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19 results on '"Jewell, Brittany E."'

1. Supplementary File 1 from Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity

Author

Awad, Dominik, primary, Cao, Pham Hong Anh, primary, Pulliam, Thomas L., primary, Spradlin, Meredith, primary, Subramani, Elavarasan, primary, Tellman, Tristen V., primary, Ribeiro, Caroline F., primary, Muzzioli, Riccardo, primary, Jewell, Brittany E., primary, Pakula, Hubert, primary, Ackroyd, Jeffrey J., primary, Murray, Mollianne M., primary, Han, Jenny J., primary, Leng, Mei, primary, Jain, Antrix, primary, Piyarathna, Badrajee, primary, Liu, Jingjing, primary, Song, Xingzhi, primary, Zhang, Jianhua, primary, Klekers, Albert R., primary, Drake, Justin M., primary, Ittmann, Michael M., primary, Coarfa, Cristian, primary, Piwnica-Worms, David, primary, Farach-Carson, Mary C., primary, Loda, Massimo, primary, Eberlin, Livia S., primary, and Frigo, Daniel E., primary

Published
2024
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2. Supplementary Figures S1-S28 from Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity

Author

Awad, Dominik, primary, Cao, Pham Hong Anh, primary, Pulliam, Thomas L., primary, Spradlin, Meredith, primary, Subramani, Elavarasan, primary, Tellman, Tristen V., primary, Ribeiro, Caroline F., primary, Muzzioli, Riccardo, primary, Jewell, Brittany E., primary, Pakula, Hubert, primary, Ackroyd, Jeffrey J., primary, Murray, Mollianne M., primary, Han, Jenny J., primary, Leng, Mei, primary, Jain, Antrix, primary, Piyarathna, Badrajee, primary, Liu, Jingjing, primary, Song, Xingzhi, primary, Zhang, Jianhua, primary, Klekers, Albert R., primary, Drake, Justin M., primary, Ittmann, Michael M., primary, Coarfa, Cristian, primary, Piwnica-Worms, David, primary, Farach-Carson, Mary C., primary, Loda, Massimo, primary, Eberlin, Livia S., primary, and Frigo, Daniel E., primary

Published
2024
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3. Data from Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity

Author

Awad, Dominik, primary, Cao, Pham Hong Anh, primary, Pulliam, Thomas L., primary, Spradlin, Meredith, primary, Subramani, Elavarasan, primary, Tellman, Tristen V., primary, Ribeiro, Caroline F., primary, Muzzioli, Riccardo, primary, Jewell, Brittany E., primary, Pakula, Hubert, primary, Ackroyd, Jeffrey J., primary, Murray, Mollianne M., primary, Han, Jenny J., primary, Leng, Mei, primary, Jain, Antrix, primary, Piyarathna, Badrajee, primary, Liu, Jingjing, primary, Song, Xingzhi, primary, Zhang, Jianhua, primary, Klekers, Albert R., primary, Drake, Justin M., primary, Ittmann, Michael M., primary, Coarfa, Cristian, primary, Piwnica-Worms, David, primary, Farach-Carson, Mary C., primary, Loda, Massimo, primary, Eberlin, Livia S., primary, and Frigo, Daniel E., primary

Published
2024
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4. Supplementary Tables 1-8 from Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity

Author

Awad, Dominik, primary, Cao, Pham Hong Anh, primary, Pulliam, Thomas L., primary, Spradlin, Meredith, primary, Subramani, Elavarasan, primary, Tellman, Tristen V., primary, Ribeiro, Caroline F., primary, Muzzioli, Riccardo, primary, Jewell, Brittany E., primary, Pakula, Hubert, primary, Ackroyd, Jeffrey J., primary, Murray, Mollianne M., primary, Han, Jenny J., primary, Leng, Mei, primary, Jain, Antrix, primary, Piyarathna, Badrajee, primary, Liu, Jingjing, primary, Song, Xingzhi, primary, Zhang, Jianhua, primary, Klekers, Albert R., primary, Drake, Justin M., primary, Ittmann, Michael M., primary, Coarfa, Cristian, primary, Piwnica-Worms, David, primary, Farach-Carson, Mary C., primary, Loda, Massimo, primary, Eberlin, Livia S., primary, and Frigo, Daniel E., primary

Published
2024
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5. Supplementary File 2 from Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity

Author

Awad, Dominik, primary, Cao, Pham Hong Anh, primary, Pulliam, Thomas L., primary, Spradlin, Meredith, primary, Subramani, Elavarasan, primary, Tellman, Tristen V., primary, Ribeiro, Caroline F., primary, Muzzioli, Riccardo, primary, Jewell, Brittany E., primary, Pakula, Hubert, primary, Ackroyd, Jeffrey J., primary, Murray, Mollianne M., primary, Han, Jenny J., primary, Leng, Mei, primary, Jain, Antrix, primary, Piyarathna, Badrajee, primary, Liu, Jingjing, primary, Song, Xingzhi, primary, Zhang, Jianhua, primary, Klekers, Albert R., primary, Drake, Justin M., primary, Ittmann, Michael M., primary, Coarfa, Cristian, primary, Piwnica-Worms, David, primary, Farach-Carson, Mary C., primary, Loda, Massimo, primary, Eberlin, Livia S., primary, and Frigo, Daniel E., primary

Published
2024
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8. Patient-derived iPSCs link elevated mitochondrial respiratory complex I function to osteosarcoma in Rothmund-Thomson syndrome

Author

Jewell, Brittany E., primary, Xu, An, additional, Zhu, Dandan, additional, Huang, Mo-Fan, additional, Lu, Linchao, additional, Liu, Mo, additional, Underwood, Erica L., additional, Park, Jun Hyoung, additional, Fan, Huihui, additional, Gingold, Julian A., additional, Zhou, Ruoji, additional, Tu, Jian, additional, Huo, Zijun, additional, Liu, Ying, additional, Jin, Weidong, additional, Chen, Yi-Hung, additional, Xu, Yitian, additional, Chen, Shu-Hsia, additional, Rainusso, Nino, additional, Berg, Nathaniel K., additional, Bazer, Danielle A., additional, Vellano, Christopher, additional, Jones, Philip, additional, Eltzschig, Holger K., additional, Zhao, Zhongming, additional, Kaipparettu, Benny Abraham, additional, Zhao, Ruiying, additional, Wang, Lisa L., additional, and Lee, Dung-Fang, additional

Published
2021
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10. Generation of an induced pluripotent stem cell line from an individual with a heterozygous RECQL4 mutation

Author

Jewell, Brittany E., primary, Liu, Mo, additional, Lu, Linchao, additional, Zhou, Ruoji, additional, Tu, Jian, additional, Zhu, Dandan, additional, Huo, Zijun, additional, Xu, An, additional, Wang, Donghui, additional, Mata, Helen, additional, Jin, Weidong, additional, Xia, Weiya, additional, Rao, Pulivarthi H., additional, Zhao, Ruiying, additional, Hung, Mien-Chie, additional, Wang, Lisa L., additional, and Lee, Dung-Fang, additional

Published
2018
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11. Establishment of a human embryonic stem cell line with homozygous TP53 R248W mutant by TALEN mediated gene editing

Author

Xu, An, primary, Zhou, Ruoji, additional, Tu, Jian, additional, Huo, Zijun, additional, Zhu, Dandan, additional, Wang, Donghui, additional, Gingold, Julian A., additional, Mata, Helen, additional, Rao, Pulivarthi H., additional, Liu, Mo, additional, Mohamed, Alaa M.T., additional, Kong, Celine Shuet Lin, additional, Jewell, Brittany E., additional, Xia, Weiya, additional, Zhao, Ruiying, additional, Hung, Mien-Chie, additional, and Lee, Dung-Fang, additional

Published
2018
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12. A homozygous p53 R282W mutant human embryonic stem cell line generated using TALEN-mediated precise gene editing

Author

Zhou, Ruoji, primary, Xu, An, additional, Wang, Donghui, additional, Zhu, Dandan, additional, Mata, Helen, additional, Huo, Zijun, additional, Tu, Jian, additional, Liu, Mo, additional, Mohamed, Alaa M.T., additional, Jewell, Brittany E., additional, Gingold, Julian, additional, Xia, Weiya, additional, Rao, Pulivarthi H., additional, Hung, Mien-Chie, additional, Zhao, Ruiying, additional, and Lee, Dung-Fang, additional

Published
2018
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17. Natural Variant of Collagen-Like Protein A in Serotype M3 Group A StreptococcusIncreases Adherence and Decreases Invasive Potential

Author

Flores, Anthony R., Jewell, Brittany E., Versalovic, Erika M., Olsen, Randall J., Bachert, Beth A., Lukomski, Slawomir, and Musser, James M.

Abstract

ABSTRACTGroup A Streptococcus(GAS) predominantly exists as a colonizer of the human oropharynx that occasionally breaches epithelial barriers to cause invasive diseases. Despite the frequency of GAS carriage, few investigations into the contributory molecular mechanisms exist. To this end, we identified a naturally occurring polymorphism in the gene encoding the streptococcal collagen-like protein A (SclA) in GAS carrier strains. All previously sequenced invasive serotype M3 GAS possess a premature stop codon in the sclAgene truncating the protein. The carrier polymorphism is predicted to restore SclA function and was infrequently identified by targeted DNA sequencing in invasive strains of the same serotype. We demonstrate that a strain with the carrier sclAallele expressed a full-length SclA protein, while the strain with the invasive sclAallele expressed a truncated variant. An isoallelic mutant invasive strain with the carrier sclAallele exhibited decreased virulence in a mouse model of invasive disease and decreased multiplication in human blood. Further, the isoallelic invasive strain with the carrier sclAallele persisted in the mouse nasopharynx and had increased adherence to cultured epithelial cells. Repair of the premature stop codon in the invasive sclAallele restored the ability to bind the extracellular matrix proteins laminin and cellular fibronectin. These data demonstrate that a mutation in GAS carrier strains increases adherence and decreases virulence and suggest selection against increased adherence in GAS invasive isolates.

Published
2015
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18. Asymptomatic Carriage of Group A StreptococcusIs Associated with Elimination of Capsule Production

Author

Flores, Anthony R., Jewell, Brittany E., Olsen, Randall J., Shelburne, Samuel A., Fittipaldi, Nahuel, Beres, Stephen B., and Musser, James M.

Abstract

ABSTRACTHumans commonly carry pathogenic bacteria asymptomatically, but despite decades of study, the underlying molecular contributors remain poorly understood. Here, we show that a group A streptococcus carriage strain contains a frameshift mutation in the hasAgene resulting in loss of hyaluronic acid capsule biosynthesis. This mutation was repaired by allelic replacement, resulting in restoration of capsule production in the isogenic derivative strain. The “repaired” isogenic strain was significantly more virulent than the carriage strain in a mouse model of necrotizing fasciitis and had enhanced growth ex vivoin human blood. Importantly, the repaired isogenic strain colonized the mouse oropharynx with significantly greater bacterial burden and had significantly reduced ability to internalize into cultured epithelial cells than the acapsular carriage strain. We conducted full-genome sequencing of 81 strains cultured serially from 19 epidemiologically unrelated human subjects and discovered the common theme that mutations negatively affecting capsule biosynthesis arise in vivoin the hasoperon. The significantly decreased capsule production is a key factor contributing to the molecular détente between pathogen and host. Our discoveries suggest a general model for bacterial pathogens in which mutations that downregulate or ablate virulence factor production contribute to carriage.

Published
2014
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19. Adipose Triglyceride Lipase Is a Therapeutic Target in Advanced Prostate Cancer That Promotes Metabolic Plasticity.

Author

Awad D, Cao PHA, Pulliam TL, Spradlin M, Subramani E, Tellman TV, Ribeiro CF, Muzzioli R, Jewell BE, Pakula H, Ackroyd JJ, Murray MM, Han JJ, Leng M, Jain A, Piyarathna B, Liu J, Song X, Zhang J, Klekers AR, Drake JM, Ittmann MM, Coarfa C, Piwnica-Worms D, Farach-Carson MC, Loda M, Eberlin LS, and Frigo DE

Subjects
Male, Humans, Mice, Animals, Lipolysis genetics, Lipid Metabolism, Lipase genetics, Lipase metabolism, Serine metabolism, Tumor Microenvironment, Calcium-Calmodulin-Dependent Protein Kinase Kinase, Prostatic Neoplasms, Castration-Resistant
Abstract

Lipid metabolism plays a central role in prostate cancer. To date, the major focus has centered on de novo lipogenesis and lipid uptake in prostate cancer, but inhibitors of these processes have not benefited patients. A better understanding of how cancer cells access lipids once they are created or taken up and stored could uncover more effective strategies to perturb lipid metabolism and treat patients. Here, we identified that expression of adipose triglyceride lipase (ATGL), an enzyme that controls lipid droplet homeostasis and a previously suspected tumor suppressor, correlates with worse overall survival in men with advanced, castration-resistant prostate cancer (CRPC). Molecular, genetic, or pharmacologic inhibition of ATGL impaired human and murine prostate cancer growth in vivo and in cell culture or organoids under conditions mimicking the tumor microenvironment. Mass spectrometry imaging demonstrated that ATGL profoundly regulates lipid metabolism in vivo, remodeling membrane composition. ATGL inhibition induced metabolic plasticity, causing a glycolytic shift that could be exploited therapeutically by cotargeting both metabolic pathways. Patient-derived phosphoproteomics identified ATGL serine 404 as a target of CAMKK2-AMPK signaling in CRPC cells. Mutation of serine 404 did not alter the lipolytic activity of ATGL but did decrease CRPC growth, migration, and invasion, indicating that noncanonical ATGL activity also contributes to disease progression. Unbiased immunoprecipitation/mass spectrometry suggested that mutation of serine 404 not only disrupts existing ATGL protein interactions but also leads to new protein-protein interactions. Together, these data nominate ATGL as a therapeutic target for CRPC and provide insights for future drug development and combination therapies., Significance: ATGL promotes prostate cancer metabolic plasticity and progression through both lipase-dependent and lipase-independent activity, informing strategies to target ATGL and lipid metabolism for cancer treatment., (©2023 American Association for Cancer Research.)

Published
2024
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