A5013327454- Cell death mechanisms and regulation
- Mitochondrial Function and Pathology
- Acute Myeloid Leukemia Research
- DNA Repair Mechanisms
- Phagocytosis and Immune Regulation
- RNA Interference and Gene Delivery
- interferon and immune responses
- Plant Molecular Biology Research
- Cancer-related Molecular Pathways
- Retinoids in leukemia and cellular processes
- Genetic Associations and Epidemiology
- Immunotherapy and Immune Responses
- Reproductive Biology and Fertility
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- CAR-T cell therapy research
- Carcinogens and Genotoxicity Assessment
- Immune Response and Inflammation
- Plant tissue culture and regeneration
- Plant Genetic and Mutation Studies
- Bacterial Genetics and Biotechnology
- RNA and protein synthesis mechanisms
- Bioinformatics and Genomic Networks
- Trace Elements in Health
- Gene expression and cancer classification
- Metabolism and Genetic Disorders
Vanderbilt University Medical Center
2013-2024
Vanderbilt University
2011-2024
Vanderbilt-Ingram Cancer Center
2012-2017
Harvard University
1991-2005
Howard Hughes Medical Institute
1994-2005
Dana-Farber Cancer Institute
1991-2005
Dana-Farber/Boston Children's Cancer and Blood Disorders Center
2003
Boston Children's Hospital
2003
Massachusetts General Hospital
2001
University of Chicago
1994-1997
Mitochondria and cytochrome c release play a role in the death of neurons glia after cerebral ischemia. In present study, we investigated whether BID, proapoptotic promoter caspase 8 substrate, was expressed brain, activated an ischemic insult vivo vitro , contributed to cell death. We detected BID cytosol mouse brain primary cultured demonstrated, by using recombinant 8, that neuronal also is substrate. After 2 h oxygen/glucose deprivation, cleavage concurrent with activation but before 3...
The proper expansion and contraction of hematopoietic cells requires tight regulation cell death. BID, a “BH3-only” molecule, amplifies death receptor signals connecting the extrinsic to intrinsic pathways by triggering mitochondrial pathway apoptosis. Bid -deficient mice, as they age, spontaneously develop myeloproliferative disorder, which progresses from myeloid hyperplasia fatal, clonal malignancy closely resembling chronic myelomonocytic leukemia (CMML). Thus, an apoptotic defect can...
Keratinocytes are potentially appealing vehicles for the delivery of secreted gene products because they can be transferred to human skin by relatively simple procedure grafting. Adult keratinocytes efficiently propagated in culture with sufficient proliferative capacity produce enough epidermis cover body surface an average adult. However, feasibility delivering proteins through grafting rests upon ( i ) strength promoter and ii efficiency protein transport basement membrane stratified...
We describe a method to determine the magnitude of protein-induced DNA bends relative set standard A tract using comparative gel electrophoresis. The bend interest was that induced by catabolite activator protein (CAP), transcriptional lac operon. comparison molecules contained both known and bound CAP. electrophoretic influence accounted for placing its binding site at end molecule where has little influence. Standard center were introduced incorporating 3-9 A6 tracts approximately 10.5...
We describe experiments that enable us to track the presence and direction of DNA bend induced by Escherichia coli catabolite activator protein (CAP) through intermediate stages transcription initiation at lac promoter. Transcriptional complexes examined were formed on superhelical templates enhance specific complex formation, detected electrophoretic analysis after restriction digestion. found is maintained even increased upon formation closed open complexes. Our results exclude hypothesis...
Reovirus infection leads to apoptosis in both cultured cells and the murine central nervous system (CNS). NF-κB-driven transcription of proapoptotic cellular genes is required for effector phase apoptotic response. Although extrinsic death-receptor signaling pathways intrinsic involving mitochondrial injury are implicated reovirus-induced apoptosis, mechanisms by which either these activated their relationship NF-κB following reovirus unknown. The Bcl-2 family member, Bid, proteolytic...
Proapoptotic BH3-interacting death domain agonist (BID) regulates apoptosis and the DNA damage response. Following replicative stress, BID associates with proteins of sensor complex, including replication protein A (RPA), ataxia telangiectasia Rad3 related (ATR), ATR-interacting (ATRIP), facilitates an efficient We have found that stimulates association RPA components complex through interaction basic cleft N-terminal RPA70 subunit. Disruption BID-RPA impairs ATR-ATRIP chromatin as well ATR...
<h3>Objective</h3> The myeloid translocation genes (MTGs) are transcriptional corepressors with both <i>Mtg8<sup>−/−</sup></i> and <i>Mtgr1<sup>−/−</sup></i> mice showing developmental and/or differentiation defects in the intestine. We sought to determine role of MTG16 intestinal integrity. <h3>Methods</h3> Baseline stress induced colonic phenotypes were examined <i>Mtg16<sup>−/−</sup></i> mice. To unmask phenotypes, we treated dextran sodium sulphate (DSS) or infected them <i>Citrobacter...
Bcl-2 family proteins reorganize mitochondrial membranes during apoptosis, to form pores and rearrange cristae. In vitro in vivo analysis integrated with human genetics reveals a novel homeostatic function for protein Bid. Loss of full-length Bid results apoptosis-independent, irregular cristae decreased respiration. Bid-/- mice display stress-induced myocardial dysfunction damage. A gene-based approach applied biobank, validated two independent GWAS studies, that genetically determined BID...
Summary In aged mice, new B‐cell development is diminished and the antibody repertoire becomes more autoreactive. Our studies suggest that (i) apoptosis contributes to reduced B lymphopoiesis in old age preferentially eliminates those precursors with higher levels of surrogate light chain (SLC) proteins (λ5/VpreB) (ii) λ5 low generate cells which show increased reactivity self‐antigen/bacterial antigen phosphorylcholine (PC). Pro‐B bone marrow as well pro‐B from young adult λ5‐deficient mice...
Mitochondrial mechanisms, particularly the release of cytochrome c, play a role in death nerve and glial cells cerebral ischemia. We have currently investigated whether BID, proapoptotic molecule bcl-2 family promoter c is expressed brain, activated by ischemia vivo, contributes to ischemic cell death. found BID cytosol mouse brain primary cultured neurons showed that neuronal substrate for caspase 8. was cleaved vivo 4 h after transitory occlusion middle artery. Further,...
We have employed transient expression assays to analyze the sequences that direct c-mos transcription in mouse oocytes. Plasmids containing chloramphenicol acetyltransferase (CAT) gene fused either a 2.4-kb or 731-bp fragment from 5'-flanking region of produced similar levels CAT activity when injected into nuclei growing BAL 31 deletions revealed up 20 bp upstream major start site could be removed without any significant loss activity. Promoter only decreased these closely approached site,...