Genetics, Genomics and Bioinformatics  http://www.gbs.uab.edu  http://www.uab.edu/graduate  Back to Main

Faculty Detail    
Name NABIHA YUSUF
Associate Professor
 
Campus Address VH 566A
Phone
E-mail  nabihayusuf@uabmc.edu
Other websites
     

Education
Graduate  Rani Durgavati University, Jabalpur, INDIA      MS Microbiology 
Graduate  University of Alabama at Birmingham      MSPH Epidemiology 
Graduate  Aligarh Muslim University, Aligarh, INDIA      PhD Immunology 

Certifications
Center of Teaching and Learning   
Center for the Integration of Research, Teaching and Learning   


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Dermatology  Dermatology Professor
Secondary  Epidemiology  Epidemiology Associate Professor
Center  Comp Arthritis, MSK, Bone & Autoimmunity Ctr  Comp Arthritis, MSK, Bone & Autoimmunity Ctr Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  Ctr for Clinical & Translational Sci  Ctr for Clinical & Translational Sci Professor
Center  GL Ctr for Craniofacial, Oral, & Dental Disorders  GL Ctr for Craniofacial, Oral, & Dental Disorders Professor
Center  UAB Immunology Institute  UAB Immunology Institute Professor
Center  UWIRC Microbiome Center  UWIRC Microbiome Center Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 
Cancer Biology 
Cell, Molecular, & Developmental Biology 
Genetics, Genomics and Bioinformatics 
Immunology 
Microbiology 
Neuroscience 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Dr. Nabiha Yusuf is an Associate Professor in UAB’s Department of Dermatology. She also has a secondary appointment in Epidemiology. She received her Master’s in Microbiology PhD in Immunology from India. She recently graduated with an MSPH degree in Epidemiology from UAB. The focus of her research is to dissect the role of innate immune responses in UVB induced cutaneous DNA damage and tumor development. Her laboratory is studying the mechanisms by which type I interferons (IFN) regulate ultraviolet (UV) radiation skin cancers. She is also performing translational studies on TLR4 inhibitor in prevention of skin cancer. Besides research, she is involved with teaching and mentorship programs in the schools of Medicine and Public Health at UAB.

Society Memberships
Organization Name Position Held Org Link
American Association for Cancer Research  Active Member  www.aacr.org 
American Association of Immunologists  Active Member  www.aai.org 
Society of Investigative Dermatology  Active Member  www.sidnet.org 



Research/Clinical Interest
Title
Innate immune mechanisms in tumor development
Description
The focus of our research is on the role of innate immunity in the development of skin carcinogenesis. In our first study, we aim to delineate the mechanisms by which type I interferons (IFN) regulate ultraviolet (UV) radiation induced cutaneous DNA damage and tumor development. Furthermore, the role of post-transcriptional regulation of type I IFN in our UV model will be assessed. The information obtained from this proposal will highlight the role played by type I IFN in the initiation and progression of UV induced cutaneous tumors, and the manner in which they can be regulated. Thus, strategies can be developed for management of pre-malignant cutaneous lesions before they develop into skin cancer. My aim is not to confine my research to skin cancer but to extend it to other disorders where type I IFNs may be key players. In another study, we are testing pharmacological inhibitors of TLR4 in in vivo pre-clinical models their efficacy in DNA repair and prevention of UV induced skin cancer. We will be performing pharmacokinetic and pharmacodynamics studies for these inhibitors in our model. This study is a follow-up on our findings, where we have shown that loss of TLR4 has a protective effect on repair against UV-induced DNA damage, immunosuppression, and skin cancer.

Selected Publications 
Publication PUBMEDID
Ahmad I, Simanyi E, Guroji P, Tamimi IA, delaRosa HJ, Nagar A, Nagar P, Katiyar SK, Elmets CA, Yusuf N. 2013. Toll-Like Receptor-4 deficiency enhances repair of ultraviolet radiation induced cutaneous DNA damage by nucleotide excision repair mechanism. J Invest Dermatol. 2013 Dec 10. doi: 10.1038/jid.2013.530.  24326454 
He D, Li H, Yusuf N, Elmets CA, Athar M, Katiyar SK, Xu H. 2012. IL-17 mediated inflammation promotes tumor growth and progression in the skin. PLos One 7:e32126.   22359662 
Naseemuddin M, Iqbal A, Nasti TH, Ghandhi JL, Kapadia AD, Yusuf N. 2011. Cell mediated immune responses through TLR4 prevents DMBA-induced mammary carcinogenesis in mice. Int J Cancer. 130:765-74.   21455984 
Lewis W, Simanyi E, Li H, Thompson CA, Nasti TH, Jaleel T, Xu H, Yusuf N. 2011. Regulation of ultraviolet radiation induced cutaneous photoimmunosuppression by Toll like receptor-4. Arch. Biochem. Biophys 508: 171-177.   21236239 
Nasti TH, Iqbal O, Geise JT, Katiyar SK, Yusuf N. 2011. Differential roles of T-cell subsets in regulation of ultraviolet radiation induced cutaneous photocarcinogenesis. Photochem Photobiol 87: 387-398.   21143237 
He D, Li H, Yusuf N, Elmets CA, Li J, Mountz J, Xu H. 2010. IL-17 promotes tumor development through the induction of tumor promoting microenvironments at tumor sites and myeloid derived suppressor cells. J Immunol. 184:2281-8.  20118280 
Yusuf N, Nasti TH, Huang CM, Huber BS, Jaleel T, Lin HY, Xu H, Elmets CA. 2009. Heat shock proteins HSP27 and HSP70 are present in the skin and are important mediators of allergic contact hypersensitivity. J Immunol., 182:675-83.  19109201 
Yusuf N, Nasti TH, Katiyar SK, Jacobs MK, Seibert MD, Ginsburg AC, Timares L, Xu H, Elmets CA. 2008. Antagonistic roles of CD4+ and CD8+ T-Cells in 7,12-dimethylbenz(a)anthracene cutaneous carcinogenesis. Cancer Res., 68 :3924-30   18483278 
Yusuf N, Nasti TH, Long JA, Naseemuddin M, Lucas AP, Elmets CA. 2008. Protective role of TLR4 during the initiation stage of cutaneous chemical carcinogenesis. Cancer Res., 68: 615-622.   18199559 

Keywords
toll like receptors, type I interferons, immune system, cancer, T-cells