Zdzisław M. Szulc
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View article: Presence and relevance of serum anti-C1P IgG antibodies in relapsing-remitting multiple sclerosis
Presence and relevance of serum anti-C1P IgG antibodies in relapsing-remitting multiple sclerosis Open
There is a growing interest in the role of sphingolipids in the background of multiple sclerosis (MS). The goal of this study was to evaluate the serum levels of antibodies against ceramide-1-phosphate (C1P) subclasses and their relationsh…
View article: Figure S7 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Figure S7 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
Effects of exogenous fumarate on HNSCC tumor metabolism in response to LCL768.
View article: Data from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Data from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
Bioactive ceramide induces cell death in part by promoting mitophagy. C18-ceramide levels are commonly reduced in head and neck squamous cell carcinoma, which correlates with poor prognosis, suggesting the potential of harnessing ceramide …
View article: Figure S5 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Figure S5 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
LCL768 reduces TCA cycle metabolism in HNSCC cells.
View article: Table S1 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Table S1 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
Key Resources Table
View article: Figure S2 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Figure S2 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
Lipidomics analysis.
View article: Figure S1 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Figure S1 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
LCL768 inhibits mitochondrial bioenergetics via inducing mitophagy.
View article: Figure S6 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Figure S6 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
Effects of LCL768 on the growth of UM-SCC-1A-derived xenograft HNSCC tumors in vivo.
View article: Figure S4 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Figure S4 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
Drp1 mutations alter its ER or mitochondrial membrane interactions and change cancer metabolism by LCL768.
View article: Figure S3 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression
Figure S3 from Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression Open
LCL768-mediated mitophagy is independent of p17, cell line, and induces Drp1’s nitrosylation.
View article: Opportunistic pathogen Porphyromonas gingivalis targets the LC3B-ceramide complex and mediates lethal mitophagy resistance in oral tumors
Opportunistic pathogen Porphyromonas gingivalis targets the LC3B-ceramide complex and mediates lethal mitophagy resistance in oral tumors Open
View article: Acid Ceramidase Inhibitor LCL-805 Antagonizes Akt Signaling and Promotes Iron-Dependent Cell Death in Acute Myeloid Leukemia
Acid Ceramidase Inhibitor LCL-805 Antagonizes Akt Signaling and Promotes Iron-Dependent Cell Death in Acute Myeloid Leukemia Open
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy requiring urgent treatment advancements. Ceramide is a cell-death-promoting signaling lipid that plays a central role in therapy-induced cell death. We previously determi…
View article: Acid Ceramidase Inhibitor LCL-805 Antagonizes Akt Signaling and Promotes Iron-Dependent Cell Death in Acute Myeloid Leukemia
Acid Ceramidase Inhibitor LCL-805 Antagonizes Akt Signaling and Promotes Iron-Dependent Cell Death in Acute Myeloid Leukemia Open
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy requiring urgent treatment advancements. Ceramide is a cell death-promoting signaling lipid that plays a central role in therapy-induced cell death. Acid ceramidase (AC),…
View article: Alterations of lipid‐mediated mitophagy result in aging‐dependent sensorimotor defects
Alterations of lipid‐mediated mitophagy result in aging‐dependent sensorimotor defects Open
The metabolic consequences of mitophagy alterations due to age‐related stress in healthy aging brains versus neurodegeneration remain unknown. Here, we demonstrate that ceramide synthase 1 (CerS1) is transported to the outer mitochondrial …
View article: Figure S6 and S7 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S6 and S7 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Figure S6. Expression and purification of NMT1. Figure S7. Kinetic analysis of purified NMT1.
View article: Figure S5 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S5 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Loss of myristoylation in Src kinase inhibits its interaction with androgen receptor (AR) and activation of AR down-stream signaling.
View article: Table S1 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Table S1 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Primer sequences used for cloning Src/Fyn mutants, shRNAs, and RT-PCR
View article: Figure S8 to S10 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S8 to S10 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Figure S8. Identifying compounds inhibiting Src myristoylation by Click chemistry. Figure S9. Structures and/or IC50 values of LCL and GRU compounds. Figure S10. Loss of myristoylation inhibits the localization of Src kinase at the cytopla…
View article: Figure S1 to S4 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S1 to S4 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Figure S1. Knockdown of NMT1 by shRNA-NMT1 inhibits Src myristoylation and proliferation of prostate cancer cells. Figure S2. Knockdown of Src and Fyn kinase inhibits the growth of prostate cancer cells. Figure S3. The contribution of myri…
View article: Figure S1 to S4 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S1 to S4 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Figure S1. Knockdown of NMT1 by shRNA-NMT1 inhibits Src myristoylation and proliferation of prostate cancer cells. Figure S2. Knockdown of Src and Fyn kinase inhibits the growth of prostate cancer cells. Figure S3. The contribution of myri…
View article: Table S1 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Table S1 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Primer sequences used for cloning Src/Fyn mutants, shRNAs, and RT-PCR
View article: Supplemental Methods and Figure Legends from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Supplemental Methods and Figure Legends from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Supplemental Methods and Figure legends
View article: Figure S5 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S5 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Loss of myristoylation in Src kinase inhibits its interaction with androgen receptor (AR) and activation of AR down-stream signaling.
View article: Figure S11 to S13 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S11 to S13 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Figure S11. The myristoyl-CoA analog, B13 has limited effect in PNT2 normal prostate cells and 293T cells. Figure S12. The additive effect of B13 with knockdown of Src kinase in regulating proliferation of 22Rv1 and PC-3 cells. Figure S13.…
View article: Figure S11 to S13 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S11 to S13 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Figure S11. The myristoyl-CoA analog, B13 has limited effect in PNT2 normal prostate cells and 293T cells. Figure S12. The additive effect of B13 with knockdown of Src kinase in regulating proliferation of 22Rv1 and PC-3 cells. Figure S13.…
View article: Data from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Data from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Protein N-myristoylation enables localization to membranes and helps maintain protein conformation and function. N-myristoyltransferases (NMT) catalyze co- or posttranslational myristoylation of Src family kinases and other o…
View article: Table S2 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Table S2 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Data collection and refinement statistics (molecular replacement)
View article: Figure S6 and S7 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S6 and S7 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Figure S6. Expression and purification of NMT1. Figure S7. Kinetic analysis of purified NMT1.
View article: Figure S8 to S10 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Figure S8 to S10 from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Figure S8. Identifying compounds inhibiting Src myristoylation by Click chemistry. Figure S9. Structures and/or IC50 values of LCL and GRU compounds. Figure S10. Loss of myristoylation inhibits the localization of Src kinase at the cytopla…
View article: Supplemental Methods and Figure Legends from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression
Supplemental Methods and Figure Legends from Blocking Myristoylation of Src Inhibits Its Kinase Activity and Suppresses Prostate Cancer Progression Open
Supplemental Methods and Figure legends