Abstract

One element that has contributed significantly to the increased research productivity of the biomedical scientists in the past and will be critical to the success of the cancer research center is the availability of additional research manpower. The CAU RCMI program supports RAs to provide assistance to its scientists. These RAs have been instrumental in the enhanced generation of data for manuscripts and proposals. In the past, the Program has supported RA positions that were made available to all RCMI-affiliated scientists on a competitive basis. Scientists who competed for these positions had to submit a proposal which fully described the research to be performed by the RA. The scientists had to also provide evidence that they had funds to support the research project. These proposals were reviewed by the RCMI IAC and by external reviewers (if needed). The RA positions were generally awarded to the successful applicants for a period of two years. It is proposed that the support for these technical support services continue as a part of the CAU RCMI program because these services are vitally important to the success of the cancer research center.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Research Centers in Minority Institutions Award (G12)
Project #
3G12RR003062-16S1
Application #
6661589
Study Section
Project Start
2002-09-19
Project End
2003-06-30
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
16
Fiscal Year
2002
Total Cost
$88,647
Indirect Cost

  Institution

Name
Clark Atlanta University
Department
Type
DUNS #
065325177
City
Atlanta
State
GA
Country
United States
Zip Code
30314

  Publications

Morton, Derrick J; Patel, Divya; Joshi, Jugal et al. (2017) ID4 regulates transcriptional activity of wild type and mutant p53 via K373 acetylation. Oncotarget 8:2536-2549
Joshi, Jugal Bharat; Patel, Divya; Morton, Derrick J et al. (2017) Inactivation of ID4 promotes a CRPC phenotype with constitutive AR activation through FKBP52. Mol Oncol 11:337-357
Komaragiri, Shravan Kumar; Bostanthirige, Dhanushka H; Morton, Derrick J et al. (2016) ID4 promotes AR expression and blocks tumorigenicity of PC3 prostate cancer cells. Biochem Biophys Res Commun 478:60-66
Wilder, Catera L; Walton, Charlene; Watson, Valencia et al. (2016) Differential cathepsin responses to inhibitor-induced feedback: E-64 and cystatin C elevate active cathepsin S and suppress active cathepsin L in breast cancer cells. Int J Biochem Cell Biol 79:199-208
Brown, Shanora G; Knowell, Ashley E; Hunt, Aisha et al. (2015) Interferon inducible antiviral MxA is inversely associated with prostate cancer and regulates cell cycle, invasion and Docetaxel induced apoptosis. Prostate 75:266-79
Muniyan, Sakthivel; Chou, Yu-Wei; Tsai, Te-Jung et al. (2015) p66Shc longevity protein regulates the proliferation of human ovarian cancer cells. Mol Carcinog 54:618-31
Chinaranagari, Swathi; Sharma, Pankaj; Bowen, Nathan J et al. (2015) Prostate cancer epigenome. Methods Mol Biol 1238:125-40
Burton, Liza J; Smith, Basil A; Smith, Bethany N et al. (2015) Muscadine grape skin extract can antagonize Snail-cathepsin L-mediated invasion, migration and osteoclastogenesis in prostate and breast cancer cells. Carcinogenesis 36:1019-27
Goodson 3rd, William H; Lowe, Leroy; Carpenter, David O et al. (2015) Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead. Carcinogenesis 36 Suppl 1:S254-96
Smith, Basil; Randle, Diandra; Mezencev, Roman et al. (2014) Camalexin-induced apoptosis in prostate cancer cells involves alterations of expression and activity of lysosomal protease cathepsin D. Molecules 19:3988-4005

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