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177 results on '"Lu, Qingxian"'

14. Additional file 1 of Characterization and clinical evaluation of microsatellite instability and loss of heterozygosity within tumor-related genes in colorectal cancer

Author

Huo, Xueyun, Feng, Dandan, Zhang, Shuangyue, Li, Zhenkun, Li, Xiaohong, Li, Changlong, Guo, Meng, Wang, Jin, Zhang, Zhongtao, Lu, Qingxian, Du, Xiaoyan, Bai, Zhigang, and Chen, Zhenwen

Subjects
Data_FILES
Abstract

Additional file 1. Tables for the additional informations and analysis.

Published
2021
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16. Enhanced NF-[kappa]B activation and cellular function in macrophages lacking l[kappa]B kinase 1 (IKK1)

Author

Li, Qiutang, Lu, Qingxian, Bottero, Virginie, Estepa, Gabriela, Morrison, Lisa, Mercurio, Frank, and Verma, Inder M.

Subjects
Autoimmunity -- Research, Macrophages -- Research, Protein kinases -- Research, Science and technology
Abstract

I[kappa]B kinase (IKK) complex plays a key regulatory role in macrophages for NF-[kappa]B activation during both innate and adaptive immune responses. Because [IKK1.sup.-/-] mice died at birth, we differentiated functional macrophages from embryonic day 15.5 IKK1 mutant embryonic liver. The embryonic liver-derived macrophage (ELDM) showed enhanced phagocytotic clearance of bacteria, more efficient antigen-presenting capacity, elevated secretion of several key proinflammatory cytokines and chemokines, and known NF[kappa]B target genes. Increased NF[kappa]B activity in IKK1 mutant ELDM was the result of prolonged degradation of I[kappa]B[alpha] in response to infectious pathogens. The delayed restoration of I[kappa]B[alpha] in pathogen-activated [IKK1.sup.-/-] ELDM was a direct consequence of uncontrolled IKK2 kinase activity. We hypothesize that IKK1 plays a checkpoint role in the proper control of IKBa kinase activity in innate and adaptive immunity. I[kappa]B[alpha] | LPS

Published
2005

20. Characterization and clinical evaluation of microsatellite instability and loss of heterozygosity within tumor-related genes in colorectal cancer

Author

Huo, Xueyun, primary, Feng, Dandan, additional, Zhang, Shuangyue, additional, Li, Zhenkun, additional, Li, Xiaohong, additional, Li, Changlong, additional, Guo, Meng, additional, Wang, Jin, additional, Zhang, Zhongtao, additional, Lu, Qingxian, additional, Du, Xiaoyan, additional, Bai, Zhigang, additional, and Chen, Zhenwen, additional

Published
2019
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21. IKK1-deficient mice exhibit abnormal development of skin and skeleton

Author

Li, Qiutang, Hwang, Jason Y., Buscher, Dirk, Lee, Kuo-Fen, Izpisua-Belmonte, Juan Carlos, Verma, Inder M., and Lu, Qingxian

Subjects
Genetic research -- Research, Mice, mutant strains -- Usage, Protein kinases -- Research, Skin -- Genetic aspects, Skeleton -- Genetic aspects, Extremities (Anatomy) -- Genetic aspects, Biological models -- Usage, Biological sciences
Abstract

IKK1-deficient mice have abnormal development of skeleton and skin. The mutant mice, which are perinatally lethal and have a wide variety of developmental defects, were generated to examine in vivo functions of IKK1. It appears from the results that IKK1 has a role in NF-kappaB activation and is involved in development of skeleton and skin. Two related kinases seem to have distinct functions and cannot be substituted for one another.

Published
1999

22. Tyro-3 family receptors are essential regulators of mammalian spermatogenesis

Author

Lu, Qingxian, Gore, Martin, Zhang, Qing, Camenish, Todd, Boast, Sharon, Casagranda, Franca, Lai, Cary, Skinner, Michael K., Klein, Rudiger, Matsushima, Glenn K., Earp, H. Shelton, Goff, Stephen P., and Lemke, Greg

Subjects
Sertoli cells -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The receptor protein-tyrosine kinases of the mammalian Tyro 3 family and their ligands are vital regulators of Sertoli-cell function. These receptors have been shown to act additively or in combination. It is possible that their combined activation in Sertoli cells is needed for the production of the germ-cell trophins that these cells must produce. The actual ligands for Tyro 3 family receptors could be hybrid molecules of Gas6 or protein S bound to testosterone or, in other cells, other steroids.

Published
1999

25. Targeted mutation in beta1,4-galactosyltransferase leads to pituitary insufficiency and neonatal lethality

Author

Lu, Qingxian, Hasty, Paul, and Shur, Barry D.

Subjects
Mutation (Biology) -- Physiological aspects, Pituitary gland -- Physiological aspects, Mice -- Genetic aspects, Biological sciences
Abstract

Despite much attention, the function of oligosaccharide chains on glycoproteins and glycolipids remains largely unknown. Our understanding of oligosaccharide function in vivo has been limited to the use of reagents and targeted mutations that eliminate entire classes of oligosaccharide chains. However, most biological functions for oligosaccharides have been attributed to specific terminal sequences on these glycoside chains; yet, there have been few studies that examine the consequences of modifying terminal oligosaccharide structures in vivo. To address this issue, mice were created bearing a targeted mutation in[Beta]1,4-galactosyltransferase (GalTase), an enzyme responsible for elaboration of many of the proposed biologically active carbohydrate epitopes. Most GalTase-null mice died within the first few weeks after birth and were characterized by stunted growth, thin skin, sparse hair, and dehydration. In addition, spermatogenesis was delayed, the lungs were poorly developed, and the adrenal cortices were poorly stratified. The few surviving adults had puffy skin (myxedema) and difficulty delivering pups at birth (dystocia) and failed to lactate (agalactosis). All of these defects are consistent with endocrine insufficiency, which was confirmed by markedly decreased levels of serum thyroxine. The polyglandular nature of the endocrine insufficiency is indicative of a failure of the anterior pituitary gland to stimulate the target endocrine organs. Previous in vitro studies have suggested that incomplete glycosylation of anterior pituitary hormones leads to the creation of hormone antagonists, which down-regulate subsequent endocrine function, producing polyglandular endocrine insufficiency. In GalTase-null mice, the anterior pituitary acquired a normal secretory phenotype during neonatal development indicative of normal glycoprotein hormone synthesis and secretion. However, as expected, the gland was devoid of GalTase activity. These results support a requirement for terminal oligosaccharide sequences for anterior pituitary hormone function. The fact that [approximately]10% of the GalTase-null mice survive the neonatal period indicates the presence of a previously unrecognized compensatory pathway for glycoprotein hormone glycosylation and/or action.

Published
1997

28. Metabolic Deregulation of the Blood-Outer Retinal Barrier in Retinitis Pigmentosa

Author

Wang, Wei, primary, Kini, Ashwini, additional, Wang, Yekai, additional, Liu, Tingting, additional, Chen, Yao, additional, Vukmanic, Eric, additional, Emery, Douglas, additional, Liu, Yongqing, additional, Lu, Xiaoqin, additional, Jin, Lei, additional, Lee, San Joon, additional, Scott, Patrick, additional, Liu, Xiao, additional, Dean, Kevin, additional, Lu, Qingxian, additional, Fortuny, Enzo, additional, James, Robert, additional, Kaplan, Henry J., additional, Du, Jianhai, additional, and Dean, Douglas C., additional

Published
2019
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30. Repression of Zeb1 and Hypoxia Cause Sequential MET and Induction of Aid, Oct4, and Dnmt1, Leading to Immortalization and Multipotential Reprogramming of Fibroblasts in Spheres

Author

Liu, Yongqing, Mukhopadhyay, Partha, Pisano, M. Michele, Lu, Xiaoqin, Huang, Li, Lu, Qingxian, and Dean, Douglas C.

Subjects
DNA (Cytosine-5-)-Methyltransferase 1, Homeodomain Proteins, Epithelial-Mesenchymal Transition, Multipotent Stem Cells, Stem Cells, Kruppel-Like Transcription Factors, Zinc Finger E-box-Binding Homeobox 1, Cell Differentiation, DNA Methylation, Fibroblasts, Hypoxia-Inducible Factor 1, alpha Subunit, Article, Cell Hypoxia, Mice, Cytidine Deaminase, Gene Knockdown Techniques, embryonic structures, Animals, DNA (Cytosine-5-)-Methyltransferases, Promoter Regions, Genetic, Transcriptome, Octamer Transcription Factor-3, Cells, Cultured
Abstract

In this study, we demonstrate that sphere formation triggers immortalization and stable reprogramming of mouse fibroblasts. Cell contact signaling in spheres causes downregulation of the epithelial-to-mesenchymal transition transcription factor Zeb1 leading to rapid mesenchymal-to-epithelial transition. Hypoxia within spheres together with loss of Zeb1 repression synergize to cause superinduction of Hif1a, which in turn leads to induction of the DNA demethylase Aid/Aicda, demethylation of the Oct4 promoter/enhancer and multipotency. Oct4 and Nanog expression diminish when cells are removed from the hypoxic environment of spheres and placed in monolayer culture, but the cells retain multipotential capacity, demonstrating stable reprogramming and a gene expression pattern resembling adult stem cells. Oct4 has been shown to induce Dnmt1 in mesenchymal stem cells, and we link Oct4 and Dnmt1 to silencing of cell cycle inhibitory cyclin dependent kinase inhibitors and Arf, and immortalization of the reprogrammed fibroblasts. Sphere formation then represents a novel and rapid protocol for immortalization and stable reprogramming of fibroblasts to multipotency that does not require exogenous expression of a stem cell factor or a lineage-specifying transcription factor.

Published
2013

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