Michael Q. Kemp

1550 WoodbrookDrive, Apartment 20,East Lansing, MI, 48823

(517) 648-4771(H)/(517) 432-1674(W)/

EDUCATION .

2000 TO 2005PhDin Nutritional Sciences with a minor in Cancer Biology, 4.0 cumulative GPA, University of Arizona, Tucson, AZ (Expected completion date 5/2005)

2000 TO 2001UniversityMedicalCenter Dietetic Internship, UMC, Tucson, AZ

1995 TO 1999B.S. in Nutritional Science with a Minor in Chemistry, 3.1 cumulative GPA/3.6 major GPA, University of Arizona, Tucson, AZ

ACCREDITATION S/MEMBERSHIPS .

2003 TO PRESENTAssociate Member. American Association of Cancer Researchers. Philadelphia, PA.

2002 TO PRESENTRegistered Dietitian, American Dietetics Association, Chicago, IL.

2001 T0 PRESENTExpertCoach, USACycling, Colorado Springs, CO

1997 TO 2001Sport Coach

EXPERIENCE .

2006 TO PRESENTBreedlove Jordan Lab, MichiganStateUniversity, East Lansing, MI. A neuroscience lab interested in hormonal modulation of the developing and adult nervous system that leads to changes in behavior.

Visiting Research Associate.Reporting to Dr. Cynthia Jordan and Dr. Marc Breedlove. Responsibilities include participating in experimental design, performing molecular and cellular experiments, mentoring graduate and undergraduate students,and grant proposal and manuscript writing.

Spinal Bulbar Muscular Atrophy (SBMA) Studies. Our group has unexpectedly discovered a new mouse model for the motoneuron disease spinal bulbar muscular atrophy (SBMA). Our model selectively over-expresses the wild-type androgen receptor (AR) in muscle tissue, which challenges the current dogma that SBMA: 1) originates in motoneurons, and 2) an expansion of CAG (glutamine) exceeding 40 repeats within the AR protein is cytotoxic and required to trigger SBMA. To support these claims we have spent the greater part of the past year characterizing our model of SBMA to show that it holds the hallmark pathological features of this disease. Our endeavors into the mechanism of SBMA have made use of potential therapeutics and retrograde tracers.

  • Therapeutics. To further characterize our model of SBMA we would like to test its responsiveness to potential therapeutics. Recently, Waza et al. (2005) demonstrated that 17-allyamino-17-demethoxygeldanamycin (17-AAG) inhibits neuronal nuclear accumulation of mutant AR and considerably ameliorates motor phenotypes of the SBMA mouse model. Successful abrogation of the disease phenotype in our transgenic mouse using 17-AAG would provide additional convincing evidence that we have a model of SBMA. Finding to such effects may also challenge the hypothesis put forward by Waza et al. regarding the method of action behind 17-AAG (17-AAGs inhibition of Hsp90 preferentially targets mutant AR for degradation). Since our model does not rely on a mutant AR to induce the SBMA phenotype, successful amelioration of the disease in our model would suggest a larger role for the induction of Hsp70 and 40 by 17-AAG.Whereas, it may suggest that the induction of Hsp70 and 40 by 17-AAG may actually prevent the SBMA phenotype by sequestering the androgen receptor in the cytoplasm. These studies may help unearth the mechanism underlying the SBMA disease but also the mechanism behind successful therapeutics.
  • Retrograde Tracers. Disruption of neurotrophin levels have been implicated in altered axonal transport and the mechanism of poly-glutamine diseases, such as SBMA. Mammalian neurons require the continual delivery of target derived neurotrophins and undergo apoptosis if the delivery of neurotrophins is interrupted. Furthermore, reduced neurotrophin levels canalter axonal transport by disrupting the phosphatidylinositol 3 Kinase/AKT pathway. To characterize the contribution of these two phenomenons in our model ofSBMA we are currently employing the use of the retrograde tracer, cholera toxin-horse radish peroxidase (CT-HRP). Preliminary results indicate that retrograde transport of the CT-HRP to motoneuron in the spinal cord is reduced. Suggesting that retrograde transport of neurotrophins is thwarted with the SBMA phenotype. Our future studies in this area will attempt to reveal whether the reduction in retrograde transport results from a reduction in target derived neurotrophins. Overall, these studies will help reveal the mechanism of action behind the SBMA disease and possibly other poly-glutamine diseases.

2001 TO 2005Mammary Gland Biology Lab, University of Arizona, Tucson, AZ.A Cancer biology laboratory housed within the nutritional sciences department.

PhD Student/Research Technician,reporting to Dr. Donato Romagnolo.Responsibilities include participating in experimental design, performing molecular and cellular experiments,and grant proposal and manuscript writing.

Techniques: Eukaryotic cell culture, agarose/acrylamide gel electrophoresis, western blotting, northern blotting, polymerase chain reaction, ligation-mediated PCR, electrophoretic mobility shift assays, stable and transient transfections, luciferase assays, site-directed mutagenesis, microarray analysis, cloning, chromatin immunoprecipations assays, flow cytometric DNA content analysis, MTT cell proliferation assays, AnnexinV assays, and Tunel assays.

Dissertation

The Protective Effects of Conjugated Linoleic Acid Against Carcinogenesis

Peer-reviewed Publications

  • Kemp MQ, Thorne PA, Wenjing L, Ornella S, and Romagnolo DF.Toxicogenomics of Polycyclic Aromatic Hydrocarbons (PAHs): Identification of the Transferrin Receptor as a Biomarker for Exposure. Environmental and Molecular Mutagenesis, 47(7). 2006.
  • Jennifer K Hockings, Patricia A. Thorne, Michael Q. Kemp, Sherif S. Morgan, Ornella Selmin, and Donato F. Romagnolo. The Ligand Status of the Aromatic Hydrocarbon Receptor Modulates Transcription Activation of BRCA1 Promoter by Estrogen. Cancer Research. 66(4):2224-32. 2006.
  • DegnerSC, Kemp MQ, Bowden GTand Romagnolo DF. Conjugated linoleic acid attenuates cycloxygenase-2 transcriptional activity via an anti-AP-1 mechanism in MCF-7 breast cancer cells. J Nutr. 137:1-7. 2006.
  • Brandon D. Jeffy, Jennifer Ku. Hockings, Michael Q. Kemp, Sherif S. Morgan, Jill A. Hager, and Donato F. Romagnolo. The Estrogen Receptor- Modulates Induction of BRCA-1 Transcription. Neoplasia, 7(9):873-882. 2005.
  • Kemp MQ, Jeffy BD, and Romagnolo DF. Conjugated Linoleic Acid Inhibits Cell Proliferation Through a p53-Dependant Mechanism: Effects on the Expression of G1-Restriction Points in Breast and Colon Cancer Cells. J Nutr. 133(11)3670-7. 2003.

Current Submissions

  • Kemp MQ,DegnerSC, K.Hockings Jennifer, Romagnolo DF. Conjugated Lionleic Acid Inhibits Polycyclic Aromatic Hydrocarbon-induced Cyclooxygenase-2 Promoter Activity through an Aromatic Hydrocarbon Receptor-dependent Mechanism.Nutr Cancer, 2006. (In Submission)
  • Romagnolo DF, DegnerSC, Kemp MQ, Hockings JK, Semlin O. Role of Dietary Constituents-Gene Interactions in Carcinogenesis. (In Submission).

Published Abstracts

  • Kemp MQ, Jeffy BD, and Romagnolo DF. Protective Effects of the Synthetic Flavonoid α-naphthoflavone Against Transcriptional, Post-transcriptional Changes, and Ultrastructural Modifications Induced by the Carcinogen Benzo[a]pyrene. 2004 AACR Annual Meeting.
  • Kemp MQ, Jeffy BD, and Romagnolo DF.Activation of the p53-dependent G1 checkpoint by conjugated linoleic acid: association with decreased Rb phosphorylation and cell cycle arrest. 2003 AACR Annual Meeting.
  • Kemp M, Bristol S, Meer M, Priestly G, and Quan S. Indications for the Utilization of FD &C Blue Food Dye in Enterally Fed Patients. 2000 Arizona Dietetic Association Annual Meeting.

2001 TO 2002CATS Team Nutrition, University of Arizona, Tucson, AZ. A Division IA sports program with student athletes in ten womens and eight mens sports programs.

Sports Nutritionistreporting to Campus Health Services R.D.,responsibilities include design and implementation of marketing materials to attract student athlete client base; Client counseling in one-on-one or group setting catering to individual and team goals;Nutritional assessments of clients completed using sport specific consideration, weight information, food intake records, diet history data acquired from interviews.

1999 TO 2001The Healthcare Center at the Forum, Tucson, AZ. A 150 room senior living service with assisted living, secured care, and critical care facilities.

Dietetic Technician reporting to Dietitian, and acting as dietitian during absence, responsibilities include nutritional assessments of patients using weight information, food intake records, labs, diet history data acquired from interviews, and drug nutrient interactions, weekly and monthly weight, fluid balance and lab assessments, government funding requisition, participated in patient care plan conferencing, developed nutritional therapies, implemented doctors approvals for nutritional therapies, patient charting, discharge summaries, and conduit between dietary and five separate departments.

  • Implemented weekly and monthly resident weight reports.
  • Design of patient care plans.

Dietary Supervisor reporting to Director of Food Services, responsibilities include overseeing meal production for 150 residents, diet menu changes, updating kitchen diet records with physicians orders, quality control of kitchen and dining facilities, interviewing, weekly scheduling of Dietary Aides, and managing a staff of 20.

1998 TO 1999St. Josephs Hospital and MedicalCenter, 703 Main Street, Paterson, NJ. A 250 patient critical care hospital in Northern New Jersey area.

As NUTRITION ASSISTANT reporting to Director of Food Services responsible for the menu preparation of 250 patients. Duties of aligning diet to match physician and dietitian orders, monitoring status and location of patients, patient diet counseling, and distribution and collection of weekly menu selections.

1998 TO 1998WellnessCenter, Tucson, AZ. A joint program between Campus health Services and the Department of Recreation committed the University of Arizona student wellness.

Nutrition Assistant completed body composition analysis on individuals, blood pressure checks, height and weight checks, and diet analysis. Staff during wellness assessments of fitness, nutrition, emotional/social health, and stress management. Conduct research to answer client questions and help expand programming.

  • Conducted research on bioelectrical impedance to enhance facilities services.

SKILLS .

Windows 95, OS 9.0/X, Word, Excel, Access, Power Point, Publisher, Photoshop, Illustrator, PageMaker, Dreamweaver, SBSS, Statview, Nutritrac and Minitab