional, Hartikainen, Erkka, additional, Wells, Carrow I, additional, Axtman, Alison D., additional, Drewry, David H., additional, Tizzard, Graham J., additional, Poso, Antti, additional, Willson, Timothy M., additional, and Johnson, Gary L., additional

Published
2023
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18. Application of Integrated Drug Screening/Kinome Analysis to Identify Inhibitors of Gemcitabine-Resistant Pancreatic Cancer Cell Growth

Author

Krulikas, Linas J., McDonald, Ian M., Lee, Benjamin, Okumu, Denis O., East, Michael P., Gilbert, Thomas S.K., Herring, Laura E., Golitz, Brian T., Wells, Carrow I., Axtman, Allison D., Zuercher, William J., Willson, Timothy M., Kireev, Dmitri, Yeh, Jen Jen, Johnson, Gary L., Baines, Antonio T., and Graves, Lee M.

Published
2018
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20. Table S2 from Combined CDK4/6 and ERK1/2 Inhibition Enhances Antitumor Activity in NF1-Associated Plexiform Neurofibroma

Author

Flint, Alyssa C., primary, Mitchell, Dana K., primary, Angus, Steven P., primary, Smith, Abbi E., primary, Bessler, Waylan, primary, Jiang, Li, primary, Mang, Henry, primary, Li, Xiaohong, primary, Lu, Qingbo, primary, Rodriguez, Brooke, primary, Sandusky, George E., primary, Masters, Andi R., primary, Zhang, Chi, primary, Dang, Pengtao, primary, Koenig, Jenna, primary, Johnson, Gary L., primary, Shen, Weihua, primary, Liu, Jiangang, primary, Aggarwal, Amit, primary, Donoho, Gregory P., primary, Willard, Melinda D., primary, Bhagwat, Shripad V., primary, Clapp, D. Wade, primary, and Rhodes, Steven D., primary

Published
2023
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21. Figure S1 from Combined CDK4/6 and ERK1/2 Inhibition Enhances Antitumor Activity in NF1-Associated Plexiform Neurofibroma

Author

Flint, Alyssa C., primary, Mitchell, Dana K., primary, Angus, Steven P., primary, Smith, Abbi E., primary, Bessler, Waylan, primary, Jiang, Li, primary, Mang, Henry, primary, Li, Xiaohong, primary, Lu, Qingbo, primary, Rodriguez, Brooke, primary, Sandusky, George E., primary, Masters, Andi R., primary, Zhang, Chi, primary, Dang, Pengtao, primary, Koenig, Jenna, primary, Johnson, Gary L., primary, Shen, Weihua, primary, Liu, Jiangang, primary, Aggarwal, Amit, primary, Donoho, Gregory P., primary, Willard, Melinda D., primary, Bhagwat, Shripad V., primary, Clapp, D. Wade, primary, and Rhodes, Steven D., primary

Published
2023
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22. Data from Combined CDK4/6 and ERK1/2 Inhibition Enhances Antitumor Activity in NF1-Associated Plexiform Neurofibroma

Author

Flint, Alyssa C., primary, Mitchell, Dana K., primary, Angus, Steven P., primary, Smith, Abbi E., primary, Bessler, Waylan, primary, Jiang, Li, primary, Mang, Henry, primary, Li, Xiaohong, primary, Lu, Qingbo, primary, Rodriguez, Brooke, primary, Sandusky, George E., primary, Masters, Andi R., primary, Zhang, Chi, primary, Dang, Pengtao, primary, Koenig, Jenna, primary, Johnson, Gary L., primary, Shen, Weihua, primary, Liu, Jiangang, primary, Aggarwal, Amit, primary, Donoho, Gregory P., primary, Willard, Melinda D., primary, Bhagwat, Shripad V., primary, Clapp, D. Wade, primary, and Rhodes, Steven D., primary

Published
2023
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24. Combined CDK4/6 and ERK1/2 Inhibition Enhances Antitumor Activity in NF1-Associated Plexiform Neurofibroma

Author

Flint, Alyssa C., primary, Mitchell, Dana K., additional, Angus, Steven P., additional, Smith, Abbi E., additional, Bessler, Waylan, additional, Jiang, Li, additional, Mang, Henry, additional, Li, Xiaohong, additional, Lu, Qingbo, additional, Rodriguez, Brooke, additional, Sandusky, George E., additional, Masters, Andi R., additional, Zhang, Chi, additional, Dang, Pengtao, additional, Koenig, Jenna, additional, Johnson, Gary L., additional, Shen, Weihua, additional, Liu, Jiangang, additional, Aggarwal, Amit, additional, Donoho, Gregory P., additional, Willard, Melinda D., additional, Bhagwat, Shripad V., additional, Clapp, D. Wade, additional, and Rhodes, Steven D., additional

Published
2023
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32. Data from GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer

Author

Bevill, Samantha M., primary, Olivares-Quintero, Jose F., primary, Sciaky, Noah, primary, Golitz, Brian T., primary, Singh, Darshan, primary, Beltran, Adriana S., primary, Rashid, Naim U., primary, Stuhlmiller, Timothy J., primary, Hale, Andrew, primary, Moorman, Nathaniel J., primary, Santos, Charlene M., primary, Angus, Steven P., primary, Zawistowski, Jon S., primary, and Johnson, Gary L., primary

Published
2023
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34. Table S1 from Discrete Adaptive Responses to MEK Inhibitor in Subpopulations of Triple-Negative Breast Cancer

Author

Goulet, Daniel R., primary, Foster, Joseph P., primary, Zawistowski, Jon S., primary, Bevill, Samantha M., primary, Noël, Mélodie P., primary, Olivares-Quintero, José F., primary, Sciaky, Noah, primary, Singh, Darshan, primary, Santos, Charlene, primary, Pattenden, Samantha G., primary, Davis, Ian J., primary, and Johnson, Gary L., primary

Published
2023
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35. Supplementary Figure 3 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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36. Supplementary Figure 2 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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37. Supplementary Figure 4 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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39. Supplementary Figure 1 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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41. Supplementary Data File 3 from GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer

Author

Bevill, Samantha M., primary, Olivares-Quintero, Jose F., primary, Sciaky, Noah, primary, Golitz, Brian T., primary, Singh, Darshan, primary, Beltran, Adriana S., primary, Rashid, Naim U., primary, Stuhlmiller, Timothy J., primary, Hale, Andrew, primary, Moorman, Nathaniel J., primary, Santos, Charlene M., primary, Angus, Steven P., primary, Zawistowski, Jon S., primary, and Johnson, Gary L., primary

Published
2023
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43. Data from Discrete Adaptive Responses to MEK Inhibitor in Subpopulations of Triple-Negative Breast Cancer

Author

Goulet, Daniel R., primary, Foster, Joseph P., primary, Zawistowski, Jon S., primary, Bevill, Samantha M., primary, Noël, Mélodie P., primary, Olivares-Quintero, José F., primary, Sciaky, Noah, primary, Singh, Darshan, primary, Santos, Charlene, primary, Pattenden, Samantha G., primary, Davis, Ian J., primary, and Johnson, Gary L., primary

Published
2023
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45. Supplementary Data File 4 from GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer

Author

Bevill, Samantha M., primary, Olivares-Quintero, Jose F., primary, Sciaky, Noah, primary, Golitz, Brian T., primary, Singh, Darshan, primary, Beltran, Adriana S., primary, Rashid, Naim U., primary, Stuhlmiller, Timothy J., primary, Hale, Andrew, primary, Moorman, Nathaniel J., primary, Santos, Charlene M., primary, Angus, Steven P., primary, Zawistowski, Jon S., primary, and Johnson, Gary L., primary

Published
2023
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46. Supplementary Data File 2 from GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer

Author

Bevill, Samantha M., primary, Olivares-Quintero, Jose F., primary, Sciaky, Noah, primary, Golitz, Brian T., primary, Singh, Darshan, primary, Beltran, Adriana S., primary, Rashid, Naim U., primary, Stuhlmiller, Timothy J., primary, Hale, Andrew, primary, Moorman, Nathaniel J., primary, Santos, Charlene M., primary, Angus, Steven P., primary, Zawistowski, Jon S., primary, and Johnson, Gary L., primary

Published
2023
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47. Figure S5 from Discrete Adaptive Responses to MEK Inhibitor in Subpopulations of Triple-Negative Breast Cancer

Author

Goulet, Daniel R., primary, Foster, Joseph P., primary, Zawistowski, Jon S., primary, Bevill, Samantha M., primary, Noël, Mélodie P., primary, Olivares-Quintero, José F., primary, Sciaky, Noah, primary, Singh, Darshan, primary, Santos, Charlene, primary, Pattenden, Samantha G., primary, Davis, Ian J., primary, and Johnson, Gary L., primary

Published
2023
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48. Data from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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