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34 results on '"Chen Ting"'

1. Sea cucumbers and their symbiotic microbiome have evolved to feed on seabed sediments

Author

Pan, Wenjie, Wang, Xuan, Ren, Chunhua, Jiang, Xiao, Gong, Sanqiang, Xie, Zhenyu, Wong, Nai-Kei, Li, Xiaomin, Huang, Jiasheng, Fan, Dingding, Luo, Peng, Yang, Yun, Ren, Xinyue, Yu, Suzhong, Qin, Zhou, Wu, Xiaofen, Huo, Da, Ma, Bo, Liu, Yang, Zhang, Xin, E, Zixuan, Liang, Jingxuan, Sun, Hongyan, Yuan, Lihong, Liu, Xujia, Cheng, Chuhang, Long, Hao, Li, Jianlong, Wang, Yanhong, Hu, Chaoqun, and Chen, Ting

Published
2024
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6. Globally invariant metabolism but density-diversity mismatch in springtails

Author

Potapov, Anton M., Guerra, Carlos A., van den Hoogen, Johan, Babenko, Anatoly, Bellini, Bruno C., Berg, Matty P., Chown, Steven L., Deharveng, Louis, Kováč, Ľubomír, Kuznetsova, Natalia A., Ponge, Jean-François, Potapov, Mikhail B., Russell, David J., Alexandre, Douglas, Alatalo, Juha M., Arbea, Javier I., Bandyopadhyaya, Ipsa, Bernava, Verónica, Bokhorst, Stef, Bolger, Thomas, Castaño-Meneses, Gabriela, Chauvat, Matthieu, Chen, Ting-Wen, Chomel, Mathilde, Classen, Aimee T., Cortet, Jerome, Čuchta, Peter, Manuela de la Pedrosa, Ana, Ferreira, Susana S. D., Fiera, Cristina, Filser, Juliane, Franken, Oscar, Fujii, Saori, Koudji, Essivi Gagnon, Gao, Meixiang, Gendreau-Berthiaume, Benoit, Gomez-Pamies, Diego F., Greve, Michelle, Tanya Handa, I., Heiniger, Charlène, Holmstrup, Martin, Homet, Pablo, Ivask, Mari, Janion-Scheepers, Charlene, Jochum, Malte, Joimel, Sophie, Claudia S. Jorge, Bruna, Jucevica, Edite, Ferlian, Olga, Iuñes de Oliveira Filho, Luís Carlos, Klauberg-Filho, Osmar, Baretta, Dilmar, Krab, Eveline J., Kuu, Annely, de Lima, Estevam C. A., Lin, Dunmei, Lindo, Zoe, Liu, Amy, Lu, Jing-Zhong, Luciañez, María José, Marx, Michael T., McCary, Matthew A., Minor, Maria A., Nakamori, Taizo, Negri, Ilaria, Ochoa-Hueso, Raúl, Palacios-Vargas, José G., Pollierer, Melanie M., Querner, Pascal, Raschmanová, Natália, Rashid, Muhammad Imtiaz, Raymond-Léonard, Laura J., Rousseau, Laurent, Saifutdinov, Ruslan A., Salmon, Sandrine, Sayer, Emma J., Scheunemann, Nicole, Scholz, Cornelia, Seeber, Julia, Shveenkova, Yulia B., Stebaeva, Sophya K., Sterzynska, Maria, Sun, Xin, Susanti, Winda I., Taskaeva, Anastasia A., Thakur, Madhav P., Tsiafouli, Maria A., Turnbull, Matthew S., Twala, Mthokozisi N., Uvarov, Alexei V., Venier, Lisa A., Widenfalk, Lina A., Winck, Bruna R., Winkler, Daniel, Wu, Donghui, Xie, Zhijing, Yin, Rui, Zeppelini, Douglas, Crowther, Thomas W., Eisenhauer, Nico, and Scheu, Stefan

Published
2023
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9. Publisher Correction: FGF signalling controls the specification of hair placode-derived SOX9 positive progenitors to Merkel cells.

Author

Nguyen, Minh Binh, Cohen, Idan, Kumar, Vinod, Xu, Zijian, Bar, Carmit, Dauber-Decker, Katherine L, Tsai, Pai-Chi, Marangoni, Pauline, Klein, Ophir D, Hsu, Ya-Chieh, Chen, Ting, Mikkola, Marja L, and Ezhkova, Elena

Abstract

The originally published version of this Article contained an error in Figure 2. In panel e, the blue bar was incorrectly labelled 'KRT8(+)/TOMATO(-)'. Furthermore, during the process of preparing a correction, the publication date of the Article was inadvertently changed to June 20th 2018. Both of these errors have been corrected in the PDF and HTML versions of the Article.

Published
2018

10. FGF signalling controls the specification of hair placode-derived SOX9 positive progenitors to Merkel cells.

Author

Nguyen, Minh Binh, Cohen, Idan, Kumar, Vinod, Xu, Zijian, Bar, Carmit, Dauber-Decker, Katherine L, Tsai, Pai-Chi, Marangoni, Pauline, Klein, Ophir D, Hsu, Ya-Chieh, Chen, Ting, Mikkola, Marja L, and Ezhkova, Elena

Subjects
Merkel Cells, Hair Follicle, Animals, Mice, Transgenic, Mice, Knockout, Mice, Green Fluorescent Proteins, Transcription Factors, Signal Transduction, Cell Lineage, Pregnancy, Models, Biological, Female, Male, NFATC Transcription Factors, Receptor, Fibroblast Growth Factor, Type 2, Basic Helix-Loop-Helix Transcription Factors, Hedgehog Proteins, Embryonic Stem Cells, SOX9 Transcription Factor, Gene Knockout Techniques, LIM-Homeodomain Proteins, Transgenic, Knockout, Models, Biological, Receptor, Fibroblast Growth Factor, Type 2
Abstract

Merkel cells are innervated mechanosensory cells responsible for light-touch sensations. In murine dorsal skin, Merkel cells are located in touch domes and found in the epidermis around primary hairs. While it has been shown that Merkel cells are skin epithelial cells, the progenitor cell population that gives rise to these cells is unknown. Here, we show that during embryogenesis, SOX9-positive (+) cells inside hair follicles, which were previously known to give rise to hair follicle stem cells (HFSCs) and cells of the hair follicle lineage, can also give rise to Merkel Cells. Interestingly, while SOX9 is critical for HFSC specification, it is dispensable for Merkel cell formation. Conversely, FGFR2 is required for Merkel cell formation but is dispensable for HFSCs. Together, our studies uncover SOX9(+) cells as precursors of Merkel cells and show the requirement for FGFR2-mediated epithelial signalling in Merkel cell specification.

Published
2018

15. Fibroblast-enriched endoplasmic reticulum protein TXNDC5 promotes pulmonary fibrosis by augmenting TGFβ signaling through TGFBR1 stabilization

Author

Lee, Tzu-Han, Yeh, Chih-Fan, Lee, Ying-Tung, Shih, Ying-Chun, Chen, Yen-Ting, Hung, Chen-Ting, You, Ming-Yi, Wu, Pei-Chen, Shentu, Tzu-Pin, Huang, Ru-Ting, Lin, Yu-Shan, Wu, Yueh-Feng, Lin, Sung-Jan, Lu, Frank-Leigh, Tsao, Po-Nien, Lin, Tzu-Hung, Lo, Shen-Chuan, Tseng, Yi-Shuan, Wu, Wan-Lin, Chen, Chiung-Nien, Wu, Chau-Chung, Lin, Shuei-Liong, Sperling, Anne I., Guzy, Robert D., Fang, Yun, and Yang, Kai-Chien

Published
2020
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16. Boosting NAD+ with a small molecule that activates NAMPT

Author

Gardell, Stephen J., Hopf, Meghan, Khan, Asima, Dispagna, Mauro, Hampton Sessions, E., Falter, Rebecca, Kapoor, Nidhi, Brooks, Jeanne, Culver, Jeffrey, Petucci, Chris, Ma, Chen-Ting, Cohen, Steven E., Tanaka, Jun, Burgos, Emmanuel S., Hirschi, Jennifer S., Smith, Steven R., Sergienko, Eduard, and Pinkerton, Anthony B.

Published
2019
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19. APOBEC3A is an oral cancer prognostic biomarker in Taiwanese carriers of an APOBEC deletion polymorphism

Author

Chen, Ting-Wen, Lee, Chi-Ching, Liu, Hsuan, Wu, Chi-Sheng, Pickering, Curtis R., Huang, Po-Jung, Wang, Jing, Chang, Ian Yi-Feng, Yeh, Yuan-Ming, Chen, Chih-De, Li, Hsin-Pai, Luo, Ji-Dung, Tan, Bertrand Chin-Ming, Chan, Timothy En Haw, Hsueh, Chuen, Chu, Lichieh Julie, Chen, Yi-Ting, Zhang, Bing, Yang, Chia-Yu, Wu, Chih-Ching, Hsu, Chia-Wei, See, Lai-Chu, Tang, Petrus, Yu, Jau-Song, Liao, Wei-Chao, Chiang, Wei-Fan, Rodriguez, Henry, Myers, Jeffrey N., Chang, Kai-Ping, and Chang, Yu-Sun

Published
2017
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20. Erratum: Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2

Author

Zhang, Haikuo, Brainson, Christine Fillmore, Koyama, Shohei, Redig, Amanda J., Chen, Ting, Li, Shuai, Gupta, Manav, Garcia-de-Alba, Carolina, Paschini, Margherita, Herter-Sprie, Grit S., Lu, Gang, Zhang, Xin, Marsh, Bryan P, Tuminello, Stephanie J., Xu, Chunxiao, Chen, Zhao, Wang, Xiaoen, Akbay, Esra A., Zheng, Mei, Palakurthi, Sangeetha, Sholl, Lynette M., Rustgi, Anil K., Kwiatkowski, David J., Alan Diehl, J., Bass, Adam J., Sharpless, Norman E., Dranoff, Glenn, Hammerman, Peter S., Ji, Hongbin, Bardeesy, Nabeel, Saur, Dieter, Watanabe, Hideo, Kim, Carla F., and Wong, Kwok-Kin

Published
2017
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22. Fibroblast-enriched endoplasmic reticulum protein TXNDC5 promotes pulmonary fibrosis by augmenting TGFβ signaling through TGFBR1 stabilization

Author

Shuei-Liong Lin, Shen-Chuan Lo, Yu-Shan Lin, Y.-H. Lee, Frank-Leigh Lu, Kai-Chien Yang, Sung-Jan Lin, Tzu-Pin Shentu, Pei-Chen Wu, Chen-Ting Hung, Ying-Chun Shih, Robert D. Guzy, Chau-Chung Wu, Wan-Lin Wu, Yen-Ting Chen, Tzu-Han Lee, Anne I. Sperling, Ru-Ting Huang, Ming-Yi You, Yueh-Feng Wu, Chiung-Nien Chen, Yun Fang, Po-Nien Tsao, Chih-Fan Yeh, Yi-Shuan Tseng, and Tzu-Hung Lin

Subjects
0301 basic medicine, Male, Protein Folding, Molecular biology, Pulmonary Fibrosis, Receptor, Transforming Growth Factor-beta Type I, General Physics and Astronomy, 02 engineering and technology, Idiopathic pulmonary fibrosis, chemistry.chemical_compound, Mice, Thioredoxins, Pulmonary fibrosis, Protein disulfide-isomerase, lcsh:Science, Mice, Knockout, Multidisciplinary, Protein Stability, 021001 nanoscience & nanotechnology, Endoplasmic Reticulum Stress, Up-Regulation, medicine.anatomical_structure, 0210 nano-technology, Signal Transduction, Science, Protein Disulfide-Isomerases, Bleomycin, General Biochemistry, Genetics and Molecular Biology, Article, Transforming Growth Factor beta1, 03 medical and health sciences, Downregulation and upregulation, medicine, Animals, Humans, Respiratory tract diseases, Lung, business.industry, Endoplasmic reticulum, General Chemistry, medicine.disease, Idiopathic Pulmonary Fibrosis, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, chemistry, Unfolded protein response, Cancer research, lcsh:Q, business, Gene Deletion
Abstract

Pulmonary fibrosis (PF) is a major public health problem with limited therapeutic options. There is a clear need to identify novel mediators of PF to develop effective therapeutics. Here we show that an ER protein disulfide isomerase, thioredoxin domain containing 5 (TXNDC5), is highly upregulated in the lung tissues from both patients with idiopathic pulmonary fibrosis and a mouse model of bleomycin (BLM)-induced PF. Global deletion of Txndc5 markedly reduces the extent of PF and preserves lung function in mice following BLM treatment. Mechanistic investigations demonstrate that TXNDC5 promotes fibrogenesis by enhancing TGFβ1 signaling through direct binding with and stabilization of TGFBR1 in lung fibroblasts. Moreover, TGFβ1 stimulation is shown to upregulate TXNDC5 via ER stress/ATF6-dependent transcriptional control in lung fibroblasts. Inducing fibroblast-specific deletion of Txndc5 mitigates the progression of BLM-induced PF and lung function deterioration. Targeting TXNDC5, therefore, could be a novel therapeutic approach against PF., Pulmonary fibrosis is a major public health problem with unclear mechanism and limited therapeutic options. Here the authors show that a fibroblast-enriched endoplasmic reticulum protein, TXNDC5, promotes pulmonary fibrosis by stabilizing TGFBR1 and show the potential of TXNDC5 as a therapeutic target against pulmonary fibrosis.

Published
2020

23. Boosting NAD+ with a small molecule that activates NAMPT

Author

Jun Tanaka, Emmanuel S. Burgos, Rebecca Falter, E. Hampton Sessions, Jeanne Brooks, Stephen J. Gardell, Steven E. Cohen, Anthony B. Pinkerton, Asima Khan, Jennifer S. Hirschi, Meghan E. Hopf, Nidhi Kapoor, Jeffrey A. Culver, Chris Petucci, Steven R. Smith, Eduard Sergienko, Chen Ting Ma, and Mauro Dispagna

Subjects
0301 basic medicine, A549 cell, Multidisciplinary, Activator (genetics), Chemistry, Science, Nicotinamide phosphoribosyltransferase, General Physics and Astronomy, 02 engineering and technology, General Chemistry, 021001 nanoscience & nanotechnology, Small molecule, General Biochemistry, Genetics and Molecular Biology, Cell biology, 03 medical and health sciences, chemistry.chemical_compound, 030104 developmental biology, Phosphorylation, lcsh:Q, NAD+ kinase, lcsh:Science, 0210 nano-technology, Intracellular, Nicotinamide mononucleotide
Abstract

Pharmacological strategies that boost intracellular NAD+ are highly coveted for their therapeutic potential. One approach is activation of nicotinamide phosphoribosyltransferase (NAMPT) to increase production of nicotinamide mononucleotide (NMN), the predominant NAD+ precursor in mammalian cells. A high-throughput screen for NAMPT activators and hit-to-lead campaign yielded SBI-797812, a compound that is structurally similar to active-site directed NAMPT inhibitors and blocks binding of these inhibitors to NAMPT. SBI-797812 shifts the NAMPT reaction equilibrium towards NMN formation, increases NAMPT affinity for ATP, stabilizes phosphorylated NAMPT at His247, promotes consumption of the pyrophosphate by-product, and blunts feedback inhibition by NAD+. These effects of SBI-797812 turn NAMPT into a “super catalyst” that more efficiently generates NMN. Treatment of cultured cells with SBI-797812 increases intracellular NMN and NAD+. Dosing of mice with SBI-797812 elevates liver NAD+. Small molecule NAMPT activators such as SBI-797812 are a pioneering approach to raise intracellular NAD+ and realize its associated salutary effects. Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate determining step for NAD+ synthesis and is of interest as a drug target. Here the authors identify and characterize a small molecule NAMPT activator SBI-797812, elucidate its mode of action and show that it increases intracellular NMN and NAD+ levels in cultured cells and elevates liver NAD+ in mice.

Published
2019

24. Boosting NAD

Author

Stephen J, Gardell, Meghan, Hopf, Asima, Khan, Mauro, Dispagna, E, Hampton Sessions, Rebecca, Falter, Nidhi, Kapoor, Jeanne, Brooks, Jeffrey, Culver, Chris, Petucci, Chen-Ting, Ma, Steven E, Cohen, Jun, Tanaka, Emmanuel S, Burgos, Jennifer S, Hirschi, Steven R, Smith, Eduard, Sergienko, and Anthony B, Pinkerton

Subjects
Molecular Structure, Intracellular Space, Enzyme Activators, Drug development, NAD, Biochemistry, Article, Small Molecule Libraries, Mice, Liver, A549 Cells, Target identification, Biocatalysis, Animals, Humans, Phosphorylation, Nicotinamide Phosphoribosyltransferase, Nicotinamide Mononucleotide
Abstract

Pharmacological strategies that boost intracellular NAD+ are highly coveted for their therapeutic potential. One approach is activation of nicotinamide phosphoribosyltransferase (NAMPT) to increase production of nicotinamide mononucleotide (NMN), the predominant NAD+ precursor in mammalian cells. A high-throughput screen for NAMPT activators and hit-to-lead campaign yielded SBI-797812, a compound that is structurally similar to active-site directed NAMPT inhibitors and blocks binding of these inhibitors to NAMPT. SBI-797812 shifts the NAMPT reaction equilibrium towards NMN formation, increases NAMPT affinity for ATP, stabilizes phosphorylated NAMPT at His247, promotes consumption of the pyrophosphate by-product, and blunts feedback inhibition by NAD+. These effects of SBI-797812 turn NAMPT into a “super catalyst” that more efficiently generates NMN. Treatment of cultured cells with SBI-797812 increases intracellular NMN and NAD+. Dosing of mice with SBI-797812 elevates liver NAD+. Small molecule NAMPT activators such as SBI-797812 are a pioneering approach to raise intracellular NAD+ and realize its associated salutary effects., Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate determining step for NAD+ synthesis and is of interest as a drug target. Here the authors identify and characterize a small molecule NAMPT activator SBI-797812, elucidate its mode of action and show that it increases intracellular NMN and NAD+ levels in cultured cells and elevates liver NAD+ in mice.

Published
2018

25. Parasitic insect-derived miRNAs modulate host development

Author

Wang, Zhi-zhi, primary, Ye, Xi-qian, additional, Shi, Min, additional, Li, Fei, additional, Wang, Ze-hua, additional, Zhou, Yue-nan, additional, Gu, Qi-juan, additional, Wu, Xiao-tong, additional, Yin, Chuan-lin, additional, Guo, Dian-hao, additional, Hu, Rong-min, additional, Hu, Na-na, additional, Chen, Ting, additional, Zheng, Bo-ying, additional, Zou, Jia-ni, additional, Zhan, Le-qing, additional, Wei, Shu-jun, additional, Wang, Yan-ping, additional, Huang, Jian-hua, additional, Fang, Xiao-dong, additional, Strand, Michael R., additional, and Chen, Xue-xin, additional

Published
2018
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26. The liver-enriched lnc-LFAR1 promotes liver fibrosis by activating TGFβ and Notch pathways

Author

Zhang, Kun, primary, Han, Xiaohui, additional, Zhang, Zhen, additional, Zheng, Lina, additional, Hu, Zhimei, additional, Yao, Qingbin, additional, Cui, Hongmei, additional, Shu, Guiming, additional, Si, Maojie, additional, Li, Chan, additional, Shi, Zhemin, additional, Chen, Ting, additional, Han, Yawei, additional, Chang, Yanan, additional, Yao, Zhi, additional, Han, Tao, additional, and Hong, Wei, additional

Published
2017
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27. Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2

Author

Zhang, Haikuo, primary, Fillmore Brainson, Christine, additional, Koyama, Shohei, additional, Redig, Amanda J., additional, Chen, Ting, additional, Li, Shuai, additional, Gupta, Manav, additional, Garcia-de-Alba, Carolina, additional, Paschini, Margherita, additional, Herter-Sprie, Grit S., additional, Lu, Gang, additional, Zhang, Xin, additional, Marsh, Bryan P., additional, Tuminello, Stephanie J., additional, Xu, Chunxiao, additional, Chen, Zhao, additional, Wang, Xiaoen, additional, Akbay, Esra A., additional, Zheng, Mei, additional, Palakurthi, Sangeetha, additional, Sholl, Lynette M., additional, Rustgi, Anil K., additional, Kwiatkowski, David J., additional, Diehl, J Alan, additional, Bass, Adam J., additional, Sharpless, Norman E., additional, Dranoff, Glenn, additional, Hammerman, Peter S., additional, Ji, Hongbin, additional, Bardeesy, Nabeel, additional, Saur, Dieter, additional, Watanabe, Hideo, additional, Kim, Carla F., additional, and Wong, Kwok-Kin, additional

Published
2017
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28. CDK4/6 or MAPK blockade enhances efficacy of EGFR inhibition in oesophageal squamous cell carcinoma

Author

Zhou, Jin, primary, Wu, Zhong, additional, Wong, Gabrielle, additional, Pectasides, Eirini, additional, Nagaraja, Ankur, additional, Stachler, Matthew, additional, Zhang, Haikuo, additional, Chen, Ting, additional, Zhang, Haisheng, additional, Liu, Jie Bin, additional, Xu, Xinsen, additional, Sicinska, Ewa, additional, Sanchez-Vega, Francisco, additional, Rustgi, Anil K., additional, Diehl, J. Alan, additional, Wong, Kwok-Kin, additional, and Bass, Adam J., additional

Published
2017
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29. Boosting NAD+ with a small molecule that activates NAMPT.

Author

Gardell, Stephen J., Hopf, Meghan, Khan, Asima, Dispagna, Mauro, Hampton Sessions, E., Falter, Rebecca, Kapoor, Nidhi, Brooks, Jeanne, Culver, Jeffrey, Petucci, Chris, Ma, Chen-Ting, Cohen, Steven E., Tanaka, Jun, Burgos, Emmanuel S., Hirschi, Jennifer S., Smith, Steven R., Sergienko, Eduard, and Pinkerton, Anthony B.

Abstract

Pharmacological strategies that boost intracellular NAD+ are highly coveted for their therapeutic potential. One approach is activation of nicotinamide phosphoribosyltransferase (NAMPT) to increase production of nicotinamide mononucleotide (NMN), the predominant NAD+ precursor in mammalian cells. A high-throughput screen for NAMPT activators and hit-to-lead campaign yielded SBI-797812, a compound that is structurally similar to active-site directed NAMPT inhibitors and blocks binding of these inhibitors to NAMPT. SBI-797812 shifts the NAMPT reaction equilibrium towards NMN formation, increases NAMPT affinity for ATP, stabilizes phosphorylated NAMPT at His247, promotes consumption of the pyrophosphate by-product, and blunts feedback inhibition by NAD+. These effects of SBI-797812 turn NAMPT into a "super catalyst" that more efficiently generates NMN. Treatment of cultured cells with SBI-797812 increases intracellular NMN and NAD+. Dosing of mice with SBI-797812 elevates liver NAD+. Small molecule NAMPT activators such as SBI-797812 are a pioneering approach to raise intracellular NAD+ and realize its associated salutary effects. Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate determining step for NAD+ synthesis and is of interest as a drug target. Here the authors identify and characterize a small molecule NAMPT activator SBI-797812, elucidate its mode of action and show that it increases intracellular NMN and NAD+ levels in cultured cells and elevates liver NAD+ in mice. [ABSTRACT FROM AUTHOR]

Published
2019
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32. Helminth-induced IL-4 expands bystander memory CD8+ T cells for early control of viral infection.

Author

Rolot, Marion, Dougall, Annette M., Chetty, Alisha, Javaux, Justine, Chen, Ting, Xiao, Xue, Machiels, Bénédicte, Selkirk, Murray E., Maizels, Rick M., Hokke, Cornelis, Denis, Olivier, Brombacher, Frank, Vanderplasschen, Alain, Gillet, Laurent, Horsnell, William G. C., and Dewals, Benjamin G.

Abstract

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8+ T cells (TVM) are non-conventional T cells displaying memory properties that can be generated through responsiveness to interleukin (IL)-4. However, it is not clear if helminth-induced type 2 immunity functionally affects the TVM compartment. Here, we show that helminths expand CD44hiCD62LhiCXCR3hiCD49dlo TVM cells through direct IL-4 signaling in CD8+ T cells. Importantly, helminth-mediated conditioning of TVM cells provided enhanced control of acute respiratory infection with the murid gammaherpesvirus 4 (MuHV-4). This enhanced control of MuHV-4 infection could further be explained by an increase in antigen-specific CD8+ T cell effector responses in the lung and was directly dependent on IL-4 signaling. These results demonstrate that IL-4 during helminth infection can non-specifically condition CD8+ T cells, leading to a subsequently raised antigen-specific CD8+ T cell activation that enhances control of viral infection. Parasitic helminth infection is known to impact upon the host response to other bystander inflammatory processes. Here the authors show that IL4 production induced by helminth infection results in expansion of bystander CD8+ memory T cells and enhanced control to viral infection. [ABSTRACT FROM AUTHOR]

Published
2018
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33. Fibroblast-enriched endoplasmic reticulum protein TXNDC5 promotes pulmonary fibrosis by augmenting TGFβ signaling through TGFBR1 stabilization

Author

Tzu-Han Lee, Chih-Fan Yeh, Ying-Tung Lee, Ying-Chun Shih, Yen-Ting Chen, Chen-Ting Hung, Ming-Yi You, Pei-Chen Wu, Tzu-Pin Shentu, Ru-Ting Huang, Yu-Shan Lin, Yueh-Feng Wu, Sung-Jan Lin, Frank-Leigh Lu, Po-Nien Tsao, Tzu-Hung Lin, Shen-Chuan Lo, Yi-Shuan Tseng, Wan-Lin Wu, Chiung-Nien Chen, Chau-Chung Wu, Shuei-Liong Lin, Anne I. Sperling, Robert D. Guzy, Yun Fang, and Kai-Chien Yang

Subjects
Science
Abstract

Pulmonary fibrosis is a major public health problem with unclear mechanism and limited therapeutic options. Here the authors show that a fibroblast-enriched endoplasmic reticulum protein, TXNDC5, promotes pulmonary fibrosis by stabilizing TGFBR1 and show the potential of TXNDC5 as a therapeutic target against pulmonary fibrosis.

Published
2020
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34. Boosting NAD+ with a small molecule that activates NAMPT

Author

Stephen J. Gardell, Meghan Hopf, Asima Khan, Mauro Dispagna, E. Hampton Sessions, Rebecca Falter, Nidhi Kapoor, Jeanne Brooks, Jeffrey Culver, Chris Petucci, Chen-Ting Ma, Steven E. Cohen, Jun Tanaka, Emmanuel S. Burgos, Jennifer S. Hirschi, Steven R. Smith, Eduard Sergienko, and Anthony B. Pinkerton

Subjects
Science
Abstract

Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate determining step for NAD+ synthesis and is of interest as a drug target. Here the authors identify and characterize a small molecule NAMPT activator SBI-797812, elucidate its mode of action and show that it increases intracellular NMN and NAD+ levels in cultured cells and elevates liver NAD+ in mice.

Published
2019
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