Gangadhara R. Sareddy
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View article: Combined Inhibition of Lysine-Specific Demethylase 1 and Kinase Signaling as a Preclinical Treatment Strategy in Glioblastoma
Combined Inhibition of Lysine-Specific Demethylase 1 and Kinase Signaling as a Preclinical Treatment Strategy in Glioblastoma Open
Introduction Lysine-specific demethylase 1 (LSD1) is overexpressed in glioblastoma, contributing to tumor growth and treatment resistance. LSD1 inhibitors have shown preclinical promise but have had limited clinical development for gliobla…
View article: DDDR-25. Targeting glioma stem cells with a fungal metabolite ophiobolin A: synthesis and evaluation of C21-ketones
DDDR-25. Targeting glioma stem cells with a fungal metabolite ophiobolin A: synthesis and evaluation of C21-ketones Open
Glioblastoma (GBM) tumors consist of ecosystems with diverse neoplastic populations, including glioma stem cells (GSCs). The latter are believed to give rise to intratumoral heterogeneity, plasticity and resistance to treatment, contributi…
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: 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: 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: 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: Figure 5 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Figure 5 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
PELP1-KD or SMIP34 treatment suppresses HCC xenograft tumor growth in vivo. Hep3B–control and Hep3B–PELP1-KD model cells were injected subcutaneously into female (A, D, and G) or male SCID mice (
View article: Figure 1 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Figure 1 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
PELP1 expression is upregulated in HCC, and high PELP1 expression is associated with poor survival of patients with HCC. Data obtained from TNMplot shows increased expression of PELP1 in patients with HCC (A). The results from TCGA-…
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: Figure 2 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Figure 2 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
PELP1-KD/SMIP34 treatment decreased cell viability, clonogenicity, and invasiveness of HCC cells. PELP1-KD in Huh7 and Hep3B cell lines were confirmed by Western blot (A). Cell viability and clonogenic assays were performed t…
View article: Figure 3 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Figure 3 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
Analysis of global transcriptional changes in PELP1-KD HCC cells. Volcano plot of differentially expressed genes with PELP1-KD in Hep3B cells is displayed (n = 3; A). PELP1-downregulated pathways were identified using …
View article: Data from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Data from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths in the United States, with a median survival period of approximately 10 months. There is an urgent need for the development of effective targeted therapie…
View article: Figure 4 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma
Figure 4 from PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Open
SMIP34 treatment blocked PELP1-mediated extranuclear signaling and decreased global protein synthesis. Huh7, SNU398, Hep3B, and SNU423 cells were treated with vehicle (DMSO 0.01%) or SMIP34 (12.5 μmol/L) to examine PELP1 degradation and th…
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 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: Data from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma
Data from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma Open
Glioblastoma (GBM) is the most prevalent and aggressive type of adult brain tumors with low 5-year overall survival rates. Epidemiologic data suggest that estrogen may decrease brain tumor growth, and estrogen receptor beta (ERβ) has been …
View article: Supplementary Fig. S1 from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma
Supplementary Fig. S1 from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma Open
Supplementary Fig.S1 shows scheme for synthesis of ER beta agonist CIDD-0149897
View article: Supplementary Fig. S2 from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma
Supplementary Fig. S2 from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma Open
Supplementary Fig.S2 shows data shows specificity of CIDD-0149897 using ER beta KO cells.
View article: Supplementary Fig. S3 from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma
Supplementary Fig. S3 from Preclinical development of brain permeable ERβ agonist for the treatment of glioblastoma Open
Supplementary Fig.S3 shows efficacy of CIDD-0149897 combination therapy.