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1

Use of chromosome walking in discovery of single-nucleotide polymorphism in noncoding regions of a candidate actin gene in Pinus radiata

100%
Li W., Li H., Wu H., Chen X.-Y.
Journal of Applied Genetics
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2010
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vol. 51
|
issue 3
275-281
EN
Untranslated regions (UTRs) of eukaryotic mRNAs play crucial roles in post-transcriptional regulation of gene expression via the modulation of nucleocytoplasmic mRNA transport, translation efficiency, subcellular localization, and message stability. Single-nucleotide polymorphisms (SNPs) in UTRs of a candidate gene may also change the post-transcriptional regulation of a gene or function by nucleotide mutation. For species that have not been entirely sequenced genomically, new methods need to be devised to discover SNPs in noncoding regions of candidate genes. In this study, based on the expressed sequence tag (EST) of Pinus radiata (Monterey pine), we obtained all the sequences of UTRs of the actin gene by using a chromosome walking method. We also detected all the SNPs in and around the coding region of the actin gene. In this way, the full genomic sequence (2154 bp) of the actin gene was identified, including the 5'UTR, introns, the coding sequence, and the 3'UTR. PCR amplification and DNA fragment sequencing from 200 unrelated P. radiata trees revealed a total of 21 SNPs in the actin gene, of which 3 were located in the 5'UTR, 3 in the introns, 10 in the coding sequence, and 5 in the 3'UTR. We show that chromosome walking can be used for obtaining the sequence of UTRs, and then, based on this sequence, to discover SNPs in the noncoding regions of candidate genes from this species without an entire genomic sequence.
2

Current advances in the management of urticaria

100%
Khalaf A. T., Li W., Jinquan T.
Archivum Immunologiae et Therapiae Experimentalis
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2008
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vol. 56
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issue 2
103-114
EN
Urticaria is a relatively common autoimmune/autoreactive skin disorder that may severely impair quality of life. Although rarely life-threatening, widespread urticaria and its associated angioedema can be an extremely disabling and difficult-to-treat condition. Patients may suffer symptoms such as pruritus and disfigurement due to wheals for years or decades. Urticaria is caused by cutaneous mast-cell degranulation attributed to immunological, non-immunological, and idiopathic causes. The last decade has seen some notable advances in the understanding of the etiology and pathogenesis of common forms of urticaria and their management. Furthermore, the wide diversity in urticaria subtypes has been identified and this reflects a partial understanding of the causes or factors that trigger it as well as the molecular and cellular mechanisms that are involved in its physiopathology. In addition, new instruments for diagnosing urticaria variants and for assessing quality of life in urticaria patients have been developed. Finally, several clinical trials have demonstrated the efficacy of novel treatment approaches for urticaria, while other therapeutic concepts are under development. The objective of this article was to review the literature to be able to offer the readers comprehensive and updated information on the basic etiological and physiopathological mechanisms and to make special emphasis on the current management of urticaria, thus promoting continuous medical education.
3

All roads lead to Rome: pathways of NKT cells promoting asthma

100%
Jinquan T., Li W., Yuling H., Lang C.
Archivum Immunologiae et Therapiae Experimentalis
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2006
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vol. 54
|
issue 5
335-340
EN
NKT cells are the prominent manipulator in asthma development. Asthmatic NKT cells migrate from thymus, spleen, liver and bone marrow into blood vessels, and then concentrate in airway bronchi mucosa. This recruitment is dependent on high expression of CCR9 and engagement of CCL25/CCR9. NKT cells promote asthma in two different pathways. One is an indirect pathway. NKT cells contact with CD3+ T cells and induce them secreting large quantity of Th2 cytokines (IL-4, IL-13), which requires the participation of dentritic cells and the synergic signaling of CCL25/CCR9 and CD226. The other is a direct pathway. Circulating asthmatic NKT cells selectively highly express Th1 cytokines . Once reached airway epithelium, most NKT cells shift to Th2-bias, highly expressing IL-4, IL-13, but not IFN-alpha. Both pathways lead to airway hyperresponsiveness and inflammation, asthma development. Comparing to the well documented suppressive regulatory T cells, CD4+CD25+ T cells, NKT cells perform as a novel active regulator in asthma. These recent understanding of NKT cells performance in the development of asthma might unveil new therapy targets and management strategies for asthma.
4

Signal transduction in human pancreatic cancer: roles of transforming growth factor beta, somatostatin receptors, and other signal intermediates

76%
Li M., Becnel L. S., Li W., Fisher W. E., Chen C., Yao Q.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
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vol. 53
|
issue 5
381-387
EN
Pancreatic cancer is a devastating disease because of the lack of early detection markers and effective treatments. It is the fourth leading cause of cancer-related death in western countries, including the United States. The mechanisms of pancreatic cancer progression remain unknown. Transforming growth factor beta (TGF-beta), a multifunctional cytokine, regulates cell growth and differentiation in healthy tissues, yet fails to do so in pancreatic cancer. Alterations of the TGF-beta and TGF-beta receptor/Smad signal transduction pathway have been implicated in pancreatic cancer. Furthermore, both the TGF-beta receptor and Smad proteins interact with a variety of cellular signal pathways, such as the somatostatin receptors (SSTRs), ERK1/2, and Wnt signal transduction cascades. This suggests that pancreatic cancer is a multi-gene-controlled malignancy and that effective treatments for pancreatic cancer should be aimed at multiple targets. In this review, we summarized the major signal intermediates involved in pancreatic cancer signal transduction pathways and specifically discussed how alterations in the regulatory functions of TGF-beta and Smad proteins allow for pancreatic carcinogenesis.
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