US 6004811A
· Seed et al.
· 1999
[cited by applicant]
US 7052906B1
· Lawson et al.
· 2006
[cited by applicant]
US 20220145325A1
· Pulé
· 2022
[cited by examiner]
US 20230256093A1
· Peruta
· 2023
[cited by examiner]
US 20240309400A1
· Pulé
· 2024
[cited by examiner]
WO WO9640199A1
· 1996
[cited by applicant]
WO WO9731113A1
· 1997
[cited by applicant]
WO WO2015075468A1
· 2015
[cited by applicant]
WO WO2015075469A1
· 2015
[cited by applicant]
WO WO2015075470A1
· 2015
[cited by applicant]
WO WO2018096361A1
· 2018
[cited by applicant]
WO WO2020183131A1
· 2020
[cited by applicant]
Kappell et al., Current Opinions in Biotechnology, vol. 3, p. 548-553, 1992 (Year: 1992).
[cited by examiner]
Houdebine et al., Journal of Biotechnology, vol. 34, p. 269-287, 1994 (Year: 1994).
[cited by examiner]
Wall et al., Theriogenology, vol. 45, p. 57-68, 1996 (Year: 1996).
[cited by examiner]
Barford et al. Revealing mechanisms for SH2 domain mediated regulation of the protein tyrosine phosphatase SHP-2. Structure (1998) 6(3):249-54 (Year: 1998).
[cited by examiner]
Houdebine Comparative Immunology, Microbiology, and Infectious Diseases, vol. 32, p. 107-121, 2009 (Year: 2009).
[cited by examiner]
Wu et al. Expression and purification of 15N-labeled 2-SH2 protein domain of SHP-2 from Homo sapiens in
[cited by examiner]
Jena et al. Redirecting T-cell specificity by introducing a tumor-specific chimeric antigen receptor. Blood (2010) 116(7):1035-1044 (Year: 2010).
[cited by examiner]
Anselmi et al., “Structural Determinants of Phosphopeptide Binding to the N-Terminal Src Homology 2 Domain of the SHP2 Phosphatase,” J. Chem. Inf. Model, 60:3157-3171 (2020).
[cited by applicant]
Baba et al., “Dual regulation of BCR-mediated growth inhibition signaling by CD72,” Eur. J. Immunol. 35:1634-1642 (2005).
[cited by applicant]
Baldan et al., “A Dominant Negative 8HP-2 Which Abrogates PD-1 Sgnalling Pathways and Restores Function of Cytotoxic CART Cells,” Blood 130:3190 (2017).
[cited by applicant]
Bunda et al., Inhibitiion of SHP2-mediated dephosphorylation of Ras suppresses oncogenesis,
[cited by applicant]
Chen et al., “CAR T-cell intrinsic PD-1 checkpoint blockade: A two-in-one approach for solid tumor immunotherapy,” OncoImmunology 4 pages (2017).
[cited by applicant]
Collection of research reports of the Uehara Memorial Foundation, vol. 28, pp. 1-4, Dec. 5, 2014.
[cited by applicant]
David et al., “The SH2 Domain-containing Tyrosine Phosphatase PTP1D Is Required for Interferon α/β-induced Gene Expression,” The Journal of Biological Chemistry 271(27):15862-15865 (1996).
[cited by applicant]
Dong et al., “Tumor-associated B7-H1 promotes T-cell apoptosis: A potential mechanism of immune evasion,” Nature Medicine 8(8):793-800 (2002).
[cited by applicant]
Hirano et al., “Blockade of B7-H1 and PD-1 by Monoclonal Antibodies Potentiates Cancer Therapeutic Immunity,” Cancer Res 65(3):1089-1096 (2005).
[cited by applicant]
International Search Report and Written Opinion from corresponding International Application No. PCT/GB2016/051576 dated Sep. 21, 2016.
[cited by applicant]
Isakov et al., ZAP-70 binding specificity to T cell receptor tyrosine-based activation motifs the tandem SH2 domains of ZAP-70 bind distinct tyrosine-based activation motifs with varying affinity,
[cited by applicant]
John et al., “Blockade of PD-1 immunosuppression boosts CART-cell therapy,” OncoImmunology 2(10):e26286-1, 4 pages (2013).
[cited by applicant]
Kim et al., Synergistic inhibition of T-cell activation by a cell-permeable ZAP-70 mutant and ctCTLA-4,
[cited by applicant]
Liu et al., “A Chimeric Switch-Receptor Targeting PD1 Augments the Efficacy of Second-Generation CAR T Cells in Advanced Solid Tumors,” Cancer Res., 76(6):1578-1590 (2016).
[cited by applicant]
Liu et al., “A Comprehensive Immunoreceptor Phosphotyrosine-based Signaling Network Revealed by Reciprocal Protein-Peptide Array Screening,” Molecular & Cell Proteomics 14.7:1846-1858 (2015).
[cited by applicant]
Lorenz, “SHP-1 and SHP-2 in T cells: two phosphatases functioning at many levels,” Immunol Rev. 228(1):342-359 (2009).
[cited by applicant]
Menger et al., “TALEN-Mediated Inactivation of PD-1 in Tumor-Reactive Lymphocytes Promotes Intratumoral T-cell Persistence and Rejection of Established Tumors,” Cancer Res., 76(8):2087-2093 (2016).
[cited by applicant]
Moon et al., “Multifactorial T-cell Hypofunction That is Reversible Can Limit the Efficacy of Chimeric Antigen Receptor-Transduced Human T cells in Solid Tumors,” Clin Cancer Res 20(16):4262-4273 (2014).
[cited by applicant]
Northrop et al., “Characterization of the roles of SH2 domain-containing proteins in T-lymphocyte activation by using dominant negative SH2 domains,” Mol Cell Biol., 16(5):2255-2263 (1996).
[cited by applicant]
Odorizzi et al., “Inhibitory Receptors on Lymphocytes: Insights from Infections,” J. Immunol., 188(7):2957-2965 (2012).
[cited by applicant]
Roitt et al., “Immunology”, Publishing House “Mir”, pp. 4-6 (2000).
[cited by applicant]
Stanford et al., “Regulation of TCR Signalling by tyrosine phosphatases: from immune homeostasis to autoimmunity,” Immunology 137(1):19 pages (2012).
[cited by applicant]
Stebbins et al., “Vav1 Dephosphorylation by the Tyrosine Phosphatase SHP-1 as a Mechanism for Inhibition of Cellular Cytotoxicity,” Molecular and Cellular Biology, 23(17):6291-6299 (2003).
[cited by applicant]
Tamada et al., “Redirecting Gene-Modified T Cells toward Various Cancer Types Using Tagged Antibodies,” Clin Cancer Res 18(23):6436-6445 (2012).
[cited by applicant]
Wang et al., “Specificity of the SH2 Domains of SHP-1 in the Interaction with the Immunoreceptor Tyrosine-Based Inhibitory Motif-Bearing Receptor gp49B,” The Journal of Immunology, 1318-1323 (1999).
[cited by applicant]
Wange et al., Tandem SH2 domains of ZAP-70 bind to T cell antigen receptor zeta and CD3 epsilon from activated Jurkat T cells,
[cited by applicant]
Yaffe, “Phosphotyrosine-Binding Domains in Signal Transduction,” Nature Reviews, Molecular Biology 31:177-186 (2002).
[cited by applicant]
Yamasaki et al., The kinse, SH3 and SH2 domains of Lck play critical roles in T-cell activation after ZAP-70 membrane localization,
[cited by applicant]