Ratna K. Vadlamudi
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View article: EXTH-104. Dual Targeting of KDM1A/LSD1 and Endoplasmic Reticulum Stress Pathways as a Therapeutic Strategy in Glioblastoma
EXTH-104. Dual Targeting of KDM1A/LSD1 and Endoplasmic Reticulum Stress Pathways as a Therapeutic Strategy in Glioblastoma Open
BACKGROUND Glioblastoma is the lethal primary brain tumor, with glioblastoma stem cells (GSCs) playing a critical role in tumor heterogeneity, drug resistance, and recurrence. Understanding the mechanisms underlying glioblastoma stemness a…
View article: Ligand-receptor interactions induce and mediate regulatory functions of BATF3 <sup>+</sup> B cells
Ligand-receptor interactions induce and mediate regulatory functions of BATF3 <sup>+</sup> B cells Open
B cells express many protein ligands, yet their regulatory functions are incompletely understood. We profiled ligand expression across murine B sublineage cells, including those activated by defined receptor signals, and assessed their reg…
View article: Figure S2 from Targeting DDR2 for Treating Pancreatic Cancer
Figure S2 from Targeting DDR2 for Treating Pancreatic Cancer Open
Supplementary Figure 2
View article: Figure S1 from Targeting DDR2 for Treating Pancreatic Cancer
Figure S1 from Targeting DDR2 for Treating Pancreatic Cancer Open
Supplementary Figure 1
View article: Supplementary Tables 1-4 from Targeting DDR2 for Treating Pancreatic Cancer
Supplementary Tables 1-4 from Targeting DDR2 for Treating Pancreatic Cancer Open
Supplementary Tables 1-4
View article: Data from Targeting DDR2 for Treating Pancreatic Cancer
Data from Targeting DDR2 for Treating Pancreatic Cancer Open
Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer with limited effective treatments, partly because of its complex tumor microenvironment. In this study, we report discoidin domain receptor 2 (DDR2), a receptor tyrosine kinase, as…
View article: Figure S3 from Targeting DDR2 for Treating Pancreatic Cancer
Figure S3 from Targeting DDR2 for Treating Pancreatic Cancer Open
Supplementary Figure 3
View article: Figure S4 from Targeting DDR2 for Treating Pancreatic Cancer
Figure S4 from Targeting DDR2 for Treating Pancreatic Cancer Open
Supplementary Figure 4
View article: EC359 Enhances Trametinib Efficacy in Ras/Raf-Driven Ovarian Cancer by Suppressing LIFR Signaling
EC359 Enhances Trametinib Efficacy in Ras/Raf-Driven Ovarian Cancer by Suppressing LIFR Signaling Open
Ovarian cancer (OCa) remains the most lethal gynecologic malignancy in the United States, with low-grade serous and mucinous subtypes frequently driven by KRAS mutations. These mutations activate downstream MAPK and PI3K/AKT signaling path…
View article: Cryo-EM structures reveal the molecular mechanism of SUMO E1–E2 thioester transfer
Cryo-EM structures reveal the molecular mechanism of SUMO E1–E2 thioester transfer Open
Post-translational modification of proteins by SUMO (small ubiquitin-like modifier) regulates fundamental cellular processes and occurs through the sequential interactions and activities of three enzymes: E1, E2 and E3. SUMO E1 activates S…
View article: Supplementary Figure S4 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary Figure S4 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Supplementary Figure S4: A-B, MDA-MB-231 (A), and BT-549 (B), cells were treated with HBS-101, stained with Annexin V, and analyzed by flow cytometry. Scatter plots illustrate Annexin V staining in control and HBS-101-treated cells.
View article: Supplementary Table S1 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary Table S1 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Supplementary Table S1. List of Antibodies used
View article: Supplementary Table S2 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary Table S2 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Supplementary Table S2. List of siRNA sequences
View article: Supplementary table S4 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary table S4 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Supplementary Table S4. List of Primer sequences
View article: Supplementary Data from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary Data from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
HBS-101 NMR spectra H-1 1
View article: Supplementary Data from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary Data from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
HBS-101 NMR spectra C-13 1
View article: Supplementary Figure S1 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary Figure S1 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Supplementary Figure S1: A. Boxplots of MDK gene expression in normal (n = 403) and BC tumor (n = 1097) gene array data (https://tnmplot.com/analysis/). B, Expression of MDK in breast invasive carcinoma based on BC subclasses. C, Expressio…
View article: Supplementary Figure S2 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary Figure S2 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Supplementary Figure S2: A, Schematic representation of the structure of HBS-101, B, Structural representation of MDK highlighting its N-terminal (cyan) and C-terminal (green) regions. The missing residues between these domains are marked,…
View article: Supplementary table S3 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary table S3 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Supplementary Table S3. The spectral NMR (proton and carbon) data for HBS-101 NMR spectra. NMR spectra were recorded on a Bruker Avance II and AV (500 MHz and 300MHz) spectrometers as deuterochloroform (CDCl3) solutions.
View article: Supplementary Figure S3 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
Supplementary Figure S3 from The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Supplementary Figure S3: A, Activity of biotin-HBS-101 on cell viability was analyzed by MTT assay (n = 3). B, The sensitivity of both scrambled and MDK-siRNA BT-549 cells to HBS-101 treatment was evaluated by measuring cell viability with…
View article: Novel LIFR-targeted combination therapy to enhance the utility of standard-of-care chemotherapy in treating ovarian cancer
Novel LIFR-targeted combination therapy to enhance the utility of standard-of-care chemotherapy in treating ovarian cancer Open
View article: Significance of Midkine Signaling in Women’s Cancers: Novel Biomarker and Therapeutic Target
Significance of Midkine Signaling in Women’s Cancers: Novel Biomarker and Therapeutic Target Open
Midkine (MDK) is a multifunctional protein that is secreted into the extracellular space. It functions as a cytokine or growth factor, modulating a variety of signaling pathways implicated in angiogenesis, antitumor immunity, metastasis, a…
View article: The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer
The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Open
Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with a poor clinical outcome. There is a dire need for the development of new targeted therapies for TNBC. Midkine (MDK), a multifunctional cytokine/growth fact…
View article: Epigenetic silencing of DNA sensing pathway by FOXM1 blocks stress ligand-dependent antitumor immunity and immune memory
Epigenetic silencing of DNA sensing pathway by FOXM1 blocks stress ligand-dependent antitumor immunity and immune memory Open
View article: Abstract 1631: Targeting ER stress for treating hepatocellular carcinoma (HCC)
Abstract 1631: Targeting ER stress for treating hepatocellular carcinoma (HCC) Open
Background: Hepatocellular carcinoma (HCC) accounts for more than 90% of instances of liver cancer, which ranks as the fifth most frequent cancer in the United States. Furthermore, Texas leads the nation in the age-adjusted incidence of HC…
View article: Supplementary Figure 2 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Supplementary Figure 2 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
Figure S2. SMIP34 treatment downregulates liver specific genes, MYC and E2F pathway targeted genes in HCC cells.
View article: Supplementary Table 1 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Supplementary Table 1 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
Supplementary Table 1. List of all the primers used for RT-qPCR.
View article: Supplementary Figure 1 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Supplementary Figure 1 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
Figure S1. Levels of PELP1 expression in 6 HCC cell lines.
View article: Targeting the Leukemia Inhibitory Factor/Leukemia Inhibitory Factor Receptor Axis Reduces the Growth of Inflammatory Breast Cancer by Promoting Ferroptosis
Targeting the Leukemia Inhibitory Factor/Leukemia Inhibitory Factor Receptor Axis Reduces the Growth of Inflammatory Breast Cancer by Promoting Ferroptosis Open
Background: Inflammatory breast cancer (IBC) is a rare subtype of breast cancer accounting for 7% of breast cancer-related fatalities. There is an urgent need to develop new targeted treatments for IBC. The progression of IBC has been asso…
View article: Tumour-intrinsic PDL1 signals regulate the Chk2 DNA damage response in cancer cells and mediate resistance to Chk1 inhibitors
Tumour-intrinsic PDL1 signals regulate the Chk2 DNA damage response in cancer cells and mediate resistance to Chk1 inhibitors Open
Our data challenge the prevailing surface PDL1 paradigm, elucidate important and previously unappreciated roles for tumour-intrinsic PDL1 in regulating the ATM/Chk2 DNA damage response axis and E3 ligase-mediated protein degradation, sugge…