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View article: Table S1 from Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling
Table S1 from Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling Open
Primers and DNA oligos used in this study
View article: Figure S3 from Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling
Figure S3 from Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling Open
SLC25A39-mediated mitochondrial GSH import is essential for metastasis but dispensable for primary tumor growth
View article: Polyamines sustain epithelial regeneration in aged intestines by modulating protein homeostasis
Polyamines sustain epithelial regeneration in aged intestines by modulating protein homeostasis Open
Ageing dampens the regenerative potential of intestinal epithelium across species including humans, yet the underlying causes remain elusive. Here we characterized the temporal dynamics of regeneration following injury induced by 5-fluorou…
View article: Autophagy maintains HEV identity and function during inflammation
Autophagy maintains HEV identity and function during inflammation Open
Summary High endothelial venules (HEVs) play a crucial role in adaptive immune responses in secondary and tertiary lymphoid organs. They are uniquely equipped with high levels of peripheral node addressins (PNAd), harboring carbohydrate st…
View article: Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling
Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling Open
Cancer cells require substantial metabolic adaptations to metastasize to distant organs, but the metabolites essential for successful colonization remain poorly defined. In this study, we used a mitochondrial metabolomics approach to compa…
View article: Constitutive expression of the transcriptional co-activator IκBζ promotes melanoma growth and immunotherapy resistance
Constitutive expression of the transcriptional co-activator IκBζ promotes melanoma growth and immunotherapy resistance Open
View article: Supplementary Figure 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 2). Epithelial and myeloid cell contributions to gene expression and 13C labeling features.
View article: Supplementary Table 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 3). Overall and recurrence-free survival summary.
View article: Figure 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
13C enrichment in the TCA cycle distinguishes tumors but not benign pulmonary lesions from the adjacent lung. A, Summary of patients with pulmonary lesions. B, Schematic of labeling from [U-13C]glucose, …
View article: Supplementary Table 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
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View article: Supplementary Figure 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 1). TCA cycle labeling and metabolite abundance in tumors and lungs from NSCLC patents.
View article: Supplementary Table 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 1). Patient Isotopologue Data.
View article: Figure 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
PDXs derived from primary NSCLC retain histological, molecular, and metabolic characteristics. A and B, Summary of histological and molecular characterization of donor tumors (A) and PDX models (B). C, H&…
View article: Supplementary Figure 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 4). Development of patient-derived xenografts from malignant tumors in the lung.
View article: Supplementary Table 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 1 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 1). Clinical and pathological data from patients recruited to this study.
View article: Supplementary Table 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 2). Transcriptomic data for NSCLC and adjacent lung tissue fragments.
View article: Figure 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
PDXs generated from primary NSCLCs spontaneously metastasize in NSG mice. A, Flow cytometry analysis of lung tissue from a mouse engrafted with mx73. Cells were stained with mouse lineage markers (CD45, CD31, and TER119) and HLA.
View article: Supplementary Table 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Table 5 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
Related to Figures 4 and 6). PDX Isotopologue Data.
View article: Figure 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
Increased 13C enrichment in the TCA cycle predicts reduced survival. A,13C enrichment in the adjacent lung and tumors with high or low TCA cycle labeling. Fractional enrichments of glycolytic (M+3) and TCA cycl…
View article: Supplementary Figure 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 4 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 3). TCA cycle metabolite abundance does not correlate with overall survival.
View article: Data from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Data from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
In patients with non–small cell lung cancer (NSCLC), the relationship between tumor metabolism and clinical outcomes is unknown. Here, 13C-labeled nutrients were intraoperatively infused into more than 90 patients with surgicall…
View article: Supplementary Figure 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figures 5 and 6): Treatment with IACS-010759 reduces distant metastasis.
View article: Figure 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 2 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
Cancer cells drive an OXPHOS expression signature in tumors. A, Heatmap of TCA cycle and ETC transcript differences between primary NSCLC and adjacent lung samples. B, RNA scores comparing matched tumor and adjacent lung for …
View article: Figure 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Figure 6 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
Inhibition of complex I with IACS-010759 limits metastasis in NSCLC PDXs. A and B, Tumor-bearing mice were treated daily with DMSO or IACS-010759 (5 mg/kg) by oral gavage for 3–4 weeks and then infused with [U-13C]…
View article: Supplementary Figure 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients
Supplementary Figure 3 from High Glucose Contribution to the TCA Cycle Is a Feature of Aggressive Non–Small Cell Lung Cancer in Patients Open
(Related to Figure 3). Relationships between TCA cycle labeling and clinical factors.
View article: Supplemental figures from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Supplemental figures from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplemental data file contains Table S1, S2 and Figures S1-S7
View article: Data from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Data from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Evolutionarily conserved selenoprotein O (SELENOO) catalyzes a posttranslational protein modification known as AMPylation that is essential for the oxidative stress response in bacteria and yeast. Given that oxidative stress experienced in…
View article: Table S3 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Table S3 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Data table of AMPylated substrates identified by mass spectrometry analysis.
View article: Figure S6 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S6 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S6 depicts markers of subcellular fractionation used to isolate crude mitochondria.
View article: Figure S2 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity
Figure S2 from Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity Open
Supplementary Figure S2 correlates SelenoO expression with survival and metastasis