A5048235777- Blood disorders and treatments
- Acute Myeloid Leukemia Research
- RNA modifications and cancer
- Immunodeficiency and Autoimmune Disorders
- RNA Research and Splicing
- DNA Repair Mechanisms
- Immune Cell Function and Interaction
- Microtubule and mitosis dynamics
- Glycosylation and Glycoproteins Research
- Cancer-related Molecular Pathways
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- T-cell and B-cell Immunology
- Cancer-related gene regulation
- Immune Response and Inflammation
- Erythrocyte Function and Pathophysiology
- Acute Lymphoblastic Leukemia research
- Ubiquitin and proteasome pathways
- Peptidase Inhibition and Analysis
- Cancer Mechanisms and Therapy
- RNA Interference and Gene Delivery
- interferon and immune responses
- Epigenetics and DNA Methylation
- Lymphoma Diagnosis and Treatment
- Blood groups and transfusion
- Monoclonal and Polyclonal Antibodies Research
Université de Montréal
2015-2024
McGill University
2015-2024
Montreal Clinical Research Institute
2015-2024
Düsseldorf University Hospital
2016
Heinrich Heine University Düsseldorf
2016
Essen University Hospital
2001-2013
University of Duisburg-Essen
2003-2010
Institut für Medizinische Informatik, Biometrie und Epidemiologie
1999-2010
Goethe University Frankfurt
2008
In-Q-Tel
2006
Pou4f3 (Brn3.1, Brn3c) is a class IV POU domain transcription factor that has central function in the development of all hair cells human and mouse inner ear sensory epithelia. A mutation POU4F3 underlies autosomal dominant non-syndromic progressive hearing loss DFNA15. Through comparison gene expression profiles E16.5 wild-type mutant deaf mice using high density oligonucleotide microarray, we identified encoding growth independence 1 ( Gfi1 ) as likely vivo target regulated by Pou4f3. To...
In the thymus, several steps of proliferative expansion and selection coordinate maturation precursors into antigen-specific T cells. Here we identify transcriptional repressor Gfi1 as an important regulator this process. Mice lacking show reduced thymic cellularity due to increased cell death rate, lack proliferation, a differentiation block in very early uncommitted CD4−/CD8−/c-Kit+ cytokine-dependent progenitors that have not yet initiated VDJ recombination. addition, Gfi1-deficient mice...
The Pim-1 oncogene encodes a serine-threonine kinase that relays signals from cytokine receptors and contributes to the formation of lymphoid tumors when expressed at high levels. Here we show protein Cdc25 C-associated 1 (C-TAK1) is binding partner substrate Pim-1. A physical interaction C-TAK1 could be shown biochemically in yeast two-hybrid assays. Immunofluorescence experiments suggested Pim-1.C-TAK1 complexes are predominantly cytoplasmic. When transiently transfected, was also found...
Transgenic mice expressing the Pim-1 kinase are predisposed to develop T-cell lymphomas with a long latency period of about 7-9 months. However, exact functional basis oncogenic activity remains obscure. C57BL/6 homozygous for lpr mutation well-described lymphoproliferative syndrome at 26-30 weeks age. This is characterized mainly by accumulation abnormal T cells in lymph nodes because lack Fas receptor-induced apoptosis. We find that backcross E mu-Pim-1 transgenics (mice transgene carries...
The Myc protein suppresses the transcription of several cyclin-dependent kinase inhibitors (CKIs) via binding to Miz1; whether this interaction is important for Myc's ability induce or maintain tumorigenesis not known. Here we show that oncogenic potential a point mutant (MycV394D) selectively deficient in Miz1 greatly attenuated. Binding continuously required repress CKI expression and inhibit accumulation trimethylated histone H3 at Lys 9 (H3K9triMe), hallmark cellular senescence, T-cell...