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141 results on '"Li, Tianxia"'

1. Recurrent RhoGAP gene fusion CLDN18-ARHGAP26 promotes RHOA activation and focal adhesion kinase and YAP-TEAD signalling in diffuse gastric cancer

Author

Zhang, Feifei, primary, Sahu, Varun, additional, Peng, Ke, additional, Wang, Yichen, additional, Li, Tianxia, additional, Bala, Pratyusha, additional, Aitymbayev, Daulet, additional, Sahgal, Pranshu, additional, Schaefer, Antje, additional, Der, Channing J, additional, Ryeom, Sandra, additional, Yoon, Sam, additional, Sethi, Nilay, additional, Bass, Adam J, additional, and Zhang, Haisheng, additional

Published
2024
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2. WRN helicase is a synthetic lethal target in microsatellite unstable cancers

Author

Chan, Edmond M., Shibue, Tsukasa, McFarland, James M., Gaeta, Benjamin, Ghandi, Mahmoud, Dumont, Nancy, Gonzalez, Alfredo, McPartlan, Justine S., Li, Tianxia, Zhang, Yanxi, Bin Liu, Jie, Lazaro, Jean-Bernard, Gu, Peili, Piett, Cortt G., Apffel, Annie, Ali, Syed O., Deasy, Rebecca, Keskula, Paula, Ng, Raymond W. S., Roberts, Emma A., Reznichenko, Elizaveta, Leung, Lisa, Alimova, Maria, Schenone, Monica, Islam, Mirazul, Maruvka, Yosef E., Liu, Yang, Roper, Jatin, Raghavan, Srivatsan, Giannakis, Marios, Tseng, Yuen-Yi, Nagel, Zachary D., D’Andrea, Alan, Root, David E., Boehm, Jesse S., Getz, Gad, Chang, Sandy, Golub, Todd R., Tsherniak, Aviad, Vazquez, Francisca, and Bass, Adam J.

Published
2019
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3. Supplement Methods from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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4. Figure S4 from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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5. Supplementary Table 3 from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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6. Supplementary Table 1, 2 and 4 from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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7. Data from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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8. Figure S6 and S7 from RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, primary, Chen, Wankun, primary, Liao, Rachel G., primary, Li, Yvonne, primary, Piccioni, Federica, primary, Wang, Jun, primary, Tan, Li, primary, Thorner, Aaron R., primary, Li, Tianxia, primary, Zhang, Yanxi, primary, Miao, Changhong, primary, Ovesen, Therese, primary, Shapiro, Geoffrey I., primary, Kwiatkowski, David J., primary, Gray, Nathanael S., primary, Meyerson, Matthew, primary, Hammerman, Peter S., primary, and Bass, Adam J., primary

Published
2023
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9. Data from Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression

Author

Rusan, Maria, primary, Li, Kapsok, primary, Li, Yvonne, primary, Christensen, Camilla L., primary, Abraham, Brian J., primary, Kwiatkowski, Nicholas, primary, Buczkowski, Kevin A., primary, Bockorny, Bruno, primary, Chen, Ting, primary, Li, Shuai, primary, Rhee, Kevin, primary, Zhang, Haikuo, primary, Chen, Wankun, primary, Terai, Hideki, primary, Tavares, Tiffany, primary, Leggett, Alan L., primary, Li, Tianxia, primary, Wang, Yichen, primary, Zhang, Tinghu, primary, Kim, Tae-Jung, primary, Hong, Sook-Hee, primary, Poudel-Neupane, Neermala, primary, Silkes, Michael, primary, Mudianto, Tenny, primary, Tan, Li, primary, Shimamura, Takeshi, primary, Meyerson, Matthew, primary, Bass, Adam J., primary, Watanabe, Hideo, primary, Gray, Nathanael S., primary, Young, Richard A., primary, Wong, Kwok-Kin, primary, and Hammerman, Peter S., primary

Published
2023
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10. Supplementary Figures 1-10 from Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression

Author

Rusan, Maria, primary, Li, Kapsok, primary, Li, Yvonne, primary, Christensen, Camilla L., primary, Abraham, Brian J., primary, Kwiatkowski, Nicholas, primary, Buczkowski, Kevin A., primary, Bockorny, Bruno, primary, Chen, Ting, primary, Li, Shuai, primary, Rhee, Kevin, primary, Zhang, Haikuo, primary, Chen, Wankun, primary, Terai, Hideki, primary, Tavares, Tiffany, primary, Leggett, Alan L., primary, Li, Tianxia, primary, Wang, Yichen, primary, Zhang, Tinghu, primary, Kim, Tae-Jung, primary, Hong, Sook-Hee, primary, Poudel-Neupane, Neermala, primary, Silkes, Michael, primary, Mudianto, Tenny, primary, Tan, Li, primary, Shimamura, Takeshi, primary, Meyerson, Matthew, primary, Bass, Adam J., primary, Watanabe, Hideo, primary, Gray, Nathanael S., primary, Young, Richard A., primary, Wong, Kwok-Kin, primary, and Hammerman, Peter S., primary

Published
2023
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14. P53-induced GAP-43 Upregulation in Primary Cortical Neurons of Rats

Author

Li, Tianxia, Jia, Yuexin, Fu, Junxian, Fu, Zhuo, Qiao, Zhidong, Liu, Xiaoyang, Lv, Ting, Tang, Rong, and Yang, Guanglu

Abstract

Objectives: In this study, we employed an in vitro culturing technique to investigate the impact of p53 on the modulation of growth-associated protein-43 (GAP-43) within the primary cortical neurons of rat specimens.Methods: (1) Within the first 24 hours after birth, the bilateral cortex was extracted from newborn Wistar rats and primary cortical neurons were cultured and identified. (2) The changes in the mRNA and protein expressions of GAP-43 induced by p53 in rat primary cortical neurons cultured in vitro were identified utilizing real-time polymerase chain reaction and western blot techniques.Results: (1) Lentiviral transfection of p53 within primary cortical neurons of rats elicited elevated levels of both mRNA and protein expressions of GAP-43, consequently culminating in a noteworthy augmentation of p53 expression. (2) The introduction of a p53 inhibitor in rat primary cortical neurons resulted in a reduction in both mRNA and protein expressions of GAP-43.Conclusion: Within primary rat cortical neurons, p53 has the potential to prompt an augmentation in both the transcriptional and protein expression levels of the GAP-43 protein.

Published
2024
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15. The Drosophila hep pathway mediates Lrrk2-induced neurodegeneration

Author

Yang, Dejun, Thomas, Joseph M., Li, Tianxia, Lee, Youngseok, Liu, Zhaohui, and Smith, Wanli W.

Subjects
Drosophila -- Health aspects, Parkinson disease -- Genetic aspects, RNA interference -- Health aspects, Gene mutation -- Health aspects, Biological sciences
Abstract

Although the pathogenesis of Parkinson's disease (PD) remains unclear, mutations in leucine-rich repeat kinase 2 (Lrrk2) are among the major causes of familial PD. Most of these mutations disrupt Lrrk2 kinase and (or) GTPase domain function, resulting in neuronal degeneration. However, the signal pathways underlying Lrrk2-induced neuronal degeneration are not fully understood. There is an expanding body of evidence that suggests a link between Lrrk2 function and MAP kinase (MAPK) cascades. To further investigate this link in vivo, genetic RNAi screens of the MAPK pathways were performed in a Drosophila model to identify genetic modifier(s) that can suppress G2019S-Lrrk2-induced PD-like phenotypes. The results revealed that the knockdown of hemipterous (hep, or JNKK) increased fly survival time, improved locomotor function, and reduced loss of dopaminergic neurons in G2019S-Lrrk2 transgenic flies. Expression of the dominant-negative allele of JNK (JNK-DN), a kinase that is downstream of hep in G2019S-Lrrk2 transgenic flies, elicited a similar effect. Moreover, treatment with the JNK inhibitor SP600125 partially reversed the G2019S-Lrrk2-induced loss of dopaminergic neurons. These results indicate that the hep pathway plays an important role in Lrrk2-linked Parkinsonism in flies. These studies provide new insights into the molecular mechanisms underlying Lrrk2-linked PD pathogenesis and aid in identifying potential therapeutic targets. Key words: Lrrk2, Parkinson's disease, JNK, neuronal degeneration, hep, dopamine neuron, Drosophila model. Meme si la pathogenese de la maladie de Parkinson (MP) demeure floue, des mutations de la proteine Lrrk2 (leucine riche repeat kinase 2) sont parmi les principales causes de la MP hereditaire. La plupart de ces mutations dereglent la fonction des domaines kinase ou GTPase de Lrrk2, resultant en une degeneration neuronale. Toutefois, les voies de signalisation qui sous-tendent la degeneration neuronale induite par Lrrk2 ne sont pas completement comprises. Ilyadeplus en plus de donnees qui suggerent qu'il existe un lien entre la fonction de Lrrk2 et les cascades des MAP kinases (MAPK). Afin d'approfondir ce lien in vivo, des criblages genetiques des voies des MAPK a l'aide d'ARNi ont ete realises chez la drosophile afin d'identifier les modificateurs genetiques qui peuvent supprimer les phenotypes de type parkinsonien induits par G2019S-Lrrk2. Les resultats ont revele que le knockdown de hemipterous (hep ou JNKK) accroissait la duree de vie des mouches, ameliorait la fonction locomotrice et reduisait la perte de neurones dopaminergiques chez les mouches transgeniques G2019S-Lrrk2. L'expression de l'allele dominant negatif de JNK (JNK-DN), une kinase qui agit en aval de hep chez les mouches transgeniques G2019S-Lrrk2, provoquait un effet similaire. De plus, un traitement avec l'inhibiteur de JNK SP600125 renversait partiellement la perte de neurones dopaminergiques induite par G2019S-Lrrk2. Ces resultats indiquent que la voie de hep joue un role important dans le parkinsonisme lie a Lrrk2 chez les mouches. Ces etudes apportent un eclairage nouveau sur les mecanismes moleculaires qui sous-tendent la pathogenese de la MP liee a Lrrk2 et contribuent a identifier des cibles therapeutiques potentielles. [Traduit par la Redaction] Mots-cles : Lrrk2, maladie de Parkinson, JNK, degeneration neuronale, hep, neurone a dopamine, modele de la drosophile., Introduction Parkinson's disease (PD) is one of the most common neurodegenerative disorders and is characterized by the selective loss of dopaminergic neurons and the presence of Lewy bodies. The clinical [...]

Published
2018
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16. Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition

Author

Wong, Gabrielle S., Zhou, Jin, Liu, Jie Bin, Wu, Zhong, Xu, Xinsen, Li, Tianxia, Xu, David, Schumacher, Steven E., Puschhof, Jens, McFarland, James, Zou, Charles, Dulak, Austin, Henderson, Les, Xu, Peng, O’Day, Emily, Rendak, Rachel, Liao, Wei-li, Cecchi, Fabiola, Hembrough, Todd, Schwartz, Sarit, Szeto, Christopher, Rustgi, Anil K., Wong, Kwok-Kin, Diehl, J. Alan, Jensen, Karin, Graziano, Francesco, Ruzzo, Annamaria, Fereshetian, Shaunt, Mertins, Philipp, Carr, Steven A., Beroukhim, Rameen, Nakamura, Kenichi, Oki, Eiji, Watanabe, Masayuki, Baba, Hideo, Imamura, Yu, Catenacci, Daniel, and Bass, Adam J.

Published
2018
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17. Developing SHP2-based combination therapy for KRAS-amplified cancer

Author

Li, Tianxia, primary, Kikuchi, Osamu, additional, Zhou, Jin, additional, Wang, Yichen, additional, Pokharel, Babita, additional, Bastl, Klavdija, additional, Gokhale, Prafulla, additional, Knott, Aine, additional, Zhang, Yanxi, additional, Doench, John G., additional, Ho, Zandra V., additional, Catenacci, Daniel V.T., additional, and Bass, Adam J., additional

Published
2023
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21. Abstract 6377: Developing combination therapy with SHP2 inhibition for CIN-type gastroesophageal adenocarcinoma with KRAS amplification

Author

Kikuchi, Osamu, primary, Li, Tianxia, additional, Zhou, Jin, additional, Wang, Yichen, additional, Bastl, Klavdija, additional, Gokhale, Prafulla C., additional, Knott, Aine, additional, Zhang, Yanxi, additional, Doench, John G., additional, Ho, Zandra, additional, Catenacci, Daniel V., additional, and Bass, Adam J., additional

Published
2022
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34. Author Correction: Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition

Author

Wong, Gabrielle S., Zhou, Jin, Bin Liu, Jie, Wu, Zhong, Xu, Xinsen, Li, Tianxia, and Xu, David

Subjects
Biological sciences, Health
Abstract

In the Supplementary Information originally published with this article, a lane was missing in the [beta]-actin blot in Supplementary Fig. 2. The lane has been added. The error has been corrected in the Supplementary Information associated with this article., Author(s): Gabrielle S. Wong [sup.1] [sup.2] , Jin Zhou [sup.1] , Jie Bin Liu [sup.1] , Zhong Wu [sup.1] , Xinsen Xu [sup.1] , Tianxia Li [sup.1] , David Xu [...]

Published
2018
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35. RAS–MAPK Reactivation Facilitates Acquired Resistance in FGFR1-Amplified Lung Cancer and Underlies a Rationale for Upfront FGFR–MEK Blockade

Author

Bockorny, Bruno, primary, Rusan, Maria, additional, Chen, Wankun, additional, Liao, Rachel G., additional, Li, Yvonne, additional, Piccioni, Federica, additional, Wang, Jun, additional, Tan, Li, additional, Thorner, Aaron R., additional, Li, Tianxia, additional, Zhang, Yanxi, additional, Miao, Changhong, additional, Ovesen, Therese, additional, Shapiro, Geoffrey I., additional, Kwiatkowski, David J., additional, Gray, Nathanael S., additional, Meyerson, Matthew, additional, Hammerman, Peter S., additional, and Bass, Adam J., additional

Published
2018
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36. Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression

Author

Rusan, Maria, primary, Li, Kapsok, additional, Li, Yvonne, additional, Christensen, Camilla L., additional, Abraham, Brian J., additional, Kwiatkowski, Nicholas, additional, Buczkowski, Kevin A., additional, Bockorny, Bruno, additional, Chen, Ting, additional, Li, Shuai, additional, Rhee, Kevin, additional, Zhang, Haikuo, additional, Chen, Wankun, additional, Terai, Hideki, additional, Tavares, Tiffany, additional, Leggett, Alan L., additional, Li, Tianxia, additional, Wang, Yichen, additional, Zhang, Tinghu, additional, Kim, Tae-Jung, additional, Hong, Sook-Hee, additional, Poudel-Neupane, Neermala, additional, Silkes, Michael, additional, Mudianto, Tenny, additional, Tan, Li, additional, Shimamura, Takeshi, additional, Meyerson, Matthew, additional, Bass, Adam J., additional, Watanabe, Hideo, additional, Gray, Nathanael S., additional, Young, Richard A., additional, Wong, Kwok-Kin, additional, and Hammerman, Peter S., additional

Published
2018
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38. Ubiqutination via K27 and K29 chains signals aggregation and neuronal protection of LRRK2 by WSB1

Author

Nucifora, Frederick C., primary, Nucifora, Leslie G., additional, Ng, Chee-Hoe, additional, Arbez, Nicolas, additional, Guo, Yajuan, additional, Roby, Elaine, additional, Shani, Vered, additional, Engelender, Simone, additional, Wei, Dong, additional, Wang, Xiao-Fang, additional, Li, Tianxia, additional, Moore, Darren J., additional, Pletnikova, Olga, additional, Troncoso, Juan C., additional, Sawa, Akira, additional, Dawson, Ted M., additional, Smith, Wanli, additional, Lim, Kah-Leong, additional, and Ross, Christopher A., additional

Published
2016
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41. The Drosophilahep pathway mediates Lrrk2-induced neurodegeneration.

Author

Yang, Dejun, Thomas, Joseph M., Li, Tianxia, Lee, Youngseok, Liu, Zhaohui, and Smith, Wanli W.

Subjects
PARKINSON'S disease, NEURODEGENERATION, BRAIN diseases, DARDARIN, DOPAMINERGIC neurons, DROSOPHILA
Abstract

Copyright of Biochemistry & Cell Biology is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2018
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42. Models for LRRK2-Linked Parkinsonism

Author

Li, Tianxia, Yang, DeJun, Sushchky, Sarah, Liu, Zhaohui, and Smith, Wanli W.

Subjects
Article Subject, nervous system diseases
Abstract

Parkinson's disease (PD) is a progressive neurodegenerative movement disorder characterized by the selective loss of dopaminergic neurons and the presence of Lewy bodies. The pathogenesis of PD is not fully understood, but it appears to involve both genetic susceptibility and environmental factors. Treatment for PD that prevents neuronal death progression in the dopaminergic system and abnormal protein deposition in the brain is not yet available. Recently, mutations in the leucine-rich repeat kinase 2 (LRRK2) gene have been identified to cause autosomal-dominant late-onset PD and contribute to sporadic PD. Here, we review the recent models for LRRK2-linked Parkinsonism and their utility in studying LRRK2 neurobiology, pathogenesis, and potential therapeutics.

Published
2011
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