Custom Protein Expression
Functional Protein, 95% Purity
Fast turnaround (2-3 weeks)
1-10 mg from E. Coli expression
for only $1790
No outsourcing to China or India


in vitro Protein Synthesis
Full-length protein in 1 week
95% Purity, From any gene
(toxic or membrane proteins)
Isotopic Labelling for NMR

50 µg~3 mg, $390 to $2500
Excellgen

Role Of IL-6 In The Pathogenesis Of Yersinia Enterocolitica Infection

Peter H Dube, Assistant Professor
Microbiology And Immunologyuniversity Of Texas Hlth Sci Ctr San Ant

Grant 5R01AI067716-03 from National Institute Of Allergy And Infectious Diseases IRG: HIBP

Project start date: 2007-06-01

Project end date: 2012-05-31


Sponsored Links Excellgen http://Excellgen.com

Protein expression & purification: E. Coli, insect and mammalian cells
Fast turn around, 3 mg of >95% purity functional protein. No outsourcing to China or India. $2500, $1800
GeneExpresso DNA Transfection Reagent
Low Cytotoxicity, Higher Transfection Efficiency than Lipofectamine 2000. $188, $138
Functional Recombinant Proteins by in vitro Protein Synthesis, 3 days, 95% Purity
Full-length, high quality protein, high yield, high throughput, any genes (toxic, low GC content), membrane proteins, isotopic labelling. $598, $398


Grants awarded to Peter H Dube

Host Response To Yersinia Pestis Infection

Peter H Dube, Assistant Professor
Microbiology And Immunologyuniversity Of Texas Hlth Sci Ctr San Ant
san Antonio, Tx 78229

Grant 5R21AI060789-02 from National Institute Of Allergy And Infectious Diseases IRG: ZRG1

Abstract: Yersinia pestis is an incidental human pathogen that is the causative agent of plague. Historically plague has been a significant source of human morbidity and mortality. In areas where plague is endemic in rodent populations humans are still at significant risk. Plague may re-emerge as a significant danger to human health due to the recent identification of multi-drug resistant strains of Y. pestis and the possibility that Y. pestis may be used as an agent of biological terrorism. Although plague has been a major health problem for more than 1500 years, relatively nothing is known about the pathogenesis of Y. pestis infection. In particular, detailed molecular data on the host response to Y. pestis infection is lacking. This data is crucial for the development of new treatments and may significantly improve vaccine strategies. Using the mouse model of Y. enterocolitica infection combined with microarray analysis of infected tissues we have gained significant insight into the host response to the enteropathogenic Yersiniae. These studies have improved our understanding of the molecular basis of the host response to Y. enterocolitica and should serve as a template for an analysis of the host response to Y. pestis. Based on our previous investigations we hypothesize that Y. pestis infection induces the expression of genes encoding immunomodulatory proteins (cytokines, chemokines, proteases, and immune effectors) and the expression of these proteins dictates the outcome of the infection. To test these hypotheses we propose 1) A comprehensive analysis of host gene expression to Y. pestis infection 2) Analysis of the effect of defined host deficiencies on the immune response to Y. pestis infection in vivo. We will utilize microarray analysis of tissues from Y. pestis infected mice including defined (cytokines) host mutants to study the host response to plague. Additionally the roles of cytokines (TARC, TGF-beta, TNF-alpha, IL-13, IL-6, IL-10) will be examined using the mouse model of infection. These studies will improve our understanding of the host immune response to Y. pestis infection

Project start date: 2007-09-20

Project end date: 2010-08-31

5R21AI060789-02 (2008): $107420


1R21AI060789-01A2 (2007): $292000

Role Of IL-6 In The Pathogenesis Of Y.enterocolitica Infection

Peter H Dube, Assistant Professor
University Of Texas Hlth Sci Ctr San Ant San Antonio, Tx 78229

Grant 1R01AI067716-01A2 from National Institute Of Allergy And Infectious Diseases IRG: HIBP

Abstract: Food and water borne infectious diseases are a significant source of morbidity and mortality world-wide. Children are especially at risk from these infections. Although often assumed to be only a problem in developing areas of the world, bacterial infections of the gastro-intestinal tract remain a serious source of disease in the US. Our long-term goal is to understand both host-response and host pathogen interactions in the gut to Yersinia enterocolitica that lead to resolution of infection or to pathology. Y. enterocolitica is an excellent pathogen to use in our studies as it has served as one of the paradigms of bacterial infectious diseases. In this proposal we expand our studies to look at the role of IL-6 in the modulation of the host response during Y. enterocolitica infection. We hypothesize that IL-6 may be a crucial regulator of inflammatory responses to infection by influencing the cytokine response of host cells involved in response to Y. enterocolitica infection. We also hypothesize that the IL-6 mediated tempering of inflammatory responses may be triggered by Y. enterocolitica encoded molecules. To test these hypotheses we propose the following specific aims 1) Identify the cells producing IL-6 in response to Y. enterocolitica infection and 2) the cells responding to IL-6 during infection in the Peyer s patch, mesenteric lymph node, and spleen. These data will give us insight into which host cells are modulating the host response to infection. 3) Test the contribution of the IL-6 modulated cytokines to the immunopathogenesis of intestinal yersiniosis. Mice deficient in IL-6 have distinct cytokine expression profiles and many of these cytokines are critical to the resolution of disease but it is unknown how mis-regulation of these cytokines contributes to pathology. These data will explore the connection between IL-6 mediated modulation of the immune response and Yersinia virulence. Altogether, these data will give us insight into how IL-6 contributes to the pathogenesis of Yersinia infection and how immune pathologies are prevented during self limiting infections. These data may provide insight into the etiology of chronic intestinal inflammation.

Keywords: infection, role, Carnivora, Peyer s patches, Yersinia, Yersinia pestis disease, back, bacteria, cell, children, communicable disease, culture, cytokine, food, gastrointestinal disorder, immune response, immune system, immunoregulation, inflammation, insight, lead, learning, lymph node, model, pathology, plasmid, play, receptor, secretion, spleen, syndrome, thinking, virulence, water

Project start date: 2007-06-01

Project end date: 2012-05-31

1R01AI067716-01A2 (2007): $365000


ROLE OF CARDS TOXIN IN M. PNEUMONIAE ASSOCIATED ASTHMA IN MICE

Peter H Dube
University Of Texas Hlth Sci Ctr San Ant, San Antonio, Tx 78229

Grant 3U19AI070412-04S1_0007 from National Institute Of Allergy And Infectious Diseases

Keywords: Accounting; Acute; Airway Hyper-responsiveness; Allergic asthma; American; Animal Model; Animal Models and Related Studies; Animals; Assay; Asthma; BALB/c; Bacterial Infections; Bioassay; Biochemical; Biologic Assays; Biological Assay; Bronchial Asthma; Causality; Cells; Chronic; Chronic Disease; Chronic Illness; Clinical; Collaborations; Community Acquired Respiratory Distress Syndrome Toxin; Complex; Complex Mixtures; Confusion; Confusional State; Control Animal; Development; Diagnostic; Disease; Disorder; Eaton Agent; Eaton Liu agent; Economics; Ensure; Environmental Factor; Environmental Risk Factor; Etiology; Experimental Designs; Experimental Models; Experimental Models, Other; Exposure to; Extrinsic asthma; Gene Expression; Genes; Genetic; Goals; Histopathology; Human; Human, General; IMPHENO; Immune; Immune response; Immune system; Immunophenotyping; Inbred BALB C Mice; Individual; Infection; Intoxication; Investigators; Length; Link; Lung; Lung diseases; M. pneumoniae; Mammals, Mice; Mammals, Rodents; Man (Taxonomy); Man, Modern; Mediating; Mental Confusion; Method LOINC Axis 6; Methodology; Mice; Mice, Inbred BALB C; Modeling; Models, Experimental; Molecular; Molecular Genetic; Molecular Genetics; Morbidity; Morbidity - disease rate; Mortality; Mortality Vital Statistics; Mouse, BALB C; Murine; Mus; Mycoplasma pneumoniae; Ovalbumin; Pathogenesis; Pathogenicity Factors; Pathology; Phenotype; Physiologic; Physiological; Play; Pneumonia; Pneumonitis; Population; Prevalence; Protocol; Protocols documentation; Pulmonary Diseases; Pulmonary Disorder; Pulmonary Inflammation; QOL; Quality of life; Reagent; Relative; Relative (related person); Research Personnel; Research Specimen; Researchers; Respiratory Disease; Respiratory Disorder; Respiratory Infections; Respiratory System Disease; Respiratory System Disorder; Respiratory System, Lung; Respiratory Tract Infections; Rodent; Rodent Model; Rodentia; Rodentias; Role; Sampling; Scientist; Specimen; Stimulus; Subtyping, Immunologic; Subtypings, Immunologic; Symptoms; Testing; Therapeutic Intervention; Toxin; Virulence; Virulence Factors; Work; ing; airway hyper-reactivity; airway hyperreactivity; airway hyperresponsiveness; airway remodeling; atopic asthma; bacterial disease; body system, allergic/immunologic; chronic disease/disorder; chronic disorder; cytokine; disease causation; disease etiology; disease/disorder; disease/disorder etiology; disorder etiology; environmental risk; experiment; experimental research; experimental study; extrinsic allergic asthma; host response; immunophenotype; immunoresponse; in vivo; insight; intervention therapy; lung disorder; model organism; mouse model; mutant; novel; null mutation; organ system, allergic/immunologic; pulmonary; research study; response; social role

Budget start date: 12-SEP-2009

Budget end date: 31-AUG-2011

PFA/PA: RFA-AI-05-027

3U19AI070412-04S1_0007 (2009): $52008


5U19AI070412-04_0007 (2009): $190613