Dawn S Chandler, PhD

College

College of Medicine

Department/Division

Pediatrics

Academic Title

Assoc Professor

Research Program

Molecular Biology and Cancer Genetics

Research Interest

Cancer, Muscular Atrophy, Spinal, Rhabdomyosarcoma, DNA Damage, Breast Cancer, Loss of Heterozygosity, Anoxia, Carcinoma, Renal Cell, von Hippel-Lindau Disease, Myopathies, Structural, Congenital

Our lab is interested in the regulation of pre-mRNA splicing and how disruption of this regulation can lead to pediatric diseases such as cancer. Current work in our lab elucidates alternative splicing as a novel mechanism by which cellular injury can control the activity of p53 and how changes in the regulation of splicing can lead to tumorigenesis. The transcription factor p53 is known to induce G1 arrest of the cell cycle and/or apoptosis. MDM2 is one of the most critical regulators of p53. Using in vitro biochemical assays and genetically engineered mouse models we are currently investigating differential RNA splicing of both the MDM2 and p53 pre-mRNAs and investigating the roles of each in normal cell function as well as disease.

Education and Background

Office Location

WA5023 Columbus Children's Research Institute

700 Children's Drive, Columbus, OH 43205

614-722-5302

614-722-5895

Dawn.Chandler@nationwidechildrens.org

Publications

Splicing factor SRSF1 negatively regulates alternative splicing of MDM2 under damage.

Comiskey DF Jr, Jacob AG, Singh RK, Tapia-Santos AS, Chandler DS

Nucleic Acids Res 43 4202-18 04/30/2015
The splicing factor FUBP1 is required for the efficient splicing of oncogene MDM2 pre-mRNA.

Jacob AG, Singh RK, Mohammad F, Bebee TW, Chandler DS

J Biol Chem 289 17350-64 06/20/2014
Stress-induced alternative splice forms of MDM2 and MDMX modulate the p53-pathway in distinct ways.

Jacob AG, Singh RK, Comiskey DF Jr, Rouhier MF, Mohammad F, Bebee TW, Chandler DS

PLoS One 9 e104444 01/01/2014
DEAR1 is a chromosome 1p35 tumor suppressor and master regulator of TGF-ß-driven epithelial-mesenchymal transition.

Lokken E, Chen J, Frazier ML, Sahin AA, Wistuba II, Sen S, Lott ST, Killary AM, Chen N, Balasenthil S, Reuther J, Frayna A, Wang Y, Chandler DS, Abruzzo LV, Rashid A, Rodriguez J, Lozano G, Cao Y

Cancer Discov 3 1172-89 10/01/2013
Stress-induced isoforms of MDM2 and MDM4 correlate with high-grade disease and an altered splicing network in pediatric rhabdomyosarcoma.

Jacob AG, O'Brien D, Singh RK, Comiskey DF Jr, Littleton RM, Mohammad F, Gladman JT, Widmann MC, Jeyaraj SC, Bolinger C, Anderson JR, Barkauskas DA, Boris-Lawrie K, Chandler DS

Neoplasia 15 1049-63 09/01/2013
miR-29 acts as a decoy in sarcomas to protect the tumor suppressor A20 mRNA from degradation by HuR.

Balkhi MY, Iwenofu OH, Bakkar N, Ladner KJ, Chandler DS, Houghton PJ, London CA, Kraybill W, Perrotti D, Croce CM, Keller C, Guttridge DC

Sci Signal 6 ra63 07/30/2013
Hypoxia is a modifier of SMN2 splicing and disease severity in a severe SMA mouse model.

Bebee TW, Dominguez CE, Samadzadeh-Tarighat S, Akehurst KL, Chandler DS

Hum Mol Genet 21 4301-13 10/01/2012

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Dawn S Chandler, PhD

College

Department/Division

Academic Title

Research Program

Research Interest

Education and Background

Office Location

Publications

Splicing factor SRSF1 negatively regulates alternative splicing of MDM2 under damage.

The splicing factor FUBP1 is required for the efficient splicing of oncogene MDM2 pre-mRNA.

Stress-induced alternative splice forms of MDM2 and MDMX modulate the p53-pathway in distinct ways.

DEAR1 is a chromosome 1p35 tumor suppressor and master regulator of TGF-ß-driven epithelial-mesenchymal transition.

Stress-induced isoforms of MDM2 and MDM4 correlate with high-grade disease and an altered splicing network in pediatric rhabdomyosarcoma.

miR-29 acts as a decoy in sarcomas to protect the tumor suppressor A20 mRNA from degradation by HuR.

Hypoxia is a modifier of SMN2 splicing and disease severity in a severe SMA mouse model.

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Dawn S Chandler, PhD

College

Department/Division

Academic Title

Research Program

Research Interest

Education and Background

Office Location

Publications

Splicing factor SRSF1 negatively regulates alternative splicing of MDM2 under damage.

The splicing factor FUBP1 is required for the efficient splicing of oncogene MDM2 pre-mRNA.

Stress-induced alternative splice forms of MDM2 and MDMX modulate the p53-pathway in distinct ways.

DEAR1 is a chromosome 1p35 tumor suppressor and master regulator of TGF-ß-driven epithelial-mesenchymal transition.

Stress-induced isoforms of MDM2 and MDM4 correlate with high-grade disease and an altered splicing network in pediatric rhabdomyosarcoma.

miR-29 acts as a decoy in sarcomas to protect the tumor suppressor A20 mRNA from degradation by HuR.

Hypoxia is a modifier of SMN2 splicing and disease severity in a severe SMA mouse model.

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