Tinghu Zhang
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View article: Overcoming EGFR resistance by monovalent and bident inhibitors targeting Cys775
Overcoming EGFR resistance by monovalent and bident inhibitors targeting Cys775 Open
Covalent targeting of EGFR cysteine 797 by osimertinib is one of the most successful breakthroughs in targeted therapy, fundamentally transforming the treatment landscape for non-small cell lung cancer (NSCLC) patients. However, resistance…
View article: Figure S3 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex
Figure S3 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex Open
Shows transcriptomic and protein analyses demonstrating TRIM21-dependent NFκB activation by PRLX, including mRNA-seq, GSEA, confocal imaging, and subcellular fractionation immunoblots.
View article: Figure S13 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex
Figure S13 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex Open
Presents pharmacokinetic analyses and in vivo efficacy of TRIM21-targeting compounds in organoid and xenograft models, including immunoblotting, plasma concentration profiles, and tumor growth studies.
View article: Figure S8 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex
Figure S8 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex Open
Shows immunoblotting, ubiquitylation proteomics, and TRIM21-TurboID proximity labeling analyses of nuclear pore complex proteins following PRLX or JWZ-8-103 treatment.
View article: Figure S4 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex
Figure S4 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex Open
Demonstrates JWZ-8-103-induced increases in TRIM21 thermal stability in PANC-1 lysates by CETSA, including quantification and immunoblot analysis.
View article: Figure S1 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex
Figure S1 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex Open
Depicts PRLX sensitivity across cancer cell lines, TRIM21 expression and functional perturbation, CRISPR/Cas9 screen results, and rescue experiments.
View article: Figure S11 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex
Figure S11 from Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex Open
Depicts live-cell imaging, lethal fraction analyses, and protein interaction/immunoblot assays demonstrating TRIM21-dependent PRLX-induced nucleoporin destabilization and rapid cancer cell death.
View article: Design and Development of DNA Damage Chemical Inducers of Proximity (DD-CIP) for Targeted Cancer Therapy
Design and Development of DNA Damage Chemical Inducers of Proximity (DD-CIP) for Targeted Cancer Therapy Open
Many chemotherapies are effective against cancers that display high levels of genome instability by disrupting or overwhelming the DNA damage response to induce cell death. PARP inhibitors (PARPi) exploit this vulnerability by stalling DNA…
View article: PRM-LIVE with Trapped Ion Mobility Spectrometry and Its Application in Selectivity Profiling of Kinase Inhibitors
PRM-LIVE with Trapped Ion Mobility Spectrometry and Its Application in Selectivity Profiling of Kinase Inhibitors Open
Parallel reaction monitoring (PRM) has emerged as a popular approach for targeted protein quantification. With high ion utilization efficiency and first-in-class acquisition speed, the timsTOF Pro provides a powerful platform for PRM analy…
View article: Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex
Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex Open
Cancer cells are acutely dependent on nuclear transport due to elevated transcriptional activity, suggesting an unrealized opportunity for selective therapeutic inhibition of the nuclear pore complex (NPC). Through large-scale phenotypic p…
View article: A Bivalent Molecular Glue Linking Lysine Acetyltransferases to Oncogene-induced Cell Death
A Bivalent Molecular Glue Linking Lysine Acetyltransferases to Oncogene-induced Cell Death Open
SUMMARY Developing cancer therapies that induce robust death of the malignant cell is critical to prevent relapse. Highly effective strategies, such as immunotherapy, exemplify this observation. Here we provide the structural and molecular…
View article: Targeted degradation of oncogenic KRASG12V triggers antitumor immunity in lung cancer models
Targeted degradation of oncogenic KRASG12V triggers antitumor immunity in lung cancer models Open
Kirsten rat sarcoma viral oncogene homolog (KRAS) is the most frequently mutated oncogene in lung adenocarcinoma, with G12C and G12V being the most predominant forms. Recent breakthroughs in KRASG12C inhibitors have transformed the clinica…
View article: Broad-spectrum activity against mosquito-borne flaviviruses achieved by a targeted protein degradation mechanism
Broad-spectrum activity against mosquito-borne flaviviruses achieved by a targeted protein degradation mechanism Open
View article: Supplementary Table S2 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S2 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S2 Overlapping dropouts (FDR <0.1) from MRTX-849 CRISPR/Cas9 screens in NSCLC cell lines
View article: Supplementary Table S11 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S11 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S11 Differential gene expression analysis of scRNA-seq data from tumor cluster in patient #2349 (MRTX-849/TNO155-resistant) vs patient #1566 (control, KRASG12V tumor)
View article: Supplementary Table S7 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S7 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S7 RPPA from MTRX-849-resistant tumor nodules from KCL mice
View article: Supplementary Table S9 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S9 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S9 RPPA data from MRTX-849/SHP099-resistant tumor nodules in KCL mice
View article: Supplementary Table S4 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S4 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S4 MaGeCK analysis of MRTX-849/TNO155 CRISPR/Cas9 screens of NSCLC cell lines
View article: Supplementary Figures 1-7 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Figures 1-7 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Figures 1-7 including Figure legends
View article: Supplementary Table S8 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S8 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S8 RNA-seq analysis of MTRX-849/SHP099-resistant tumor nodules from KCL mice
View article: Supplementary Table S7 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S7 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S7 RPPA from MTRX-849-resistant tumor nodules from KCL mice
View article: Supplementary Table S2 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S2 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S2 Overlapping dropouts (FDR <0.1) from MRTX-849 CRISPR/Cas9 screens in NSCLC cell lines
View article: Supplementary Table S3 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S3 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S3 RNA-seq analysis of H2030 and H2122 cells treated with MRTX-849 or vehicle for 48 hr
View article: Supplementary Table S5 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S5 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S5 MaGeCK analysis of TNO155 CRISPR/Cas9 screens of NSCLC cell lines
View article: Supplementary Table S1 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S1 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S1 MaGeCK analysis of MRTX-849 CRISPR/Cas9 SL screens of NSCLC cell lines
View article: Supplementary Table S6 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S6 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S6 RNA-seq analysis of MTRX-849-resistant tumor nodules from KCL mice
View article: Supplementary Figure Legend from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Figure Legend from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Figure Legends
View article: Supplementary Table S11 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S11 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S11 Differential gene expression analysis of scRNA-seq data from tumor cluster in patient #2349 (MRTX-849/TNO155-resistant) vs patient #1566 (control, KRASG12V tumor)
View article: Supplementary Table S10 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S10 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S10 Differential gene expression analysis of scRNA-seq data from tumor cluster in patient #1778 (AMG-510-resistant tumor) vs patient #1566 (control, KRASG12V tumor)
View article: Supplementary Table S10 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy
Supplementary Table S10 from Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRAS<sup>G12C</sup> Inhibitor Efficacy Open
Supplementary Table S10 Differential gene expression analysis of scRNA-seq data from tumor cluster in patient #1778 (AMG-510-resistant tumor) vs patient #1566 (control, KRASG12V tumor)