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Self‐Assembly of Helical Nanofibrous Chiral Covalent Organic Frameworks
Despite significant progress on the design and synthesis of covalent organic frameworks (COFs), precise control over microstructures of such materials remains challenging. Herein, two chiral COFs with well-defined one-handed double-helical nanofibrous morphologies were constructed via an unprecedented template-free method, capitalizing on the diastereoselective formation of aminal linkages. Detailed time-dependent experiments reveal the spontaneous transformation of initial rod-like aggregates into the double-helical microstructures. We have further demonstrated that the helical chirality and circular dichroism signal can be facilely inversed by simply adjusting the amount of acetic acid during synthesis. Moreover, by transferring chirality to achiral fluorescent molecular adsorbents, the helical COF nanostructures can effectively induce circularly polarized luminescence with the highest luminescent asymmetric factor (glum ) up to ≈0.01
Supplementary Table S2 from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Table S2. Detailed information of human pancreatic tissue array.</p
Supplementary Table S1 from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Table S1. MAGeCK analysis of CRISPR screen results to identify regulator of immune evasion in orthotopic PDAC mouse models.</p
SUPPLEMENTARY DATA FIGURES from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Figure S1. In vivo CRISPR screens to identify critical drivers of immune evasion; Supplementary Figure S2. Effects of Ripk2 depletion on tumor growth; Supplementary Figure S3. RIPK2 is overexpressed in human and mouse PDAC tissues; Supplementary Figure S4. Ablation of RIPK2 disrupts the desmoplastic TME; Supplementary Figure S5. RIPK2 modulates the immune profile and impairs anti-tumor T cell response; Supplementary Figure S6. RIPK2 restricts the activation and effector states of CD8+ T cells by impairing antigen presentation; Supplementary Figure S7. RIPK2 promotes MHC-I trafficking to lysosomes via NBR1; Supplementary Figure S8. RIPK2 ubiquitination promotes NBR1-mediated MHC-I degradation; Supplementary Figure S9. RIPK2 ablation potentiates the efficacy of PD-1 blockade; Supplementary Figure S10. Diagram illustrating RIPK2-mediated degradation of MHC I through autophagy–lysosome system.</p
Supplementary Table S4 from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Table S4. Primers used for qPCR or generating knockout/knockdown constructs.</p
Supplementary Table S4 from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Table S4. Primers used for qPCR or generating knockout/knockdown constructs.</p
Supplementary Table S3 from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Table S3. Detailed information of reagents and resources used in this study.</p
Supplementary Table S3 from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Table S3. Detailed information of reagents and resources used in this study.</p
Supplementary Table S2 from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Table S2. Detailed information of human pancreatic tissue array.</p
SUPPLEMENTARY DATA FIGURES from Receptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
Supplementary Figure S1. In vivo CRISPR screens to identify critical drivers of immune evasion; Supplementary Figure S2. Effects of Ripk2 depletion on tumor growth; Supplementary Figure S3. RIPK2 is overexpressed in human and mouse PDAC tissues; Supplementary Figure S4. Ablation of RIPK2 disrupts the desmoplastic TME; Supplementary Figure S5. RIPK2 modulates the immune profile and impairs anti-tumor T cell response; Supplementary Figure S6. RIPK2 restricts the activation and effector states of CD8+ T cells by impairing antigen presentation; Supplementary Figure S7. RIPK2 promotes MHC-I trafficking to lysosomes via NBR1; Supplementary Figure S8. RIPK2 ubiquitination promotes NBR1-mediated MHC-I degradation; Supplementary Figure S9. RIPK2 ablation potentiates the efficacy of PD-1 blockade; Supplementary Figure S10. Diagram illustrating RIPK2-mediated degradation of MHC I through autophagy–lysosome system.</p