1998 — 2000 |
Singer, Cherie |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Il1 Beta and Map Kinase Mediated Airway Responses @ University of Nevada Reno
mitogen activated protein kinase; respiratory muscles; smooth muscle; interleukin 1; asthma; enzyme activity; muscle contraction; gene induction /repression; cell migration; inflammation; immunogenetics; muscle cells; stress proteins; animal genetic material tag; immunocytochemistry; dogs; tissue /cell culture;
|
0.915 |
2005 — 2008 |
Singer, Cherie |
K01Activity Code Description: For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Interferon Regulation of T-Bet in Airway Smooth Muscle @ University of Nevada Reno
DESCRIPTION (provided by applicant): A Mentored Career Development Award will allow me to become an innovative, recognized investigator and instructor by expanding my research skills, enhancing my ideas for my own research program in airway smooth muscle biology, and providing me with opportunities to continue to develop expertise in teaching through the outlined career development and research plans. I believe that my previous training and research experience at both large and small universities has given me an excellent foundation in which to begin an independent research career. As a graduate student, I endured a rigorous program of study that emphasized critical and analytical thinking, oral communication and presentation skills, and research excellence in the neurosciences. As a post-doctoral fellow, I developed an interest in the role of airway smooth muscle (ASM) in inflammatory events that contribute to airway diseases and took advantage of opportunities to gain teaching experience. I continue my interest in airway smooth muscle biology with this proposal by examining the T-box transcription factor T-bet in ASM. The proposed career development plan will facilitate my goals through intellectual interactions with colleagues, students and my mentor, Dr. William T. Gerthoffer, along with participation in structured activities including University service, attendance at scientific meetings, and involvement in teaching, career development and laboratory management workshops and seminars. The research project described here examines the hypothesis that ASM expression of T-bet participates in the development of a secretory smooth muscle cell phenotype that affects the inflammatory response by increasing T helper cell 1 (Th1) cytokine secretion. The experiments described will examine IFNgamma regulation of T-bet expression in ASM, determine whether T-bet expression contributes to the development of a secretory smooth muscle cell phenotype by upregulating Th1 cytokines, and addresses whether T-bet alters the functions of ASM cells such as proliferation, migration and contraction. There are few places that I would have the opportunity to interact with faculty that are as recognized for their expertise in smooth muscle cell biology than at the University of Nevada School of Medicine. This award will allow me to begin to ask novel questions about the secretory phenotype of ASM in this supportive research environment that is committed to furthering junior faculty development.
|
0.915 |
2008 — 2009 |
Singer, Cherie |
P20Activity Code Description: To support planning for new programs, expansion or modification of existing resources, and feasibility studies to explore various approaches to the development of interdisciplinary programs that offer potential solutions to problems of special significance to the mission of the NIH. These exploratory studies may lead to specialized or comprehensive centers. |
Cobre: Unr: Molecular Biology Core (B) @ University of Nevada Reno
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Core B is the Molecular Biology Core. This core will serve all of the cobre projects by providing general cloning and expression of recombinant proteins, recombinant adenovirus production, Southern, Northern and Western analysis. In addition, Core B will design primers and probes for real-time PCR and DNA seqeuence analysis along with co-immunoprecipitation assay development. In addition, this core will perform all preparative work required by the COBRE projects for the subsequent analysis and identification of proteins and protein profiling. The University of Nevada has a well-established proteomics facility, the Nevada Proteomics Center, that can adequately perform all the necessary protein analysis such as protein mass and sequence determination.
|
0.915 |
2016 — 2019 |
Singer, Cherie |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Microrna-25 Attenuates Allergic Inflammation by Altering Airway Smooth Muscle Phenotype and Function @ University of Nevada Reno
? DESCRIPTION (provided by applicant): In vitro studies have established that airway smooth muscle (ASM) cells exhibit phenotypic plasticity in response to inflammatory events mediated by transcriptional and post-transcriptional mechanisms that have not been fully elucidated. microRNA (miRNA)-mediated gene silencing has emerged as an regulator of gene expression and studies of miRNA function in ASM hold promise for the development of novel miRNA-based tools for prognosis and therapy. The long-term goal of our studies is to identify the miRNA-mediated gene- silencing mechanisms determining ASM cell phenotype in asthma. Our laboratory was the first to characterize miRNA expression in ASM following a pro-inflammatory stimulus and identified miR-25 as a target of the inflammatory response that regulates plasticity of ASM cells. This proposal will test the hypothesis that expression of miR-25 attenuates allergic asthma pathogenesis by altering ASM phenotype. In Specific Aim 1, we will determine whether miR-25 expression in a mouse model of allergic inflammation attenuates hyperreactivity, remodeling and alters ASM contractile force using a unique transgenic mouse model of smooth muscle-targeted miR-25 expression. These mice will be used to assess the effects of miR-25 on AHR, remodeling and ASM contractility following acute and chronic models of ovalbumin-sensitization and challenge. In Specific Aim 2, we will study the effect of smooth muscle-targeted miR-25 expression on increased ASM mass in vivo following acute and chronic ovalbumin-sensitization and challenge by assessing proliferative markers and mitogenic signaling pathways to address the molecular mechanisms underlying this miR-25 function. In Specific Aim 3, we will determine whether miR-25 affects the phenotype of asthmatic ASM cells using gain and loss of miR-25 function studies, as well as effects on identified targets of miR-25 mediated gene-silencing. This unique experimental approach, coupled with correlations in human diseased cells, will provide mechanistic data describing miR-25 function in the lung and be an essential step towards developing novel therapeutic strategies targeting miRNA in asthma.
|
0.915 |