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Professor,
Microbiology, Immunology & Molecular Genetics
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Member,
ACCESS Program: Dept. of Microbiology, Immunology, & Molecular Genetics,
JCCC Gene Regulation Program Area,
JCCC Signal Transduction and Therapeutics Program Area
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Contact Information:
| Work Address: |
Office
Factor
Los Angeles, CA 90095
UNITED STATES
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| Work Address: |
Laboratory
Factor
Los Angeles, CA 90095
UNITED STATES
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| Work Address: |
210A BSRB
CAMPUS - 736422
CA
UNITED STATES
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Work Phone Number:
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(310) 825-8896
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Research Interests:
Molecular Mechanisms in Immune Responses and Cancer Therapy
Cheng laboratory at UCLA studies signal transduction and gene expression network through the TNF receptor, Toll-like receptor (TLR), and Nod families during the process of innate and adaptive immune responses. The TNF receptor family members are involved in regulating cell survival, adaptive immune and inflammatory responses. The TLR family members are involved in innate immune responses through detecting pathogen-associated molecular patterns (PAMPs) out side of the cells. The Nod family members were first recognized in plant as plant resistant proteins. Mutations in the nod2 are associated with about 25% of the human Crohn's disease. They share similar leucine rich repeats as the TLR family members and are considered as receptors for intracellular pathogens. Interestingly, most members in TNF receptor, TLR and Nod families use the TRAF family proteins as their adapters for activating similar signal transduction pathways such as the NF-kB, JNK, p38, ERK, PI3K, and IRF3. We have established a comprehensive system using biochemical and microarray analysis, cell-based assays, as well as animal models to determine the role and the specificity of individual receptors, signaling pathways and their targeting molecules in immune and inflammatory responses to bacterial and viral infections, as well as in cancer therapy.
Upon recognition of different subsets of PAMPs, ten TLRs are believed to initiate unique profiles of innate and adaptive immune responses to combat different type of pathogens. This functional specificity of TLRs is regulated by a subset of overlapped and distinct signal transduction and gene expression networks (gene program). We have recently identified two TLR-mediated major gene programs. The inflammatory and phagocytosis gene program involves MyD88-dependent activation of signaling pathways such as p38, and induction of inflammatory genes such as IL-1b and phagocytosis related genes such as Marco, which results in induction of inflammatory responses and enhancement of pathogen uptake by innate immune cells. Different TLRs have different abilities to activate this gene program, TLR9 being the strongest and TLR3 being weakest. The anti-viral gene program specifically activated by TLR3 and TLR4 but bot by other TLRs and TNF receptors. This gene program involves a subset of immediate early response genes that are regulated by the interferon regulatory factor 3 (IRF3) and a group of secondary response genes activated by autocrine production of interferon beta (IFNb). Selective activation of this program by TLR3/4 was shown to mediate a protective effect against viral infection. Our studies further demonstrated that this program is dispensable from the TLR-mediated inflammatory responses suggesting the possibility of activating anti-viral activity without inducing inflammation.
We demonstrated that receptor-interacting protein 2(RIP2) is a critical kinase for signal transduction through the Nod family of receptors. We recently created mice with knockout of the receptor-interacting protein 2 (RIP2) gene. RIP2-deficient mice are extremely susceptible to infection by intracellular bacteria such as Listeria manocytogenes, which is likely due to their defect in detecting bacterial infections during innate immune responses and generating Th1 cells during adaptive immune responses (Nature 416:190-194, 2002). Macrophages derived from RIP2-deficient mice do not respond to stimulation with Nod2 ligand, the muramyl dipeptide (MDP). Th1 cells and NK cells Macrophages derived from RIP2-deficient mice are defective in their production of IFNg, which is critical for controlling intracellular pathogens.
As a member of the TNF receptor superfamily, CD40 plays essential roles in normal humoral immune responses, including immunoglobulin isotype switching, antibody affynity maturation, memory B-cell formation and T-cell activation. On the other hand, recent studies indicated that abnormal signaling through CD40 is associated with many inflammatory diseases, including chronic rejection following tissue transplantation, athersclerosis, alzheimer??A?s disease and autoimmune diseases such as rheumatoid arthritis, lupus nephritis and multiple sclerosis. My laboratory is interested in dissecting the molecular mechanisms of CD40-mediated physiological and pathological functions. We hope to use mouse models for thymus-dependent antigen response, heart transplantation, atherosclerosis, and inflammatory bowel disease (IBD) to determine the roles of CD40-expressing B-lymphocytes, macrophage and dendritic cells in CD40-mediated normal immune responses and abnormal inflammatory responses.
Our Laboratory is also interested in understanding the mechanisms of chemoresistance and developing novel strategies to improve cancer treatment. We have recently demonstrated that the MEKK1-dependent signal transduction pathway is essential for cell apoptosis in response to microtubule or actin disruption. We found many chemotherapy agents commonly used in clinic, which suppose to kill tumor cells, can actually activate alternative cell survival pathways (such as the NF-kB-dependent up-regulation of Bcl-x and Bfl-1 genes) to protect tumor cells. Blocking the NF-kB-dependent up-regulation of Bcl-x and Bfl-1 genes can greatly reduce chemoresistance and sensitize chemotherapy-mediated apoptosis. My Laboratory is currently evaluating the possibility of using the combination of NF-kB inhibitors and chemotherapy agents for cancer therapy. Finally, we found that most of Epstein-Barr virus-associated nasopharyngeal carcinoma and a significant portion of other epithelial cancers have relative high NF-kB activity and express elevated levels of epidermal growth factor receptor (EGFR). We are evaluating the possibility of treating these cancers with NF-kB and EGFR antagonists.
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Additional Information:
Dr. Cheng is a Professor in Microbiology, Immunology and Molecular Genetics at UCLA. He had his PhD training in Molecular Biology with Dr. Arthur Skoultchi at Albert Einstein College of Medicine, and had his postdoctoral training in Molecular Immunology with Dr. David Baltimore at Rockefeller University and Massachusetts Institute of Technology (MIT). Dr. Cheng is an expert on immune responses in host defense against infections and cancers as well as their associations with inflammatory and metabolic diseases. He has authored close to 100 peer-reviewed articles, many of which are published in top journals like Nature and Science. He has been the principal investigator in many research grants from government and private sources. Dr. Cheng has received many awards, including Stop Cancer Award, Leukemia & Lymphoma Society Scholar Award, Leukemia & Lymphoma Society Stohlman Scholar Award and NIH Merit Award.
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Hwang S, Kim KS, Flano E, Wu TT, Tong LM, Park AN, Song MJ, Sanchez DJ, O'Connell RM, Cheng G, Sun R, Conserved herpesviral kinase promotes viral persistence by inhibiting the IRF-3-mediated type I interferon response, Cell Host Microbe, 2009, 5 (2), 166-78.
Miyahira, AK, Shahangian, A., Hwang, S., Sun, R. Cheng G, TANK-binding kinase-1 plays an important role during in vitro and in vivo type I interferon responses to DNA virus infections, J Immunol., 2009, 182 (4), 2248-57.
Cheng LS., Hwang S., Huang TH, Sheu TC, Sun R., Morrison SL, Cheng G, and Shahangian A, Antibody-fused interferons as an effective approach to enhance target specificity and antiviral efficacy of type I interferons, Cell Res. advance online publication, 2008.
Zarnegar BJ, Wang Y.,, Mahoney DJ, Dempsey PD, Cheung HH, He J, Shiba T, Yang X., Yeh WC, Mak TW, Korneluk RG, and Cheng G, Noncanonical NF-κB Activation Requires the Coordinated Assembly of the cIAP1/2-NIK Regulatory Complex by TRAF2 and TRAF3, Nature Immunology, 2008, 9 (12), 1371-8.
Pietras EM, Cheng G, A New TRADDition in intracellular antiviral signaling, Science Signaling, 2008, 1 (30), 36.
Zanegar, B., Yamazak S. He JQ, Cheng G, Control of Canonical NF-κB Activation through the NIK-IKK-Complex Pathway, PNAS, 2008, 105 (9), 3503-3508.
Sanchez DJ, Miranda D Jr, Arumugaswami V, Hwang S, Singer AE, Senaati A, Shahangian A, Song MJ, Sun R, Cheng G., A Repetitive Region of Gamma-herpesvirus Genomic DNA Is a Ligand for Induction of Type I Interferon, J Virol., 2008, 82 (5), 2208-17.
Miller, L. S. Pietras, E. M. Garcia, N. Cheung, A. L. Blauvelt, A. Cheng, G. Modlin, R. L., IL-1R activation is required for IL-17-dependent neutrophil recruitment against Staphylococcus aureus skin infections, Journal of Investigative Dermatology, 2008, 128, S190-S190.
Oganesyan, G. Saha, S. K. Pietras, E. M. Guo, B. Miyahira, A. K. Zarnegar, B. Cheng, G. , IRF3-dependent type I interferon response in B cells regulates CpG-mediated antibody production, Journal of Biological Chemistry, 2008, 283 ( 2), 802-808.
Tricker, E. Cheng, G. , With a little help from my friends: modulation of phagocytosis through TLR activation, Cell Research, 2008, 18 ( 7), 711-712.
Wong PK., Yu, F., Shahangian, A., Cheng, G., Sun, R., and Ho, CM, Closed-loop Control of Cellular Functions By using a Stochastic Search Algorithm, PNAS, 2008, 105, 5105-5110.
Chow, EKH., Pierstorff, E., Cheng, G., and Ho, D, Copolymeric Nanofilm Platform for Controlled and Localized Therapeutic Delivery, ACS Nano, 2008, 2 (1), 33-40.
Zhai Y, Qiao B, Shen XD, Gao F, Busuttil RW, Cheng G, Platt JL, Volk HD, Kupiec-Weglinski JW, Evidence for the Pivotal Role of Endogenous Toll-Like Receptor 4 Ligands in Liver Ischemia and Reperfusion Injury, Transplantation., 2008, 85 (7), 1016-1022.
Pietras EM, Cheng G., New tricks for old NODs, Genome Biol., 2008, 9 (4), 217.
Zheng D., Chen G., Guo B., Cheng G, and Tang H, PLP2, a potent deubiquitinase from murine hepatitis virus, can strongly inhibit cellular type I interferon production, Cell Res. , 2008, 11, 1105-13.
Velázquez, P, Wei, B, McPherso,n M, Mendoza, LM, Nguyen, SL, Turovskaya, O, Kronenberg, M, Huang, TT, Schrage, M, Lobato, LN, Fujiwara, D, Brewer, S, Arditi, M, Cheng, G, Sartor, RB, Newberry, RD, Braun, J., Villous B cells of the small intestine are specialized for invariant NK T cell dependence, J Immunol., 2008, 180 (7), 4629-38.
Miller, LS., Pietras, EM., Uricchio, LH., Hirano, K.,Rao, S., Lin, H., O'Connell, RM., Iwakura,, Y., Ambrose L. Cheung, AL., Cheng G., Modlin, RL, Inflammasome-mediated production of IL-1β is required for neutrophil recruitment against Staphylococcus aureus in vivo, J. Immunol., 2007, 179 (10), 6933-42.
Chow, EKH., Chu, B., Cheng G., Tai, YC., Pierstorff, P., and Ho., D, Copolymer-mediated Fabrication of Versatile Electro-Active and Inflammation Attenuating Substrates for Biological Interrogation, NANO: Brief Reports and Reviews, 2007, 2 (6), 351-359.
Chang, EY., Guo B, Doyle, S. Cheng G., Involvement of the Type I interferon production and signaling pathway in lipopolysaccharide-induced IL-10 production, J. Immunol, 2007, 178 (1), 6705-9.
Lee DJ, Sieling PA, Ochoa MT, Krutzik SR, Guo B, Hernandez M, Rea TH, Cheng G, Colonna M, Modlin RL., LILRA2 Activation Inhibits Dendritic Cell Differentiation and Antigen Presentation to T Cells, J Immunol., 2007, 179 (12), 8128-36.
O'connell RM, Taganov KD, Boldin MP, Cheng G, Baltimore D, MicroRNA-155 is induced during the macrophage inflammatory response, PNAS, 2007, 104 (5), 1604-9.
Miller, L. S. Pietras, E. M. Uricchio, L. O'Connell, R. M. Hirano, K. A. Rao, S. Cheung, A. L. Cheng, G. Modlin, R. L. , IL-1 beta and the inflammasome but not IL-1 alpha mediate IL-1R-dependent neutrophil recruitment against Staphylococcus aureus skin infection, Journal of Investigative Dermatology, 2007, 127, S130-S130.
He, J. Q. Oganesyan, G. Saha, S. K. Zarnegar, B. Cheng, G. , TRAF3 and its biological function, Tnf Receptor Associated Factors (Trafs), 2007, 597, 48-59.
Kayagaki, N., Phung, Q., Chan, S., Chaudhari R, Quan, C., O'Rourke, KM., Eby, M., Pietras, E, Cheng, G., Bazan, JF., Zhang, Z., Arnott, D., Dixit, VM.., DUBA: A Deubiquitinase That Regulates Type I Interferon Production., Science, 2007, 318 (5856), 1628-32.
Guo B, Cheng G., Modulation of the interferon antiviral response by the TBK1/IKKI adaptor protein tank, J Biol Chem., 2007, 282 (16), 11817-26.
Chow EK, Razani B, Cheng G., Innate immune system regulation of nuclear hormone receptors in metabolic diseases, J Leukoc Biol., 2007, 82 (2), 187-95.
He JQ, Saha SK, Kang JR, Zarnegar B, Cheng G., Specificity of TRAF3 in its negative regulation of the noncanonical NF-kappa B pathway, J Biol Chem, 2006, 282 (6), 3688-94.
Chow EK, Castrillo A, Shahangian A, Pei L, O'Connell RM, Modlin RL, Tontonoz P, Cheng G., A role for IRF3-dependent RXRalpha repression in hepatotoxicity associated with viral infections, J Exp Med. , 2006, 203, 2589-602.
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Oganesyan, G., Saha, SK, Guo, B., He, J., Shahangian, A., Zarnegar B., Perry, AK., Cheng, G. , Critical role of TRAF3 in the Toll-like receptor-dependent and independent antiviral response. , Nature, 2006, 439, 208-211.
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Miller, LS., O'Connell, RM., Gutierrez, MA., Pietras, EM., Shahangian, A., Gross, CE., Thirumala, A., Cheung, AL., Cheng , G., Modlin, RL. , MyD88 mediates neutrophil recruitment initiated by IL-1R but not TLR2 activation in immunity against Staphylococcus aureus , Immunity, 2006, 24, 79-91.
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Saha, SK., Pietras, EM., He, JQ., Kang, JR., Liu, SY., Oganesyan, G., Shahangian, A., Zarnegar, B., Shiba TL., and Cheng, G. , Regulation of antiviral responses by a direct and specific interaction between TRAF3 and Cardif. , EMBO J. , 2006, 25, 3257-3263.
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He, JQ., Zarnegar, B., Yamazaki, S., Oganesyan, G., Saha, SK., Doyle, S., Dempsey, P., and Cheng, G. , Rescue of TRAF3 null mice by p100 NF-kB deficiency. , J Exp Med, 2006, 203, 2413-2418.
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Deng, JC., Cheng, G. Newstead, MW., Zeng, X., Kobayashi, K., Flavell, R., Standiford, TJ. , Sepsis-Induced Suppression of Lung Innate Immunity is mediated by IRAK-M. , Journal of clinical investigation (JCI), 2006, 116, 2532-2542.
Renn, CN, Sanchez, DJ, Ochoa, MT, Legaspi, AJ, Oh, CK, Liu, PT, Krutzik, SR, Sieling, PA, Cheng, G, Modlin, RL. , TLR activation of Langerhans cell-like dendritic cells triggers an antiviral immune response , J Immunol., 2006, 177, 298-305.
Saha, SK and Cheng, G. , TRAF3: A New Regulator of Type I Interferons, Cell Cycle, 2006, 5, 804-807.
Pietras, EM., Saha, SK. and Cheng, G. , The Interferon Response to bacterial and viral infections. , Journal of Endotoxin Research, 2006, 12, 246-50.
O'Connell, RM, Saha, SK and Cheng, G. , Combating bacterial pathogens through host defense gene programs. , Current Immunology Reviews, 2005, 1, 43-54.
Miller, L. S. O'Connell, R. M. Gutierrez, M. A. Kim, J. Thirumala, A. Cheung, A. L. Cheng, G. Modlin, R. L. , Critical role of lL-1R in controlling Staphylococcus aureus skin infections: comparison to TNF-alpha RI, Journal of Investigative Dermatology, 2005, 124 (4), A115-A115.
O'Connell RM, Vaidya VA, Perry AK, Saha SK, Dempsey PW, and Cheng G , Immune activation of type I IFNs by Listeria monocytogenes occurs independent of TLR4, TLR2 and receptor interacting protein 2 but involves tank-binding kinase 1., J. Immunol., 2005, 174, 1602-1607.
Damalas, A. Weis, L. Nordgard, S. H. Kristensen, V. N. Gardner, K. Cheng, G. Gelinas, C. Levrero, M. Strano, S. Borresen-Dale, A. L. Rotter, V. Oren, M. Blandino, G. , Mutant p53 exerts its gain of function through activation of the NF-kappa B pathway, Breast Cancer Research, 2005, 7, S53-S53.
Liu B, Yang R, Wong KA, Getman C, Stein N, Teitell MA, Cheng G, Wu H, Shuai K, Negative regulation of NF-kappaB signaling by PIAS1., Molecular and cellular biology. , 2005, 25 (3), 1113-23.
Chow, EK., O'Connell, RM, Schilling, S., , Wang, XF., Fu, XY., and Cheng , G. , TLR Agonists Regulate PDGF-B Production and Cell Proliferation through TGF-beta/Type I IFN Crosstalk , EMBO J. , 2005, 24, 4071-4081.
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Perry, AK., Chen, G., Zheng, DH., Tang, H., Cheng, G. , The host type I interferon response to viral and bacterial infections., Cell Res. , 2005, 15, 407-422.
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Chin,AI., Dempsey, PW. And Cheng, G, Rip2: a key molecule that regulates both innate and acquired immunity, Current Medicinal Chemistry, 2005, 4, 35-42.
Jazirehi, AR., Huerta-Yepez, S., Cheng, G. and Bonavida, B, Rituximab (chimeric anti-CD20 mAb) inhibits the constitute NIK/IKK/IkB/NF-kB signaling pathway in non-Hodgkin’s lymphoma (NHL) B-cell lines: role in sensitization to chemotherapeutic drug-induced apoptosis, Cancer Research, 2005, 65, 264-276.
Shen, DX., Ke, B., Zhai, Y., Gao, F., Busuttil, RW., Cheng, G., Kupiec-Weglinski, JW, Toll-Like Receptor and Heme Oxygenase-1 Signaling in Hepatic Ischemia/Reperfusion Injury, Am J Transplant, 2005, 5 (8), 1793-1800.
Bo, Q. Zhai, Y. Gao, W. Gao, F. Busuttil, R. W. Cheng, G. Kupiec-Weglinski, J. W., Type-1 interferon-dependent hepatocyte production of IP-10, American Journal of Transplantation, 2004, 4, 248-248.
Perry, A. K. Chow, E. K. Goodnough, J. B. Yeh, W. C. Cheng, G. , Differential requirement for TANK-binding kinase-1 in type I interferon responses to toll-like receptor activation and viral infection, Journal of Experimental Medicine, 2004, 199 ( 12), 1651-1658.
Miller, L. S. O'Connell, R. M. Kim, J. Cheng, G. Modlin, R. L. , Contrasting roles of TLR2 and MyD88 in an in vivo model of skin infection with Staphylococcus aureus, Journal of Investigative Dermatology, 2004, 122 (3), A120-A120.
Zhai Y, Shen XD, O'Connell R, Gao F, Lassman C, Busuttil RW, Cheng G, Kupiec-Weglinski JW, Cutting edge: TLR4 activation mediates liver ischemia/reperfusion inflammatory response via IFN regulatory factor 3-dependent MyD88-independent pathway., Journal of immunology (Baltimore, Md. : 1950) , 2004, 173 (12), 7115-9.
Modlin RL, Cheng G, From plankton to pathogen recognition., Nature medicine. , 2004, 10 (11), 1173-4.
Ni CZ, Oganesyan G, Welsh K, Zhu X, Reed JC, Satterthwait AC, Cheng G, Ely KR, Key molecular contacts promote recognition of the BAFF receptor by TNF receptor-associated factor 3: implications for intracellular signaling regulation., Journal of immunology (Baltimore, Md. : 1950) , 2004, 173 (12), 7394-400.
Joseph SB, Bradley MN, Castrillo A, Bruhn KW, Mak PA, Pei L, Hogenesch J, O'connell RM, Cheng G, Saez E, Miller JF, Tontonoz P, LXR-dependent gene expression is important for macrophage survival and the innate immune response, Cell, 2004, 119 (2), 299-309.
Huerta-Yepez S, Vega M, Jazirehi A, Garban H, Hongo F, Cheng G, Bonavida B, Nitric oxide sensitizes prostate carcinoma cell lines to TRAIL-mediated apoptosis via inactivation of NF-kappa B and inhibition of Bcl-xl expression., Oncogene. , 2004, 23 (29), 4993-5003.
Doyle SE, O'Connell RM, Miranda GA, Vaidya SA, Chow EK, Liu PT, Suzuki S, Suzuki N, Modlin RL, Yeh WC, Lane TF, Cheng G, Toll-like receptors induce a phagocytic gene program through p38., The Journal of experimental medicine. , 2004, 199 (1), 81-90.
O'Connell RM, Saha SK, Vaidya SA, Bruhn KW, Miranda GA, Zarnegar B, Perry AK, Nguyen BO, Lane TF, Taniguchi T, Miller JF, Cheng G, Type I interferon production enhances susceptibility to Listeria monocytogenes infection., The Journal of experimental medicine. , 2004, 200 (4), 437-45.
Zarnegar B, He JQ, Oganesyan G, Hoffmann A, Baltimore D, Cheng G, Unique CD40-mediated biological program in B cell activation requires both type 1 and type 2 NF-kappaB activation pathways, Proc Natl Acad Sci U S A, 2004, 101 (21), 8108-13.
Ronni T, Agarwal V, Haykinson M, Haberland ME, Cheng G, Smale ST, Common interaction surfaces of the toll-like receptor 4 cytoplasmic domain stimulate multiple nuclear targets., Molecular and cellular biology. , 2003, 23 (7), 2543-55.
Castrillo A, Joseph SB, Vaidya SA, Haberland M, Fogelman AM, Cheng G, Tontonoz P, Crosstalk between LXR and toll-like receptor signaling mediates bacterial and viral antagonism of cholesterol metabolism, Molecular cell. , 2003, 12 (4), 805-16.
Brown HJ, Song MJ, Deng H, Wu TT, Cheng G, Sun R, NF-kappaB inhibits gammaherpesvirus lytic replication., Journal of virology. , 2003, 77 (15), 8532-40.
Dadgostar H, Doyle SE, Shahangian A, Garcia DE, and Cheng G , T3JAM, a novel protein that specifically interacts with TRAF3 and promotes the activation of JNK, FEBS Letters, 2003, 553 (3), 403-40.
Chen, MC, Hwang, MJ, Chou, YC, Chen, WH, Cheng, G, Nakano, H, Luh, TY, Mai, SC, Hsieh, SL, The role of ASK1 in Lymphotoxin-beta receptor-mediated cell death, J Biol Chem, 2003, 278, 16073-81.
Dempsey PW, Doyle SE, He JQ, Cheng G, The signaling adaptors and pathways activated by TNF superfamily., Cytokine & growth factor reviews. , 2003, 14 (3-4), 193-209.
Doyle SE, O'Connell R, Vaidya SA, Chow EK, Yee K, Cheng G, Toll-like receptor 3 mediates a more potent antiviral response than Toll-like receptor 4., Journal of immunology (Baltimore, Md. : 1950) , 2003, 170 (7), 3565-71.
Vaidya SA, Cheng G, Toll-like receptors and innate antiviral responses, Curr Opin Immunol, 2003, 15 (4), 402-7.
Dadgostar H, Zarnegar B, Hoffmann A, Qin XF, Truong U, Rao G, Baltimore D, Cheng G, Cooperation of Multiple Signaling Pathways in CD40-Regulated Gene Expression in B Lymphocytes., Proceedings of the National Academy of Sciences of the USA, 2002, 99 (3), 1497-1502.
Li C, Ni CZ, Havert ML, Cabezas E, He J, Kaiser D, Reed JC, Satterthwait AC, Cheng G, Ely KR, Downstream regulator TANK binds to the CD40 recognition site on TRAF3., Structure (Cambridge, Mass. : 2001) , 2002, 10 (3), 403-11.
Doyle, S. E. Vaidya, S. A. O'Connell, R. Dadgostar, H. Dempsey, P. W. Wu, T. T. Rao, G. Sun, R. Haberland, M. E. Modlin, R. L. Cheng, G. , IRF3 mediates a TLR3/TLR4-specific antiviral gene program, Immunity, 2002, 17 (3), 251-263.
Chin AI, Dempsey PW, Bruhn K, Miller JF, Xu Y, Cheng G, Involvement of receptor-interacting protein 2 in innate and adaptive immune responses., Nature, 2002, 416 (6877), 190-4.
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Wang Y, Kelly CG, Karttunen JT, Whittall T, Lehner PJ, Duncan L, MacAry P, Younson JS, Singh M, Oehlmann W, Cheng G, Bergmeier L, Lehner T, CD40 is a cellular receptor mediating mycobacterial heat shock protein 70 stimulation of CC-chemokines, Immunity, 2001, 15 (6), 971-83.
Kwan G, Burnside J, Kurosahi T, Cheng G, MEKK1 is required for JNK activation and apoptosis in response to microtubule disruption., Molecular and Cellular Biology, 2001, 21 (21), 7183-7190.
Fischbein MP, Ardehali A, Yun J, Schoenberger S, Laks H, Irie Y, Dempsey P, Cheng G, Fishbein MC, Bonavida B, CD40 signaling replaces CD4+ lymphocytes and its blocking prevents chronic rejection of heart transplants., Journal of Immunology, 2000, 165 (12), 7316-22.
Cheng Q, Lee HH, Ying Li, Parks T, Cheng G, Upregulation of Bcl-x and Bfl-1 as a potential mechanism of chemoresistance, which can be overcome by NF-kB inhibition., Oncogene, 2000, 19 (42), 4936-4940.
Lee HH, Dempsey PW, Parks TP, Zhu X, Baltimore D, Cheng G, Specificities of CD40 signaling: involvement of TRAF2 in CD40-induced NF-kappaB activation and intercellular adhesion molecule-1 up-regulation., Proceedings of the National Academy of Sciences of the United States of America. , 1999, 96 (4), 1421-6.
Chin A, Shu J, Shi CS, Yao ZB, Kehrl JH, Cheng G, TANK Potentiates Tumor Necrosis Factor Receptor-Associated Factor-Mediated c-Jun N-Terminal Kinase/Stress-Activated Protein Kinase Activation through the Germinal Center Kinase Pathway, Molecular and Cellular Biology, 1999, 19 (10), 6665-6672.
Dadgostar H, Cheng G, An Intact Zinc Ring Finger Is Required for Tumor Necrosis Factor Receptor-associated Factor-mediated Nuclear Factor-keppaB Activation but Is Dispensable for c-Jun N-terminal Kinase Signaling., The Journal of Biological Chemistry, 1998, 273 (38), 24775-24780.
Brodeur SR, Cheng G, Baltimore D, Thorley-Lawson DA, Localization of the major NF-kB activation site and the sole TRAF3 binding site of LMP-1 defines two distinct signalling motifs., The Journal of Biological Chemistry, 1997, 272 (32), 19777-19784.
Cheng G, Baltimore D, TANK, a co-inducer with TRAF2 of TNF- and CD40L-mediated NF-kB activation., Genes & Development, 1996, 10, 963-973.
Xu Y, Cheng G, Baltimore D, Targeted disruption of TRAF3 leads to postnatal lethality and defective T-dependent immune responses., Immunity, 1996, 5 (5), 407-15.
Cheng G, Cleary AM, Ye ZS, Hong DI, Lederman S, Baltimore D, Involvement of CRAF1, a relative of TRAF, in CD40 signaling., Science, 1995, 267 (5203), 1494-8.
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