Allison N. Lau
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View article: Whole body MondoA deletion protects against diet-induced obesity through uncontrolled multi-organ substrate utilization and futile cycling
Whole body MondoA deletion protects against diet-induced obesity through uncontrolled multi-organ substrate utilization and futile cycling Open
Objective Delineating the nodal control points that maintain whole-body energy homeostasis is critical for understanding potential treatments of obesity and cardiometabolic diseases. The nutrient-sensing transcription factor MondoA is a re…
View article: Effects of aging on glucose and lipid metabolism in mice
Effects of aging on glucose and lipid metabolism in mice Open
Aging is accompanied by multiple molecular changes that contribute to aging-associated pathologies, such as accumulation of cellular damage and mitochondrial dysfunction. Tissue metabolism can also change with age, in part because mitochon…
View article: Supplemental Table 8 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 8 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Amino Acid- Mass Spec
View article: Supplemental Table 2 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 2 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
TMA Clinical Data
View article: Data from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Data from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate and lacks effective therapeutics. Therefore, it is of paramount importance to identify new targets. Using multiplex data from patient tissue, three-dimensional cocultu…
View article: Supplemental Table 8 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 8 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Amino Acid- Mass Spec
View article: Key Resources Table from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Key Resources Table from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Lists all key resources and reagents
View article: Supplementary Figures from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplementary Figures from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
18 supplementary figures and corresponding legends
View article: Supplemental Table 1 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 1 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Microarray
View article: Supplemental Table 4 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 4 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
RNAseq
View article: Supplemental Table 3 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 3 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
TMA IHC Scores
View article: Supplemental Table 1 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 1 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Microarray
View article: Supplemental Table 3 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 3 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
TMA IHC Scores
View article: Supplementary Figures from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplementary Figures from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
18 supplementary figures and corresponding legends
View article: Supplemental Tables 5-7 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Tables 5-7 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Sup Tables 5-7- Amino Acid Biochrom
View article: Supplemental Table 2 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 2 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
TMA Clinical Data
View article: Supplemental Table 4 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Table 4 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
RNAseq
View article: Data from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Data from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate and lacks effective therapeutics. Therefore, it is of paramount importance to identify new targets. Using multiplex data from patient tissue, three-dimensional cocultu…
View article: Key Resources Table from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Key Resources Table from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Lists all key resources and reagents
View article: Supplemental Tables 5-7 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression
Supplemental Tables 5-7 from Netrin G1 Promotes Pancreatic Tumorigenesis through Cancer-Associated Fibroblast–Driven Nutritional Support and Immunosuppression Open
Sup Tables 5-7- Amino Acid Biochrom
View article: Figure S2 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Figure S2 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Fig. S2. N-acetyl alanine does not protect from gemcitabine toxicity and nucleoside levels in PDAC cells are not effected by treatment with gemcitabine or conditioned media (A) Dose response curves with N-acetyl-alanine without (solid line…
View article: Data from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Data from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer deaths in the United States. The deoxynucleoside analogue gemcitabine is among the most effective therapies to treat PDAC, however, nearly all patients treated with gemci…
View article: Data from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Data from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer deaths in the United States. The deoxynucleoside analogue gemcitabine is among the most effective therapies to treat PDAC, however, nearly all patients treated with gemci…
View article: Figure S3 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Figure S3 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Fig. S3. Absolute quantification of the indicated species in 3 day CM. (A-D) 8-MDP and dipyridamole were applied to PSC2s conditioning the media at 6.67 uM. A83 was applied to PSC2s conditioning the media at 5 uM. Data show 3 biological re…
View article: Supplementary Figure Legends from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Supplementary Figure Legends from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Supplementary Figure Legends
View article: Figure S2 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Figure S2 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Fig. S2. N-acetyl alanine does not protect from gemcitabine toxicity and nucleoside levels in PDAC cells are not effected by treatment with gemcitabine or conditioned media (A) Dose response curves with N-acetyl-alanine without (solid line…
View article: Figure S1 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Figure S1 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Fig. S1. Conditioned media does not affect growth of PDAC cells except at 100% supplementation but does protect human PDAC cell lines regardless of P53 status. (A-E) Arbitrary units of resazurin fluorescence representing growth of PDAC cel…
View article: Figure S5 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Figure S5 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Fig. S5. PSC lines exhibit heterogeneity in expression of fibroblast activation markers (A) Staining of the indicated PSCs lines with DAPI and aSMA and PDGFRb antibodies. Scale bars are indicated in the bottom right corner of each image. (…
View article: Figure S4 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Figure S4 from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Fig. S4. Boiling does not inactivate ENT inhibitors 8-MDP and dipyridamole. Dose response curves with gemcitabine supplemented with boiled or untreated media containing 6.67 uM of ENT inhibitors 8-MDP or dipyridamole. Data represent the me…
View article: Supplementary Figure Legends from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance
Supplementary Figure Legends from Deoxycytidine Release from Pancreatic Stellate Cells Promotes Gemcitabine Resistance Open
Supplementary Figure Legends