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Your search keyword '"Gu, Chunfang"' showing total 39 results
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39 results on '"Gu, Chunfang"'

3. PPIP5K2 and PCSK1 are Candidate Genetic Contributors to Familial Keratoconus.

Author

Khaled, Mariam Lofty, Bykhovskaya, Yelena, Gu, Chunfang, Liu, Alice, Drewry, Michelle D, Chen, Zhong, Mysona, Barbara A, Parker, Emily, McNabb, Ryan P, Yu, Hongfang, Lu, Xiaowen, Wang, Jing, Li, Xiaohui, Al-Muammar, Abdulrahman, Rotter, Jerome I, Porter, Louise F, Estes, Amy, Watsky, Mitchell A, Smith, Sylvia B, Xu, Hongyan, Abu-Amero, Khaled K, Kuo, Anthony, Shears, Stephen B, Rabinowitz, Yaron S, and Liu, Yutao

Subjects
Cornea, Animals, Humans, Mice, Keratoconus, Disease Models, Animal, Genetic Predisposition to Disease, Proprotein Convertase 1, Phosphotransferases (Phosphate Group Acceptor), Corneal Topography, Chromosome Mapping, Pedigree, Genotype, Mutation, Genome, Human, Quality of Life, Adult, Female, Male, Genetic Linkage, Whole Exome Sequencing, Disease Models, Animal, Phosphotransferases, Genome, Human
Abstract

Keratoconus (KC) is the most common corneal ectatic disorder affecting >300,000 people in the US. KC normally has its onset in adolescence, progressively worsening through the third to fourth decades of life. KC patients report significant impaired vision-related quality of life. Genetic factors play an important role in KC pathogenesis. To identify novel genes in familial KC patients, we performed whole exome and genome sequencing in a four-generation family. We identified potential variants in the PPIP5K2 and PCSK1 genes. Using in vitro cellular model and in vivo gene-trap mouse model, we found critical evidence to support the role of PPIP5K2 in normal corneal function and KC pathogenesis. The gene-trap mouse showed irregular corneal surfaces and pathological corneal thinning resembling KC. For the first time, we have integrated corneal tomography and pachymetry mapping into characterization of mouse corneal phenotypes which could be widely implemented in basic and translational research for KC diagnosis and therapy in the future.

Published
2019

14. Development of Novel IP6K Inhibitors for the Treatment of Obesity and Obesity-Induced Metabolic Dysfunctions

Author

Zhou, Yubai, primary, Mukherjee, Sandip, additional, Huang, Daowei, additional, Chakraborty, Molee, additional, Gu, Chunfang, additional, Zong, Guangning, additional, Stashko, Michael A., additional, Pearce, Kenneth H., additional, Shears, Stephen B., additional, Chakraborty, Anutosh, additional, Wang, Huanchen, additional, and Wang, Xiaodong, additional

Published
2022
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15. Analysis of Inositol Phosphate Metabolism by Capillary Electrophoresis Electrospray Ionization Mass Spectrometry (CE-ESI-MS)

Author

Qiu, Danye, primary, Wilson, Miranda S., additional, Eisenbeis, Verena B., additional, Harmel, Robert K., additional, Riemer, Esther, additional, Haas, Thomas M., additional, Wittwer, Christopher, additional, Jork, Nikolaus, additional, Gu, Chunfang, additional, Shears, Stephen B., additional, Schaaf, Gabriel, additional, Kammerer, Bernd, additional, Fiedler, Dorothea, additional, Saiardi, Adolfo, additional, and Jessen, Henning J., additional

Published
2020
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16. InsP 7 is a small-molecule regulator of NUDT3-mediated mRNA decapping and processing-body dynamics

Author

Sahu, Soumyadip, primary, Wang, Zhenzhen, additional, Jiao, Xinfu, additional, Gu, Chunfang, additional, Jork, Nikolaus, additional, Wittwer, Christopher, additional, Li, Xingyao, additional, Hostachy, Sarah, additional, Fiedler, Dorothea, additional, Wang, Huanchen, additional, Jessen, Henning J., additional, Kiledjian, Megerditch, additional, and Shears, Stephen B., additional

Published
2020
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20. Corrigendum to ‘Inositol hexakisphosphate kinase 1 is a metabolic sensor in pancreatic β-cells’ [Cellular Signalling 46 (2018) 120–128]

Author

Rajasekaran, Subu Surendran, primary, Kim, Jaeyoon, additional, Gaboardi, Gian-Carlo, additional, Gromada, Jesper, additional, Shears, Stephen B., additional, dos Santos, Karen Tiago, additional, Nolasco, Eduardo Lima, additional, de Souza Ferreira, Sabrina, additional, Illies, Christopher, additional, Köhler, Martin, additional, Gu, Chunfang, additional, Ryu, Sung Ho, additional, Martins, Joilson O., additional, Darè, Elisabetta, additional, Barker, Christopher J., additional, and Berggren, Per-Olof, additional

Published
2019
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21. IL-17R–EGFR axis links wound healing to tumorigenesis in Lrig1+ stem cells

Author

Chen, Xing, primary, Cai, Gang, additional, Liu, Caini, additional, Zhao, Junjie, additional, Gu, Chunfang, additional, Wu, Ling, additional, Hamilton, Thomas A., additional, Zhang, Cun-jin, additional, Ko, Jennifer, additional, Zhu, Liang, additional, Qin, Jun, additional, Vidimos, Allison, additional, Koyfman, Shlomo, additional, Gastman, Brian R., additional, Jensen, Kim B., additional, and Li, Xiaoxia, additional

Published
2018
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22. Act1 is a negative regulator in T and B cells via direct inhibition of STAT3

Author

Zhang, Cun-Jin, primary, Wang, Chenhui, additional, Jiang, Meiling, additional, Gu, Chunfang, additional, Xiao, Jianxin, additional, Chen, Xing, additional, Martin, Bradley N., additional, Tang, Fangqiang, additional, Yamamoto, Erin, additional, Xian, Yibo, additional, Wang, Han, additional, Li, Fengling, additional, Sartor, R. Balfour, additional, Smith, Howard, additional, Husni, M. Elaine, additional, Shi, Fu-Dong, additional, Gao, Ji, additional, Carman, Julie, additional, Dongre, Ashok, additional, McKarns, Susan C., additional, Coppieters, Ken, additional, Jørgensen, Trine N., additional, Leonard, Warren J., additional, and Li, Xiaoxia, additional

Published
2018
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23. Inositol hexakisphosphate kinase 1 is a metabolic sensor in pancreatic β-cells

Author

Rajasekaran, Subu Surendran, primary, Kim, Jaeyoon, additional, Gaboardi, Gian-Carlo, additional, Gromada, Jesper, additional, Shears, Stephen B., additional, dos Santos, Karen Tiago, additional, Nolasco, Eduardo Lima, additional, Ferreira, Sabrina de Souza, additional, Illies, Christopher, additional, Köhler, Martin, additional, Gu, Chunfang, additional, Ryu, Sung Ho, additional, Martins, Joilson O., additional, Darè, Elisabetta, additional, Barker, Christopher J., additional, and Berggren, Per-Olof, additional

Published
2018
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30. The flavonoid cyanidin blocks binding of the cytokine interleukin-17A to the IL-17RA subunit to alleviate inflammation in vivo

Author

Liu, Caini, primary, Zhu, Liang, additional, Fukuda, Koichi, additional, Ouyang, Suidong, additional, Chen, Xing, additional, Wang, Chenhui, additional, Zhang, Cun-jin, additional, Martin, Bradley, additional, Gu, Chunfang, additional, Qin, Luke, additional, Rachakonda, Suguna, additional, Aronica, Mark, additional, Qin, Jun, additional, and Li, Xiaoxia, additional

Published
2017
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34. A novel IL-17 signaling pathway controlling keratinocyte proliferation and tumorigenesis via the TRAF4–ERK5 axis

Author

Wu, Ling, primary, Chen, Xing, additional, Zhao, Junjie, additional, Martin, Bradley, additional, Zepp, Jarod A., additional, S. Ko, Jennifer, additional, Gu, Chunfang, additional, Cai, Gang, additional, Ouyang, Wenjun, additional, Sen, Ganes, additional, Stark, George R., additional, Su, Bing, additional, Vines, Charlotte M., additional, Tournier, Cathy, additional, Hamilton, Thomas A., additional, Vidimos, Allison, additional, Gastman, Brian, additional, Liu, Caini, additional, and Li, Xiaoxia, additional

Published
2015
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35. IL-17R–EGFR axis links wound healing to tumorigenesis in Lrig1+ stem cells

Author

Chen, Xing, Cai, Gang, Liu, Caini, Zhao, Junjie, Gu, Chunfang, Wu, Ling, Hamilton, Thomas A., Zhang, Cun-jin, Ko, Jennifer, Zhu, Liang, Qin, Jun, Vidimos, Allison, Koyfman, Shlomo, Gastman, Brian R., Jensen, Kim B., and Li, Xiaoxia

Abstract

Lrig1 marks a distinct population of stem cells restricted to the upper pilosebaceous unit in normal epidermis. Here we report that IL-17A–mediated activation of EGFR plays a critical role in the expansion and migration of Lrig1+ stem cells and their progenies in response to wounding, thereby promoting wound healing and skin tumorigenesis. Lrig1-specific deletion of the IL-17R adaptor Act1 or EGFR in mice impairs wound healing and reduces tumor formation. Mechanistically, IL-17R recruits EGFR for IL-17A–mediated signaling in Lrig1+ stem cells. While TRAF4, enriched in Lrig1+ stem cells, tethers IL-17RA and EGFR, Act1 recruits c-Src for IL-17A–induced EGFR transactivation and downstream activation of ERK5, which promotes the expansion and migration of Lrig1+ stem cells. This study demonstrates that IL-17A activates the IL-17R–EGFR axis in Lrig1+ stem cells linking wound healing to tumorigenesis.

Published
2019
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36. Inositol Pyrophosphate Profiling of Two HCT116 Cell Lines Uncovers Variation in InsP8 Levels.

Author

Gu, Chunfang, Wilson, Miranda S. C., Jessen, Henning J., Saiardi, Adolfo, and Shears, Stephen B.

Subjects
*CANCER immunology, *INOSITOL pyrophosphates, *CELL lines, *DIPLOIDY, *CYTOLOGY, *INFLAMMATION
Abstract

The HCT116 cell line, which has a pseudo-diploid karotype, is a popular model in the fields of cancer cell biology, intestinal immunity, and inflammation. In the current study, we describe two batches of diverged HCT116 cells, which we designate as HCT116NIH and HCT116UCL. Using both gel electrophoresis and HPLC, we show that HCT116UCL cells contain 6-fold higher levels of InsP8 than HCT116NIH cells. This observation is significant because InsP8 is one of a group of molecules collectively known as ‘inositol pyrophosphates’ (PP-InsPs)—highly ‘energetic’ and conserved regulators of cellular and organismal metabolism. Variability in the cellular levels of InsP8 within divergent HCT116 cell lines could have impacted the phenotypic data obtained in previous studies. This difference in InsP8 levels is more remarkable for being specific; levels of other inositol phosphates, and notably InsP6 and 5-InsP7, are very similar in both HCT116NIH and HCT116UCL lines. We also developed a new HPLC procedure to record 1-InsP7 levels directly (for the first time in any mammalian cell line); 1-InsP7 comprised <2% of total InsP7 in HCT116NIH and HCT116UCL lines. The elevated levels of InsP8 in the HCT116UCL lines were not due to an increase in expression of the PP-InsP kinases (IP6Ks and PPIP5Ks), nor to a decrease in the capacity to dephosphorylate InsP8. We discuss how the divergent PP-InsP profiles of the newly-designated HCT116NIH and HCT116UCL lines should be considered an important research opportunity: future studies using these two lines may uncover new features that regulate InsP8 turnover, and may also yield new directions for studying InsP8 function. [ABSTRACT FROM AUTHOR]

Published
2016
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37. A novel IL-17 signaling pathway controlling keratinocyte proliferation and tumorigenesis via the TRAF4–ERK5 axis

Author

Wu, Ling, Chen, Xing, Zhao, Junjie, Martin, Bradley, Zepp, Jarod A., Ko, Jennifer S., Gu, Chunfang, Cai, Gang, Ouyang, Wenjun, Sen, Ganes, Stark, George R., Su, Bing, Vines, Charlotte M., Tournier, Cathy, Hamilton, Thomas A., Vidimos, Allison, Gastman, Brian, Liu, Caini, and Li, Xiaoxia

Abstract

Although IL-17 is emerging as an important cytokine in cancer promotion and progression, the underlining molecular mechanism remains unclear. Previous studies suggest that IL-17 (IL-17A) sustains a chronic inflammatory microenvironment that favors tumor formation. Here we report a novel IL-17–mediated cascade via the IL-17R–Act1–TRAF4–MEKK3–ERK5 positive circuit that directly stimulates keratinocyte proliferation and tumor formation. Although this axis dictates the expression of target genes Steap4 (a metalloreductase for cell metabolism and proliferation) and p63 (a transcription factor for epidermal stem cell proliferation), Steap4 is required for the IL-17–induced sustained expansion of p63+ basal cells in the epidermis. P63 (a positive transcription factor for the Traf4 promoter) induces TRAF4 expression in keratinocytes. Thus, IL-17–induced Steap4-p63 expression forms a positive feedback loop through p63-mediated TRAF4 expression, driving IL-17–dependent sustained activation of the TRAF4–ERK5 axis for keratinocyte proliferation and tumor formation.

Published
2015
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38. Capillary electrophoresis mass spectrometry identifies new isomers of inositol pyrophosphates in mammalian tissues.

Author

Qiu D, Gu C, Liu G, Ritter K, Eisenbeis VB, Bittner T, Gruzdev A, Seidel L, Bengsch B, Shears SB, and Jessen HJ

Abstract

Technical challenges have to date prevented a complete profiling of the levels of myo -inositol phosphates (InsPs) and pyrophosphates (PP-InsPs) in mammalian tissues. Here, we have deployed capillary electrophoresis mass spectrometry to identify and record the levels of InsPs and PP-InsPs in several tissues obtained from wild type mice and a newly created PPIP5K2 knockout strain. We observe that the mouse colon harbours unusually high levels of InsPs and PP-InsPs. Additionally, the PP-InsP profile is considerably more complex than previously reported for animal cells: using chemically synthesized internal stable isotope references and high-resolution mass spectra, we characterize two new PP-InsP isomers as 4/6-PP-InsP 5 and 2-PP-InsP 5 . The latter has not previously been described in nature. The analysis of feces and the commercial mouse diet suggests that the latter is one potential source of noncanonical isomers in the colon. However, we also identify both molecules in the heart, indicating unknown synthesis pathways in mammals. We also demonstrate that the CE-MS method is sensitive enough to measure PP-InsPs from patient samples such as colon biopsies and peripheral blood mononuclear cells (PBMCs). Strikingly, PBMCs also contain 4/6-PP-InsP 5 and 2-PP-InsP 5 . In summary, our study substantially expands PP-InsP biology in mammals., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

Published
2022
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39. IL-17R-EGFR axis links wound healing to tumorigenesis in Lrig1 + stem cells.

Author

Chen X, Cai G, Liu C, Zhao J, Gu C, Wu L, Hamilton TA, Zhang CJ, Ko J, Zhu L, Qin J, Vidimos A, Koyfman S, Gastman BR, Jensen KB, and Li X

Subjects
Adaptor Proteins, Signal Transducing genetics, Adaptor Proteins, Signal Transducing metabolism, Animals, CSK Tyrosine-Protein Kinase, Carcinogenesis genetics, Carcinogenesis pathology, Epidermis pathology, ErbB Receptors genetics, HeLa Cells, Humans, Membrane Glycoproteins genetics, Mice, Mice, Knockout, Nerve Tissue Proteins genetics, Receptors, Interleukin-17 genetics, Stem Cells pathology, src-Family Kinases genetics, src-Family Kinases metabolism, Carcinogenesis metabolism, Epidermis metabolism, ErbB Receptors metabolism, Membrane Glycoproteins metabolism, Nerve Tissue Proteins metabolism, Receptors, Interleukin-17 metabolism, Signal Transduction, Stem Cells metabolism, Wound Healing
Abstract

Lrig1 marks a distinct population of stem cells restricted to the upper pilosebaceous unit in normal epidermis. Here we report that IL-17A-mediated activation of EGFR plays a critical role in the expansion and migration of Lrig1 + stem cells and their progenies in response to wounding, thereby promoting wound healing and skin tumorigenesis. Lrig1-specific deletion of the IL-17R adaptor Act1 or EGFR in mice impairs wound healing and reduces tumor formation. Mechanistically, IL-17R recruits EGFR for IL-17A-mediated signaling in Lrig1 + stem cells. While TRAF4, enriched in Lrig1 + stem cells, tethers IL-17RA and EGFR, Act1 recruits c-Src for IL-17A-induced EGFR transactivation and downstream activation of ERK5, which promotes the expansion and migration of Lrig1 + stem cells. This study demonstrates that IL-17A activates the IL-17R-EGFR axis in Lrig1 + stem cells linking wound healing to tumorigenesis., (© 2018 Chen et al.)

Published
2019
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