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Your search keyword '"Yang, FaJun"' showing total 5 results
Start Over Author "Yang, FaJun" Publisher nature publishing group
5 results on '"Yang, FaJun"'

1. E2F1 represses β-catenin transcription and is antagonized by both pRB and CDK8

Author

Morris, Erick J., Ji, Jun-Yuan, Yang, Fajun, Di Stefano, Luisa, Herr, Anabel, Moon, Nam-Sung, Kwon, Eun-Jeong, and Haigis, Kevin M.

Subjects
DNA-ligand interactions -- Research -- Health aspects -- Chemical properties -- Physiological aspects, Apoptosis -- Causes of -- Research -- Physiological aspects -- Health aspects -- Chemical properties, Genetic transcription -- Evaluation -- Research -- Health aspects -- Chemical properties -- Physiological aspects, DNA binding proteins -- Physiological aspects -- Chemical properties -- Health aspects -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation, Evaluation, Physiological aspects, Chemical properties, Research, Health aspects, Causes of
Abstract

The E2F1 transcription factor can promote proliferation or apoptosis when activated, and is a key downstream target of the retinoblastoma tumour suppressor protein (pRB). Here we show that E2F1 is [...]

Published
2008

2. A nuclear receptor-like pathway regulating multidrug resistance in fungi

Author

Thakur, Jitendra K., Arthanari, Haribabu, Yang, Fajun, Pan, Shih-Jung, Fan, Xiaochun, Breger, Julia, Frueh, Dominique P., Gulshan, Kailash, Li, Darrick K., Mylonakis, Eleftherios, Struhl, Kevin, Moye-Rowley, W. Scott, Cormack, Brendan P., Wagner, Gerhard, and Naar, Anders M.

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Multidrug resistance (MDR) is a serious complication during treatment of opportunistic fungal infections that frequently afflict immunocompromised individuals, such as transplant recipients and cancer patients undergoing cytotoxic chemotherapy. Improved knowledge [...]

Published
2008

3. An ARC/Mediator subunit required for SREBP control of cholesterol and lipid homeostasis

Author

Yang, Fajun, Vought, Bryan W., Satterlee, John S., Walker, Amy K., Jim Sun, Z.-Y., Watts, Jennifer L., DeBeaumont, Rosalie, Mako Saito, R., Hyberts, Sven G., Yang, Shaosong, Macol, Christine, Iyer, Lakshmanan, Tjian, Robert, van den Heuvel, Sander, Hart, Anne C., Wagner, Gerhard, and Naar, Anders M.

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Fajun Yang [1, 2, 9]; Bryan W. Vought [3, 9]; John S. Satterlee [1]; Amy K. Walker [1, 4]; Z.-Y. Jim Sun [3]; Jennifer L. Watts [5]; Rosalie DeBeaumont [...]

Published
2006
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4. The Hippo Signaling Transducer TAZ Regulates Mammary Gland Morphogenesis and Carcinogen-induced Mammary Tumorigenesis.

Author

Denson KE, Mussell AL, Shen H, Truskinovsky A, Yang N, Parashurama N, Chen Y, Frangou C, Yang F, and Zhang J

Subjects
Adaptor Proteins, Signal Transducing metabolism, Adaptor Proteins, Signal Transducing physiology, Animals, Apoptosis, Carcinogenesis metabolism, Cell Proliferation, Cell Transformation, Neoplastic, Epithelial Cells metabolism, Female, Hippo Signaling Pathway, Humans, Mammary Neoplasms, Animal metabolism, Mice, Mice, Inbred C57BL, Mice, Transgenic, Protein Serine-Threonine Kinases metabolism, Protein Serine-Threonine Kinases physiology, Signal Transduction, Trans-Activators, Transcription Factors metabolism, Transcriptional Coactivator with PDZ-Binding Motif Proteins, Intracellular Signaling Peptides and Proteins metabolism, Intracellular Signaling Peptides and Proteins physiology, Mammary Glands, Animal metabolism
Abstract

Hippo signaling pathway is an evolutionarily conserved pathway that controls organ size by regulating cell proliferation, apoptosis and stem cell self-renewal. TAZ (transcriptional coactivator with the PDZ-binding motif) is a key downstream effector of the mammalian Hippo pathway. Here, using a transgenic mouse model with mammary-gland-specific expression of constitutively active TAZ, we found that TAZ induction in mammary epithelial cells was associated with an increase in mammary glandular size, which probably resulted from adipocyte hypertrophy. Consistent with its known oncogenic potential, we observed tumor formation in TAZ transgenic mice after administration of the carcinogen 7,12-dimethylbenzanthracene (DMBA) and demonstrated that tumorigenesis was reliant on the presence of TAZ. Our findings establish a previously unknown roles of TAZ in regulating both mammary gland morphogenesis as well as carcinogen-induced mammary tumor formation.

Published
2018
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5. E2F1 represses beta-catenin transcription and is antagonized by both pRB and CDK8.

Author

Morris EJ, Ji JY, Yang F, Di Stefano L, Herr A, Moon NS, Kwon EJ, Haigis KM, Näär AM, and Dyson NJ

Subjects
Adenomatous Polyposis Coli Protein metabolism, Apoptosis, Cell Line, Cyclin-Dependent Kinase 8, Gene Expression Regulation, Genes, myc genetics, Glycogen Synthase Kinase 3 metabolism, Humans, Retinoblastoma Protein genetics, Signal Transduction, TCF Transcription Factors metabolism, Wnt Proteins metabolism, Cyclin-Dependent Kinases metabolism, E2F1 Transcription Factor antagonists & inhibitors, E2F1 Transcription Factor metabolism, Retinoblastoma Protein metabolism, Transcription, Genetic, beta Catenin antagonists & inhibitors, beta Catenin metabolism
Abstract

The E2F1 transcription factor can promote proliferation or apoptosis when activated, and is a key downstream target of the retinoblastoma tumour suppressor protein (pRB). Here we show that E2F1 is a potent and specific inhibitor of beta-catenin/T-cell factor (TCF)-dependent transcription, and that this function contributes to E2F1-induced apoptosis. E2F1 deregulation suppresses beta-catenin activity in an adenomatous polyposis coli (APC)/glycogen synthase kinase-3 (GSK3)-independent manner, reducing the expression of key beta-catenin targets including c-MYC. This interaction explains why colorectal tumours, which depend on beta-catenin transcription for their abnormal proliferation, keep RB1 intact. Remarkably, E2F1 activity is also repressed by cyclin-dependent kinase-8 (CDK8), a colorectal oncoprotein. Elevated levels of CDK8 protect beta-catenin/TCF-dependent transcription from inhibition by E2F1. Thus, by retaining RB1 and amplifying CDK8, colorectal tumour cells select conditions that collectively suppress E2F1 and enhance the activity of beta-catenin.

Published
2008
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