Augustine M.K. Choi
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View article: High-fat diet obesity exacerbates acute lung injury-induced dysregulation of fatty acid oxidation in alveolar epithelial type 2 cells
High-fat diet obesity exacerbates acute lung injury-induced dysregulation of fatty acid oxidation in alveolar epithelial type 2 cells Open
High-fat diet obesity is linked to increased lung injury and bronchoalveolar lavage fluid (BALF) fatty acids in a hyperoxic ARDS model. In the present study, obesity not only upregulated intracellular lipids and effectors of fatty acid mit…
View article: Chitinase 3–like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα– and CD24-Siglec10–Mediated Phagocytosis
Chitinase 3–like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα– and CD24-Siglec10–Mediated Phagocytosis Open
Innate immune responses such as phagocytosis are critically linked to the generation of adaptive immune responses against the neoantigens in cancer and the efferocytosis that is essential for homeostasis in diseases characterized by lung i…
View article: Retraction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3
Retraction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3 Open
Chitinase 1 (CHIT1) plays a role in the pathogenesis of pulmonary fibrosis by modulating canonical and noncanonical TGF-β signaling via interaction with TGFBRAP1 and FOXO3. These findings highlight the CHIT1/SMAD7 axis as a potential bioma…
View article: The Asthma Risk Gene, GSDMB, Promotes Mitochondrial DNA-induced ISGs Expression
The Asthma Risk Gene, GSDMB, Promotes Mitochondrial DNA-induced ISGs Expression Open
Released mitochondrial DNA (mtDNA) in cells activates cGAS-STING pathway, which induces expression of interferon-stimulated genes (ISGs) and thereby promotes inflammation, as frequently seen in asthmatic airways. However, whether the genet…
View article: Chitinase 3-like-1 (CHI3L1) Inhibits Innate Anti-Tumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα and CD24-Siglec10-Mediated Phagocytosis
Chitinase 3-like-1 (CHI3L1) Inhibits Innate Anti-Tumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα and CD24-Siglec10-Mediated Phagocytosis Open
Innate immune responses such as phagocytosis are critically linked to the generation of adaptive immune responses against the neoantigens in cancer and the efferocytosis that is essential for homeostasis in diseases characterized by lung i…
View article: Alveolar type II epithelial cell FASN maintains lipid homeostasis in experimental COPD
Alveolar type II epithelial cell FASN maintains lipid homeostasis in experimental COPD Open
Alveolar epithelial type II (AEC2) cells strictly regulate lipid metabolism to maintain surfactant synthesis. Loss of AEC2 cell function and surfactant production are implicated in the pathogenesis of the smoking-related lung disease chron…
View article: Auto-immunoproteomics analysis of COVID-19 ICU patients revealed increased levels of autoantibodies related to the male reproductive system
Auto-immunoproteomics analysis of COVID-19 ICU patients revealed increased levels of autoantibodies related to the male reproductive system Open
Background: Coronavirus disease (COVID-19) manifests many clinical symptoms, including an exacerbated immune response and cytokine storm. Autoantibodies in COVID-19 may have severe prodromal effects that are poorly understood. The interact…
View article: Retraction Notice to: mTORC1-Induced HK1-Dependent Glycolysis Regulates NLRP3 Inflammasome Activation
Retraction Notice to: mTORC1-Induced HK1-Dependent Glycolysis Regulates NLRP3 Inflammasome Activation Open
(Cell Reports 12, 102–115; July 7, 2015) This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the editors of…
View article: CEACAM6: A Novel Marker of Chronic Obstructive Pulmonary Disease Susceptibility?
CEACAM6: A Novel Marker of Chronic Obstructive Pulmonary Disease Susceptibility? Open
"CEACAM6: A Novel Marker of COPD Susceptibility?." American Journal of Respiratory and Critical Care Medicine, 0(ja), pp.
View article: Correction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3
Correction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3 Open
Chitinase 1 (CHIT1) plays a role in the pathogenesis of pulmonary fibrosis by modulating canonical and noncanonical TGF-β signaling via interaction with TGFBRAP1 and FOXO3. These findings highlight the CHIT1/SMAD7 axis as a potential bioma…
View article: Mitochondria in health, disease, and aging
Mitochondria in health, disease, and aging Open
Mitochondria are well known as organelles responsible for the maintenance of cellular bioenergetics through the production of ATP. Although oxidative phosphorylation may be their most important function, mitochondria are also integral for …
View article: Supplementary Table 1 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Table 1 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
XLSX file - 144K, Metabolomics data (raw and processed).
View article: Supplementary Figure 3 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 3 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 34K, Effect of chloroquine on the metabolome of Tsc2+/+ MEFs.
View article: Supplementary Figure 5 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 5 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 204K, mTORC1 signaling upon chloroquine/6-AN treatment and effect of mTORC1 inhibition on the proliferation of Tsc2-/- cells treated with the dual drug combination.
View article: Supplementary Figure 6 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 6 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 98K, Autophagy and pentose phosphate pathway inhibition suppresses proliferation of Tsc2-null cystadenoma 105K cells.
View article: Supplementary Table 1 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Table 1 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
XLSX file - 144K, Metabolomics data (raw and processed).
View article: Supplementary Figure 3 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 3 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 34K, Effect of chloroquine on the metabolome of Tsc2+/+ MEFs.
View article: Supplementary Figure 6 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 6 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 98K, Autophagy and pentose phosphate pathway inhibition suppresses proliferation of Tsc2-null cystadenoma 105K cells.
View article: Supplementary Figure 8 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 8 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 42K, Parthenolide rescues proliferation in Tsc2-/- MEFs.
View article: Data from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Data from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
The mammalian target of rapamycin complex 1 (mTORC1) is hyperactive in many human cancers and in tuberous sclerosis complex (TSC). Autophagy, a key mTORC1-targeted process, is a critical determinant of metabolic homeostasis. Metabolomic pr…
View article: Supplementary Figure 2 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 2 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 55K, Effect of chloroquine on the metabolome of Tsc2+/+ MEFs.
View article: Supplementary Figure 1 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 1 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 61K, Effect of chloroquine in Tsc2-deficient models.
View article: Supplementary Figure 4 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide
Supplementary Figure 4 from Autophagy-Dependent Metabolic Reprogramming Sensitizes TSC2-Deficient Cells to the Antimetabolite 6-Aminonicotinamide Open
PDF file - 35K, Chloroquine treatment induces ROS production.