@article{wang_2015, title={Single cell sequencing and systems immunology preface}, journal={Single cell sequencing and systems immunology}, author={Wang, X. D.}, year={2015}, pages={V-} }
 @article{wang_sistrunk_marval_kim_rodriguez-puebla_2012, title={Combined effect of cyclin D3 expression and abrogation of cyclin D1 prevent mouse skin tumor development}, volume={11}, ISSN={["1551-4005"]}, DOI={10.4161/cc.11.2.18774}, abstractNote={We have previously demonstrated that ras-mediated skin tumorigenesis depends on signaling pathways that act preferentially through cyclin D1 and D2. Interestingly, the expression of cyclin D3 inhibits skin tumor development, an observation that conflicts with the oncogenic role of D-type cyclins in the mouse epidermis. Here, we show that simultaneous up and downregulation of particular members of the D-type cyclin family is a valuable approach to reduce skin tumorigenesis. We developed the K5D3/cyclin D1-/- compound mouse, which overexpresses cyclin D3 but lacks expression of cyclin D1 in the skin. Similar to K5D3 transgenic mice, keratinocytes from K5D3/cyclin D1-/- compound mice show a significant reduction of cyclin D2 levels. Therefore, this model allows us to determine the effect of cyclin D3 expression when combined with reduced or absent expression of the remaining two members of the D-type cyclin family in mouse epidermis. Our data show that induced expression of cyclin D3 compensates for the reduced level of cyclin D1 and D2, resulting in normal keratinocyte proliferation. However, simultaneous ablation of cyclin D1 and downregulation of cyclin D2 via cyclin D3 expression resulted in a robust reduction in ras-mediated skin tumorigenesis. We conclude that modulation of the levels of particular members of the D-type cyclin family could be useful to inhibit tumor development and, in particular, ras-mediated tumorigenesis.}, number={2}, journal={CELL CYCLE}, author={Wang, Xian and Sistrunk, Christopher and Marval, Paula L. Miliani and Kim, Yongbaek and Rodriguez-Puebla, Marcelo L.}, year={2012}, month={Jan}, pages={335–342} }
 @article{wang_adler_2008, title={Epithelial brush border proteomics and associated dysfunction.}, volume={1}, journal={404nOtfound}, author={Wang, X. and Adler, K. B.}, year={2008}, pages={27–33} }
 @misc{wang_bai_li_adler_wang_2008, title={Role of airway epithelial cells in development of asthma and allergic rhinitis}, volume={102}, ISSN={["0954-6111"]}, DOI={10.1016/j.rmed.2008.01.017}, abstractNote={Asthma and allergic rhinitis frequently coexist in the same patient. There is a similarity and variation as well as potential relationship between asthma and allergic rhinitis. There is an increasing evidence to suggest a major involvement of airway epithelial cells in the pathogenesis of asthma and allergic rhinitis. The present review describes the importance of the airway epithelial cell in the development of allergic airway diseases, its role as the primary airway defense against exposure of the airway and lung to inflammatory stimuli and antigens and as an important player through activation of epithelial Toll-like receptors (TLRs) to provide an important link between innate immunity and allergic disease. Additionally, airway epithelial cells can act as inflammatory promoters capable of directing dendritic cells (DCs) towards a T helper 2 (Th2) response, and as active producers of several inflammatory/anti-inflammatory mediators. It is hypothesized that airway epithelial cells may play as both inflammatory initiator and immuno-pathological feedback regulation between allergic rhinitis and asthma via release of systemic inflammatory mediators. Thus, airway epithelial cells may be valuable therapeutic targets for discovery and development of new drugs and/or new therapeutic strategies to treat asthma and allergic rhinitis.}, number={7}, journal={RESPIRATORY MEDICINE}, author={Wang, YaoLi and Bai, Chunxue and Li, Ka and Adler, Kenneth B. and Wang, Xiangdong}, year={2008}, month={Jul}, pages={949–955} }
 @article{wang_2007, title={Proteomics in the study of organ dysfunction}, volume={4}, number={1}, journal={Expert Review of Proteomics}, author={Wang, X. D.}, year={2007}, pages={1–3} }
 @article{wang_adler_erjefalt_bai_2007, title={Role of airway epithelial dysfunction in development of acute lung injury and acute respiratory distress syndrome.}, volume={1}, DOI={10.1586/17476348.1.1.149}, abstractNote={Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are common and important stages of both pulmonary and systemic critical illnesses. ALI/ARDS is categorized as primary or secondary based on the etiology of the disease. There is increasing evidence to suggest the involvement of airway epithelial cells in the pathogenesis of ALI/ARDS. The airway epithelial cell is a new candidate as a biological target responsible for development of the disease and the role of these cells in the pathogenesis of ALI/ARDS is under investigation. This review describes the importance of the airway epithelial cell in the development of ALI/ARDS, its role as the first line of lung defense facing local and primary challenges, its role as an important player in the development of airway inflammation and remodeling, as an inflammatory promoter for initiating both local and systemic inflammation and as an active producer of several inflammatory and anti-inflammatory mediators. It is hypothesized that airway epithelial cells may contribute to ALI/ARDS via Toll-like receptor-involved mediators, reactive oxygen species-involved reactions and an imbalance between protease and antiprotease activation. The airway epithelial cell may be a valuable therapeutic target for discovering and developing new drugs and/or new therapeutic strategies for ALI/ARDS.}, journal={404nOtfound}, author={Wang, X. and Adler, K. B. and Erjefalt, J. and Bai, C.}, year={2007}, pages={149–155} }
 @misc{zhao_adler_bai_tang_wang_2006, title={Epithelial proteomics in multiple organs and tissues: Similarities and variations between cells, organs, and diseases}, volume={5}, ISSN={["1535-3907"]}, DOI={10.1021/pr050389v}, abstractNote={Epithelial cells play an important role in physiological and pathophysiological situations, with organ-, tissue-, type-, and function-specific patterns. Proteome analysis has been used to study epithelial-origin diseases and identify novel prognostic, diagnostic, and therapeutic markers. The present review compares the variation of sample preparation for epithelial proteomic analysis, search similarities, and differences of epithelial proteomics between different cells, locations, and diseases. We focus on specificity of proteomic markers for epithelial-involved diseases. Proteomic alterations in epithelial cell lines were mapped to understand protein patterns, differentiation, oncogenesis, and pathogenesis of epithelial-origin diseases. Changes of proteomic patterns depend on different epithelial cell lines, challenges, and preparation. Epithelial protein profiles associated with intracellular locations and protein function. Epithelial proteomics has been greatly developed to link clinical questions, e.g., disease severity, biomarkers for disease diagnosis, and drug targets. There is an exciting and attractive start to link epithelial proteomics with histology of clinical samples. From the present review, we can find that most of disease-associated investigation of epithelial proteomics has been focused on epithelial-origin cancer. There is a significant gap of epithelial proteomics between acute and chronic organ injury, inflammation, and multiple organ dysfunction. Epithelial proteomics will provide powerful information on the relationships between biological molecules and disease mechanisms. Epithelial proteomics strategies and approaches should become more global, multidimensional, and systemic.}, number={4}, journal={JOURNAL OF PROTEOME RESEARCH}, author={Zhao, H and Adler, KB and Bai, CX and Tang, FD and Wang, XD}, year={2006}, month={Apr}, pages={743–755} }