Dr. David W. Koh M.D.
Pulmonologist | Pulmonary Disease
1302 Franklin Ave #2200 Normal IL, 61761About
Dr. David Koh practices Pulmonology in Normal, IL. A pulmonologist is a physician who possesses specialized knowledge and skill in the diagnosis and treatment of pulmonary conditions and diseases. Dr. Koh manages patients who need life support and mechanical ventilation, and is specially trained in diseases and conditions of the chest, particularly pneumonia, asthma, tuberculosis, emphysema, and complicated chest infections.
Education and Training
University of Illinois College of Medicine 1990
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Identification of an inhibitor binding site of poly(ADP-ribose) glycohydrolase.
- SAR analysis of adenosine diphosphate (hydroxymethyl)pyrrolidinediol inhibition of poly(ADP-ribose) glycohydrolase.
- Identification of three critical acidic residues of poly(ADP-ribose) glycohydrolase involved in catalysis: determining the PARG catalytic domain.
- Poly(ADP-ribosyl)ation regulation of life and death in the nervous system.
- Differential effect of PARP-2 deletion on brain injury after focal and global cerebral ischemia.
- Enhanced DNA accessibility and increased DNA damage induced by the absence of poly(ADP-ribose) hydrolysis.
- Activation of cell death mediated by apoptosis-inducing factor due to the absence
- Synergistic cytotoxicity of N-methyl-N'-nitro-N-nitrosoguanidine and absence of poly(ADP-ribose) glycohydrolase involves chromatin decondensation.
- Poly(ADP-ribosyl)ation pathways in mammals: the advantage of murine PARG null mutation.
- Silencing of Apoptosis-Inducing factor and poly(ADP-ribose) glycohydrolase reveals novel roles in breast cancer cell death after chemotherapy.
- Inhibition of poly(ADP-ribose) polymerase-1 or poly(ADP‑ribose) glycohydrolase individually, but not in combination, leads to improved chemotherapeutic efficacy in HeLa cells.
- Roles of poly(ADP-ribose) glycohydrolase in DNA damage and apoptosis.
- Quantitative proteomic analysis in HCV-induced HCC reveals sets of proteins with potential significance for racial disparity.
- Inhibition of the transient receptor potential melastatin-2 channel causes increased DNA damage and decreased proliferation in breast adenocarcinoma cells.
- Enhanced cytotoxicity in triple-negative and estrogen receptor‑positive breast adenocarcinoma cells due to inhibition of the transient receptor potential melastatin-2 channel.
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