Search

Your search keyword '"Gao, Tianyan"' showing total 424 results
Start Over Author "Gao, Tianyan"
424 results on '"Gao, Tianyan"'

2. YingLong: Skillful High Resolution Regional Short Term Forecasting with Boundary Smoothing

Author

Xu, Pengbo, Gao, Tianyan, Wang, Yu, Yin, Junping, Zhang, Juan, Zheng, Xiaogu, Zhang, Zhimin, Hu, Xiaoguang, and Chen, Xiaoxu

Subjects
Physics - Atmospheric and Oceanic Physics
Abstract

In the realm of numerical weather forecasting, achieving higher resolution demands increased computational resources and time investment, and leveraging deep learning networks trained solely on data significantly reduces the time expenditure during forecasting. Recently, several global forecasting artificial-intelligence-based models are developed, which are mainly trained on reanalysis dataset with a spatial resolution of approximately 25km. However, regional forecasting prefers a higher spatial resolution, and boundary information for the region also plays an important role in regional forecasting, which turns out to be a major difference from global forecasting. Here we introduce a high resolution, short-term regional weather forecasting, artificial-intelligence-based model called 'YingLong', which is capable of hourly predicting weather fields including wind speed, temperature, and specific humidity at a 3km resolution. YingLong utilizes a parallel structure of global and local blocks to capture multiscale meteorological features and is trained on analysis dataset. Additionally, the necessary information around the regional boundary is introduced to YingLong through the boundary smoothing strategy, which significantly improves the regional forecasting results. By comparing forecast results with those from WRF-ARW, one of the best numerical prediction models, YingLong demonstrates superior forecasting performances in most cases, especially on surface variables.

Published
2024

9. Upregulation of Fatty Acid Synthase Increases Activity of β-Catenin and Expression of NOTUM to Enhance Stem-like Properties of Colorectal Cancer Cells.

Author

Kelson, Courtney O., Tessmann, Josiane Weber, Geisen, Mariah E., He, Daheng, Wang, Chi, Gao, Tianyan, Evers, B. Mark, and Zaytseva, Yekaterina Y.

Subjects
FATTY acid synthases, GENETIC regulation, GENE expression, CANCER cell growth, COLORECTAL cancer, CATENINS
Abstract

Dysregulated fatty acid metabolism is an attractive therapeutic target for colorectal cancer (CRC). We previously reported that fatty acid synthase (FASN), a key enzyme of de novo synthesis, promotes the initiation and progression of CRC. However, the mechanisms of how upregulation of FASN promotes the initiation and progression of CRC are not completely understood. Here, using Apc/VillinCre and ApcMin mouse models, we show that upregulation of FASN is associated with an increase in activity of β-catenin and expression of multiple stem cell markers, including Notum. Genetic and pharmacological downregulation of FASN in mouse adenoma organoids decreases the activation of β-catenin and expression of Notum and significantly inhibits organoid formation and growth. Consistently, we demonstrate that NOTUM is highly expressed in human CRC and its expression positively correlates with the expression of FASN in tumor tissues. Utilizing overexpression and shRNA-mediated knockdown of FASN, we demonstrate that upregulation of FASN increases β-catenin transcriptional activity, NOTUM expression and secretion, and enhances stem-like properties of human CRC cells. Pharmacological inhibition of NOTUM decreases adenoma organoids growth and proliferation of cancer cells. In summary, upregulation of FASN enhances β-catenin signaling, increases NOTUM expression and stem-like properties of CRC cells, thus suggesting that targeting FASN upstream of the β-catenin/NOTUM axis may be an effective preventative therapeutic strategy for CRC. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

12. Dysregulation of mitochondrial function by PLK1-mediated PDHA1 phosphorylation promotes Cr(VI)-associated lung cancer progression

Author

Zhang, Qiongsi, primary, Li, Zhiguo, additional, Rao, Xiongjian, additional, Allison, Derek B., additional, Qiao, Qi, additional, Zhang, Zhuangzhuang, additional, Kong, Yifan, additional, Zhang, Yanquan, additional, Wang, Ruixin, additional, Liu, Jinghui, additional, Wang, Xinyi, additional, Li, Chaohao, additional, Mao, Fengyi, additional, Katz, Wendy, additional, Shao, Qing, additional, Gao, Tianyan, additional, and Liu, Xiaoqi, additional

Published
2024
Full Text
View/download PDF

16. Pleckstrin homology domain leucine-rich repeat protein phosphatases set the amplitude of receptor tyrosine kinase output

Author

Reyes, Gloria, Niederst, Matt, Cohen-Katsenelson, Ksenya, Stender, Joshua D, Kunkel, Maya T, Chen, Muhan, Brognard, John, Sierecki, Emma, Gao, Tianyan, Nowak, Dawid G, Trotman, Lloyd C, Glass, Christopher K, and Newton, Alexandra C

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Rare Diseases, Brain Disorders, Cancer, 2.1 Biological and endogenous factors, Aetiology, Animals, Cell Line, Transformed, ErbB Receptors, MAP Kinase Signaling System, Mice, Mice, Knockout, Models, Biological, Nuclear Proteins, Phosphatidylinositol 3-Kinases, Phosphoprotein Phosphatases, Protein Kinase C, Proto-Oncogene Proteins c-akt, Rats, Repetitive Sequences, Amino Acid, Transcription, Genetic
Abstract

Growth factor receptor levels are aberrantly high in diverse cancers, driving the proliferation and survival of tumor cells. Understanding the molecular basis for this aberrant elevation has profound clinical implications. Here we show that the pleckstrin homology domain leucine-rich repeat protein phosphatase (PHLPP) suppresses receptor tyrosine kinase (RTK) signaling output by a previously unidentified epigenetic mechanism unrelated to its previously described function as the hydrophobic motif phosphatase for the protein kinase AKT, protein kinase C, and S6 kinase. Specifically, we show that nuclear-localized PHLPP suppresses histone phosphorylation and acetylation, in turn suppressing the transcription of diverse growth factor receptors, including the EGF receptor. These data uncover a much broader role for PHLPP in regulation of growth factor signaling beyond its direct inactivation of AKT: By suppressing RTK levels, PHLPP dampens the downstream signaling output of two major oncogenic pathways, the PI3 kinase/AKT and the Rat sarcoma (RAS)/ERK pathways. Our data are consistent with a model in which PHLPP modifies the histone code to control the transcription of RTKs.

Published
2014

26. Supplementary Data from Potent Synergistic Effect on C-Myc–Driven Colorectal Cancers Using a Novel Indole-Substituted Quinoline with a Plk1 Inhibitor

Author

Xie, Yanqi, primary, Zhang, Wen, primary, Guo, Lichao, primary, Kril, Liliia M., primary, Begley, Kristin L., primary, Sviripa, Vitaliy M., primary, Chen, Xi, primary, Liu, Xifu, primary, Lee, Eun Y., primary, He, Daheng, primary, Wang, Chi, primary, Gao, Tianyan, primary, Liu, Xiaoqi, primary, Evers, B. Mark, primary, Watt, David S., primary, and Liu, Chunming, primary

Published
2023
Full Text
View/download PDF

29. Figure S4 from Erbin Suppresses KSR1-Mediated RAS/RAF Signaling and Tumorigenesis in Colorectal Cancer

Author

Stevens, Payton D., primary, Wen, Yang-An, primary, Xiong, Xiaopeng, primary, Zaytseva, Yekaterina Y., primary, Li, Austin T., primary, Wang, Chi, primary, Stevens, Ashley T., primary, Farmer, Trevor N., primary, Gan, Tong, primary, Weiss, Heidi L., primary, Inagaki, Masaki, primary, Marchetto, Sylvie, primary, Borg, Jean-Paul, primary, and Gao, Tianyan, primary

Published
2023
Full Text
View/download PDF

30. Table S2 from Erbin Suppresses KSR1-Mediated RAS/RAF Signaling and Tumorigenesis in Colorectal Cancer

Author

Stevens, Payton D., primary, Wen, Yang-An, primary, Xiong, Xiaopeng, primary, Zaytseva, Yekaterina Y., primary, Li, Austin T., primary, Wang, Chi, primary, Stevens, Ashley T., primary, Farmer, Trevor N., primary, Gan, Tong, primary, Weiss, Heidi L., primary, Inagaki, Masaki, primary, Marchetto, Sylvie, primary, Borg, Jean-Paul, primary, and Gao, Tianyan, primary

Published
2023
Full Text
View/download PDF

31. Data from Erbin Suppresses KSR1-Mediated RAS/RAF Signaling and Tumorigenesis in Colorectal Cancer

Author

Stevens, Payton D., primary, Wen, Yang-An, primary, Xiong, Xiaopeng, primary, Zaytseva, Yekaterina Y., primary, Li, Austin T., primary, Wang, Chi, primary, Stevens, Ashley T., primary, Farmer, Trevor N., primary, Gan, Tong, primary, Weiss, Heidi L., primary, Inagaki, Masaki, primary, Marchetto, Sylvie, primary, Borg, Jean-Paul, primary, and Gao, Tianyan, primary

Published
2023
Full Text
View/download PDF

38. An obligatory role for neurotensin in high-fat-diet-induced obesity

Author

Li, Jing, Song, Jun, Zaytseva, Yekaterina Y., Liu, Yajuan, Rychahou, Piotr, Jiang, Kai, Starr, Marlene E., Kim, Ji Tae, Harris, Jennifer W., Yiannikouris, Frederique B., Katz, Wendy S., Nilsson, Peter M., Orho-Melander, Marju, Chen, Jing, Zhu, Haining, Fahrenholz, Timothy, Higashi, Richard M., Gao, Tianyan, Morris, Andrew J., Cassis, Lisa A., Fan, Teresa W.-M., Weiss, Heidi L., Dobner, Paul R., Melander, Olle, Jia, Jianhang, and Evers, B. Mark

Subjects
Ketogenic diet -- Health aspects, Obesity -- Physiological aspects, Neurotensin -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Obesity and its associated comorbidities (for example, diabetes mellitus and hepatic steatosis) contribute to approximately 2.5 million deaths annually (1) and are among the most prevalent and challenging conditions confronting [...]

Published
2016

45. Potent Synergistic Effect on C-Myc–Driven Colorectal Cancers Using a Novel Indole-Substituted Quinoline with a Plk1 Inhibitor

Author

Xie, Yanqi, primary, Zhang, Wen, additional, Guo, Lichao, additional, Kril, Liliia M., additional, Begley, Kristin L., additional, Sviripa, Vitaliy M., additional, Chen, Xi, additional, Liu, Xifu, additional, Lee, Eun Y., additional, He, Daheng, additional, Wang, Chi, additional, Gao, Tianyan, additional, Liu, Xiaoqi, additional, Evers, B. Mark, additional, Watt, David S., additional, and Liu, Chunming, additional

Published
2021
Full Text
View/download PDF

47. Protein phosphatase PHLPP1 controls the light-induced resetting of the circadian clock

Author

Masubuchi, Satoru, Gao, Tianyan, O'Neill, Audrey, Eckel-Mahan, Kristin, Newton, Alexandra C., and Sassone-Corsi, Paolo

Subjects
Phosphatases -- Physiological aspects, Circadian rhythms -- Research, Science and technology
Abstract

The pleckstrin homology domain leucine-rich repeat protein phosphatase 1 (PHLPP1) differentially attenuates Akt, PKC, and ERK1/2 signaling, thereby controlling the duration and amplitude of responses evoked by these kinases. PHLPP1 is expressed in the mammalian central clock, the suprachiasmatic nucleus, where it oscillates in a circadian fashion. To explore the role of PHLPP1 in vivo, we have generated mice with a targeted deletion of the PHLPP1 gene. Here we show that PHLPP1-null mice, although displaying normal circadian rhythmicity, have a drastically impaired capacity to stabilize the circadian period after light-induced resetting, producing a large phase shift after light resetting. Our findings reveal that PHLPP1 exerts a previously unappreciated role in circadian control, governing the consolidation of circadian periodicity after resetting. Per | period | after-effect | suprachiasmatic nucleus | phase shift doi/ 10.1073/pnas.0910292107

Published
2010

Catalog

Books, media, physical & digital resources
See catalog results