A5035075796- RNA Research and Splicing
- DNA Repair Mechanisms
- RNA and protein synthesis mechanisms
- Telomeres, Telomerase, and Senescence
- Photosynthetic Processes and Mechanisms
- RNA modifications and cancer
- Chemical Synthesis and Analysis
- Protein Structure and Dynamics
- Cancer-related Molecular Pathways
- Microtubule and mitosis dynamics
- Mitochondrial Function and Pathology
- Advanced Proteomics Techniques and Applications
- Modular Robots and Swarm Intelligence
- Ubiquitin and proteasome pathways
- Metabolism and Genetic Disorders
- Cancer Treatment and Pharmacology
- PI3K/AKT/mTOR signaling in cancer
- Viral Infections and Immunology Research
- PARP inhibition in cancer therapy
- Enzyme Structure and Function
- Epigenetics and DNA Methylation
- Antioxidant Activity and Oxidative Stress
- Monoclonal and Polyclonal Antibodies Research
- Hippo pathway signaling and YAP/TAZ
- Biotin and Related Studies
Massachusetts Institute of Technology
2007-2023
Washington State Department of Agriculture
2013
Center for Cancer Research
2007-2009
Center for Environmental Health
2007
University of Oregon
2002-2005
Howard Hughes Medical Institute
2000
Montana State University
1992-1993
National Institute of Allergy and Infectious Diseases
1993
DNA damage checkpoints arrest cell cycle progression to facilitate repair. The ability survive genotoxic insults depends not only on the initiation of but also checkpoint maintenance. While activation has been studied extensively, molecular mechanisms involved in sustaining and ultimately inactivating are largely unknown. Here, we explored feedback that control maintenance termination function by computationally identifying an evolutionary conserved mitotic phosphorylation network within...
In response to DNA damage, cells arrest at specific stages in the cell cycle. This must fulfill least 3 requirements: it be activated promptly; sustained as long damage is present prevent loss of genomic information; and after arrest, re-enter into appropriate cycle phase ensure proper ploidy. Multiple molecular mechanisms capable arresting have been identified mammalian cells; however, unknown whether each mechanism meets all requirements or they act together confer functions arrest. To...
Summary The heat‐shock proteins DnaJ, DnaK, and GrpE are involved in the replication of various species DNA Escherichia coli , addition to their roles other processes, including protein disaggregation export. We have cloned Borrelia burgdorferi homologues these genes. sequence analysis revealed an open reading frame encoding a that is 62% identical E. DnaK protein. Genes homologous grpE dnaJ genes, products 28% 39% homologues, located up‐ downstream, respectively, B. dnaK gene. No obvious...
CRS2-associated factors 1 and 2 (CAF1 CAF2) are closely related proteins that function in concert with chloroplast RNA splicing (CRS2) to promote the of specific sets group II introns maize chloroplasts. The CRS2-CAF complexes bind tightly their cognate vivo, CAF subunit determining intron specificity complex. In this work we show stable absence targets CRS2 binds a 22 amino acid motif COOH-terminal region CAF2 is conserved CAF1. Yeast two-hybrid assays co-fractionation studies using...
It is not easy to find candidate sites within a given protein where the geometry of polypeptide chain matches that metal-binding in known structures. By choosing location T4 lysozyme inherently flexible, it was possible engineer two-histidine site binds different divalent cations. Crystallographic analysis shows binding zinc distorted tetrahedral while cobalt and nickel octahedral. Insofar as spectroscopic data can be measured, they indicate similar modes coordination are retained solution....
Abstract Peptide 11, CDPGYIGSR-NH2, is a segment of laminin which blocks tumor cell invasion. A high affinity receptor in cells thought to be blocked by the carboxyl-terminal YIGSR, and conformational energy calculations suggest that glycine YIGSR allows an important bend. We replaced residue peptide 11 with either D-alanine or L-alanine allow disfavor proposed found Gly7-->D-Ala7 analog equal inhibiting invasion basement membrane matrix. The Gly7-->L-Ala7 was much less capable inhibition....
Abstract NOTE: This abstract was not presented at the conference. The DNA damage signaling network can be considered a computational device in which input is type and extent of output cell cycle arrest repair, permanent or death. A protein kinases makes these cellular decisions, but how commits to different outcomes unclear. To understand fates are determined we have generated level understanding this decision process works through synergistic application experimental methods. project builds...
SUMMARY Genotoxic stress in mammalian cells, including that caused by anti-cancer chemotherapy, can induce temporary cell cycle arrest, DNA damage-induced senescence (DDIS) or apoptotic death. Despite obvious clinical importance, it is unclear how the signals emerging from damage are integrated together with other cellular signaling pathways monitoring cell’s environment and/or internal state to control these different fates. Here, using a combination of single cell-based measurements and...
Genotoxic stress in mammalian cells, including that caused by anti-cancer chemotherapy, can induce temporary cell cycle arrest, DNA damage-induced senescence (DDIS) or apoptotic death. Despite obvious clinical importance, it is unclear how the signals emerging from damage are integrated together with other cellular signaling pathways monitoring cell’s environment and/or internal state to control these different fates. Here, using a combination of single cell-based measurements and tensor...