Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Carbohydrate doai
Reexamination Certificate
1998-09-22
2003-05-13
Nguyen, Dave T. (Department: 1636)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Carbohydrate doai
C435S455000, C435S325000, C435S069100, C530S350000, C536S023500
Reexamination Certificate
active
06562797
ABSTRACT:
FIELD OF THE INVENTION
This invention relates to Fas-mediated cellular functions and methods for the regulation of Fas-mediated cellular functions in a population of cells.
BACKGROUND OF THE INVENTION
Programmed cell death (PCD) is a physiologic process essential to the normal development and homeostatic maintenance of multicellular organisms (reviewed in Vaux et al. (1994)
Cell
76:777-779 and Ellis et al. (1991)
Ann. Rev. Cell Biol.
7:663-698). Apoptosis, often equated with PCD, refers to the morphologic alterations exhibited by “actively” dying cells which include cell shrinkage, membrane blebbing and chromatin condensation. (For a general review of apoptosis, see Tomei, L. D. and Cope, F. O.
Apoptosis: The Molecular Basis of Cell Death
(1991) Cold Spring Harbor Press, N.Y.; Tomei, L. D.; Cope, F. O.
Apoptosis II: The Molecular Basis of Apoptosis in Disease
(1994) Cold Spring Harbor Press, N.Y.; Duvall and Wyllie (1986)
Immun. Today
7(4):115-119 and Cohen (1993)
Immunol. Today
14:126-130.) In contrast, necrosis, sometimes referred to as accidental cell death, is defined by the swelling and lysis of cells that are exposed to toxic stimuli.
Apoptosis has been linked to many biological processes, including embryogenesis, development of the immune system, elimination of virus-infected cells, and the maintenance of tissue homeostasis. Apoptosis also occurs as a result of human immunodeficiency virus (HIV) infection of CD4
+
T lymphocytes (T cells). Indeed, one of the major characteristics of AIDS is the gradual depletion of CD4
+
T lymphocytes during the development of the disease. Several mechanisms, including apoptosis, have been suggested to be responsible for the CD4 depletion. It is speculated that apoptotic mechanisms might be mediated either directly or by the virus replication as a consequence of the HIV envelope gene expression, or indirectly by priming uninfected cells to apoptosis when triggered by different agents.
The depletion of CD4
+
T cells results in the impairment of the cellular immune response. It has been reported that an inappropriate activation-induced T cell PCD causes the functional and numerical abnormalities of T
H
cells from HIV-infected patients, that leads to the near collapse of the patient's immune system. (Brunner, T. et al. (1995)
Nature
373:441-444; Dhein, J. et al. (1995)
Nature
373:438-441; and Ju, S-T. et al. (1995)
Nature
373:444-448).
Therefore, it is advantageous to block apoptosis and the ensuing depletion of T cells, especially in HIV infected individuals. Accordingly, a need exists to maintain T cell function and viability in HIV infected individuals and to provide systems to screen for new drugs that may assist in maintaining the cellular immune response. This invention satisfies this need and provides related advantages as well.
SUMMARY OF THE INVENTION
This invention provides a novel purified mammalian protein designated FADD having the ability to bind the cytoplasmic region or domain of the Fas receptor.
Also provided by this invention are nucleic acid molecules that encode the mammalian protein which binds the intracellular domain of Fas.
An antibody, such as a monoclonal antibody, with specific affinity for FADD is further provided by this invention.
Methods of using the proteins, nucleic acids and antibodies described above are further provided herein.
REFERENCES:
patent: 4107297 (1978-08-01), Omura et al.
patent: 4683195 (1987-07-01), Mullis et al.
patent: 4683202 (1987-07-01), Mullis
patent: 4754065 (1988-06-01), Levenson et al.
patent: 4800159 (1989-01-01), Mullis et al.
patent: 5258454 (1993-11-01), Berg et al.
patent: 5674734 (1997-10-01), Leder et al.
patent: WO 93/25685 (1993-12-01), None
patent: WO 93/25694 (1993-12-01), None
patent: WO 94/18317 (1994-08-01), None
patent: WO 94/21817 (1994-09-01), None
patent: WO 94/24297 (1994-10-01), None
patent: WO 94/25621 (1994-11-01), None
patent: WO 94/27583 (1994-12-01), None
patent: WO 95/31544 (1995-11-01), None
patent: WO 96/01642 (1996-01-01), None
patent: WO 96/18641 (1996-06-01), None
patent: WO 96/20721 (1996-07-01), None
patent: WO 96/25945 (1996-08-01), None
patent: WO 96/36698 (1996-11-01), None
patent: WO 96/40713 (1996-12-01), None
patent: WO 97/03998 (1997-02-01), None
patent: WO 97/18313 (1997-05-01), None
patent: WO 98/03648 (1998-01-01), None
N. Miller et. al.; Targeted vectors for gene therapy; Feb. 1995, FASEB Journal, vol. 9 ;190-199.*
N. Wivel et. al.; Methods Of Gene Delivery; Jun. 1998, Hematology/ Oncology Clinics of North America; vol. 12, 483-501.*
I. Verma et.al.; Gene therapy-promises, problems and prospects; Sep., 1997; Nature, vol. 389; 239-242.*
M. Deonarian; Ligand-targeted receptor-mediated vectors for gene delivery; 1998, Exp. Opin. Ther. Patents 8(1), 53-69.*
Daniel et. al.; The kiss of death: promises and failures of death receptors and ligands in cancer therapy, 2001, Leukemia 15: 1022-1032.*
Yeh et.al.; Gene targeting in the analysis of mammalian apoptosis and TNF receptor superfamily signaling, 1999, Immunoiogical Reviews vol. 169: 283-302.*
Allison et al., “The yin and yang of T cell costimulation”Science270:932-933 (1995).
Anderson, “Human gene therapy”Science256:808-813 (1992).
Baglioni, “Mechanisms of cytotoxicity, cytolysis, and growth stimulation by TNF”Tumor Necrisis Factors. The Molecules and Their Emerging Role in MedicineB. Beutler, M.D., ed., Raven Press, New York. A title page and table of contents are enclosed herewith (1992).
Barres et al., “Cell death and control of cell survival in the oligodendrocyte lineage” Cell 70:31-46 (1992).
Beidler et al., “The baculovirus p35 protein inhibits fas- and tumor necrosis factor-induced apoptosis”J. Biol. Chem. 270:16526-16528 (1995).
Blau et al., “Molecular medicine: Gene therapy—a novel form of drug delivery”N. Eng. J. Med. 333:1204-1207 (1995).
Boldin et al., “A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain”J. Biol. Chem. 270:7795-7798 (1995).
Boldin et al., “Self-association of the ‘death domains’ of the p55 tumor necrosis factor (TNF) receptor and Fas/APO1 prompts signaling for TNF and Fas/APO1 effects”J. Biol. Chem. 270:387-391 (1995).
Bordignon et al., “Retroviral vector-mediated high-efficiency expression of adenosine deaminase (ADA) in hematopoietic long-term cultures of ADA-deficient marrow cells”Proc. Natl. Acad. Sci. USA86:6748-6752 (1989).
Bose et al., “Ceramide synthase mediated daunorubicin-induced apoptosis: An alternative mechanism for generating death signals”Cell82:405-414 (1995).
Boudreau et al., “Suppression of ICE and apoptosis in mammary epithelial cells by extracellular matrix”Science267:891-893 (1995).
Boulakia et al., “Bcl-2 and adenovirus E1B 19 kDa protein prevent E1A-induced processing of CPP32 and cleavage of poly (ADP-ribose) polymerase”Oncogene12:529-535 (1996).
Brunner et al., “Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas”Nature373:441-444 (1995).
Bump et al., “Inhibition of ICE family protease by baculovirus antiapoptotic protein p 35”Science269:1885-1888 (1995).
Casciola-Rosen et al., “Specific cleavage of the 70-kDa protein compound of the U1 small nuclear ribonucleoprotein is a characteristic biochemical feature of apoptotic cell death”J. Biol. Chem. 269:30757-30760 (1994).
Cerretti et al., “Molecular cloning of the interleukin-1&bgr; converting enzyme”Science256:97-100 (1992).
Chinnaiyan et al. “Signal Transduction by DR3, a Death Domain-Containing Receptor Related to TNFR-1 and CD95”Science274:990-992 (1996).
Chinnaiyan et al., “FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis”Cell81:505-512 (1995).
Chinnaiyan et al., “FADD/MORTI is a common mediator of CD95 (Fas/APO-1) and tumor necrosis factor receptor-induced apoptosis”J. Biol. Chem. 271:4961-4965 (1996).
Chinnaiyan et al., “Molecular ordering of the cell death pathway”J. Biol. Chem. 271:4573-4576 (1996).
Clem et al., “Control of programmed cell death by the bacu
Dixit Vishva M.
O'Rourke Karen
Medlen & Carroll, LLP.
Nguyen Dave T.
Nguyen Quang
The Regents of the University of Michigan
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