The overall goal of the HPDCF is to provide members of the Rheumatic Disease Core Center research base with fast and efficient state-of-the-art monoclonal antibody (Mab) production at economical prices. This goal is implemented through four specific aims: 1. To produce hybridomas and monoclonal antibodies (Mabs) for Rheumatic Diseases Core Center (RDCC) members in a timely and economical manner. 2. To provide RDCC members with state-of-the-art phage display technology and assist investigators in the utilization of single chain (scFv) antibody reagents. 3. To develop novel and efficient immunization strategies that facilitate the production of Mabs to problematic antigens. 4. To serve as a storage and distribution center for Mabs that are frequently utilized by members of the RDCC research base. The laboratory is committed to achieving a 100% success rate for the production of solicited Mabs. As a result, the HPDCF not only performs routine services, but also participates in research relating to the design and implementation of novel strategies for the generation of monoclonal reagents. Several of the innovative immunization protocols utilized by our laboratory have greatly facilitated the production of hybridomas to difficult antigens. Our recently incorporate phage display unit has already generated specific and highly functional single chain antibody molecules (scFv) to antigens that were refractory to antibody production using traditional methodology. If the need should arise, we will utilize our patented chicken recombinant antibody technology as a means for obtaining high affinity antibodies to highly conserved mammalian antigens.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
1P30AR048311-01
Application #
6547718
Study Section
Special Emphasis Panel (ZAR1)
Project Start
2001-09-28
Project End
2006-08-31
Budget Start
Budget End
Support Year
1
Fiscal Year
2001
Total Cost
Indirect Cost
Name
University of Alabama Birmingham
Department
Type
DUNS #
004514360
City
Birmingham
State
AL
Country
United States
Zip Code
35294
Yang, Zhengrong; Hildebrandt, Ellen; Jiang, Fan et al. (2018) Structural stability of purified human CFTR is systematically improved by mutations in nucleotide binding domain 1. Biochim Biophys Acta Biomembr 1860:1193-1204
Smith, Samuel R; Schaaf, Kaitlyn; Rajabalee, Nusrah et al. (2018) The phosphatase PPM1A controls monocyte-to-macrophage differentiation. Sci Rep 8:902
Chen, Wei; Zhu, Guochun; Jules, Joel et al. (2018) Monocyte-Specific Knockout of C/ebp? Results in Osteopetrosis Phenotype, Blocks Bone Loss in Ovariectomized Mice, and Reveals an Important Function of C/ebp? in Osteoclast Differentiation and Function. J Bone Miner Res 33:691-703
Wang, Yong; Schafer, Cara C; Hough, Kenneth P et al. (2018) Myeloid-Derived Suppressor Cells Impair B Cell Responses in Lung Cancer through IL-7 and STAT5. J Immunol 201:278-295
Jones, Robert B; Dorsett, Kaitlyn A; Hjelmeland, Anita B et al. (2018) The ST6Gal-I sialyltransferase protects tumor cells against hypoxia by enhancing HIF-1? signaling. J Biol Chem 293:5659-5667
Bandari, Shyam K; Purushothaman, Anurag; Ramani, Vishnu C et al. (2018) Chemotherapy induces secretion of exosomes loaded with heparanase that degrades extracellular matrix and impacts tumor and host cell behavior. Matrix Biol 65:104-118
Jo, SeongHo; Chen, Junqin; Xu, Guanlan et al. (2018) miR-204 Controls Glucagon-Like Peptide 1 Receptor Expression and Agonist Function. Diabetes 67:256-264
Stafman, Laura L; Williams, Adele P; Garner, Evan F et al. (2018) Targeting PIM Kinases Affects Maintenance of CD133 Tumor Cell Population in Hepatoblastoma. Transl Oncol 12:200-208
Hamilton, Jennie A; Wu, Qi; Yang, PingAr et al. (2018) Cutting Edge: Intracellular IFN-? and Distinct Type I IFN Expression Patterns in Circulating Systemic Lupus Erythematosus B Cells. J Immunol 201:2203-2208
Yang, Zhenhua; Shah, Kushani; Busby, Theodore et al. (2018) Hijacking a key chromatin modulator creates epigenetic vulnerability for MYC-driven cancer. J Clin Invest 128:3605-3618

Showing the most recent 10 out of 340 publications