Carol Lenaghan
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View article: Supplementary Figures 1-5 from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors
Supplementary Figures 1-5 from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors Open
Supp Fig 1 Tumour efficacy Supp Fig 2 In vitro gene expression modulation Supp Fig 3 In vivo biomarker analysis Supp Fig 4 HCC70 In vivo FDG uptake imaging Supp Fig 5 U87MG in vivo FDG uptake imaging
View article: Data from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors
Data from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors Open
Loss of the tumor suppressor PTEN confers a tumor cell dependency on the PI3Kβ isoform. Achieving maximal inhibition of tumor growth through PI3K pathway inhibition requires sustained inhibition of PI3K signaling; however, efficacy is ofte…
View article: Supplementary Materials text from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel
Supplementary Materials text from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel Open
Supplementary Materials text. Supplementary text to support supplementary data.
View article: Supplementary Methods from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors
Supplementary Methods from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors Open
Supplementary methods for in vivo studies
View article: Supplementary Tables 1-3 and Figure 1-7 from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel
Supplementary Tables 1-3 and Figure 1-7 from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel Open
Supplementary Tables 1-3 and Figure 1-7. Supp Table 1 Summary of cell line origins and verification. Supp Table 2 Summary of antibodies used in all experimental analysis Supp Fig 1 AZD8186 inhibits PI3K pathway in PTEN null but not PTEN WT…
View article: Supplementary Materials text from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel
Supplementary Materials text from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel Open
Supplementary Materials text. Supplementary text to support supplementary data.
View article: Data from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel
Data from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel Open
Loss of PTEN protein results in upregulation of the PI3K/AKT pathway, which appears dependent on the PI3Kβ isoform. Inhibitors of PI3Kβ have potential to reduce growth of tumors in which loss of PTEN drives tumor progression. We have devel…
View article: Data from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors
Data from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors Open
Loss of the tumor suppressor PTEN confers a tumor cell dependency on the PI3Kβ isoform. Achieving maximal inhibition of tumor growth through PI3K pathway inhibition requires sustained inhibition of PI3K signaling; however, efficacy is ofte…
View article: Supplementary Tables 1-3 from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors
Supplementary Tables 1-3 from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors Open
Supplementary Table 1: Cell lines; Supplementary Table 2: Antibodies; Supplementary Table 3: Gene lists
View article: Data from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel
Data from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel Open
Loss of PTEN protein results in upregulation of the PI3K/AKT pathway, which appears dependent on the PI3Kβ isoform. Inhibitors of PI3Kβ have potential to reduce growth of tumors in which loss of PTEN drives tumor progression. We have devel…
View article: Supplementary Tables 1-3 and Figure 1-7 from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel
Supplementary Tables 1-3 and Figure 1-7 from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel Open
Supplementary Tables 1-3 and Figure 1-7. Supp Table 1 Summary of cell line origins and verification. Supp Table 2 Summary of antibodies used in all experimental analysis Supp Fig 1 AZD8186 inhibits PI3K pathway in PTEN null but not PTEN WT…
View article: Supplementary Tables 1-3 from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors
Supplementary Tables 1-3 from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors Open
Supplementary Table 1: Cell lines; Supplementary Table 2: Antibodies; Supplementary Table 3: Gene lists
View article: Supplementary Figures 1-5 from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors
Supplementary Figures 1-5 from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors Open
Supp Fig 1 Tumour efficacy Supp Fig 2 In vitro gene expression modulation Supp Fig 3 In vivo biomarker analysis Supp Fig 4 HCC70 In vivo FDG uptake imaging Supp Fig 5 U87MG in vivo FDG uptake imaging
View article: Supplementary Methods from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors
Supplementary Methods from Combined Inhibition of PI3Kβ and mTOR Inhibits Growth of PTEN-null Tumors Open
Supplementary methods for in vivo studies
View article: Supplementary Figures 1-9 from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Supplementary Figures 1-9 from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Supplemtary figures 1-9
View article: Supplemental data figure legends from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Supplemental data figure legends from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Supplemental data figure legends
View article: Supplementary Table Results from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Supplementary Table Results from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Supplementary Table results
View article: Data from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Data from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Purpose: PTEN-null tumors become dependent on the PI3Kβ isoform and can be targeted by molecules such as the selective PI3Kβ inhibitor AZD8186. However, beyond the modulation of the canonical PI3K pathway, the consequences of inhibiting PI…
View article: Supplementary Table Results from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Supplementary Table Results from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Supplementary Table results
View article: Supplementary Table Methods from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Supplementary Table Methods from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Supplementary Table Methods
View article: Data from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Data from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Purpose: PTEN-null tumors become dependent on the PI3Kβ isoform and can be targeted by molecules such as the selective PI3Kβ inhibitor AZD8186. However, beyond the modulation of the canonical PI3K pathway, the consequences of inhibiting PI…
View article: Supplemental data figure legends from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Supplemental data figure legends from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Supplemental data figure legends
View article: Supplementary Figures 1-9 from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Supplementary Figures 1-9 from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Supplemtary figures 1-9
View article: Supplementary Table Methods from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors
Supplementary Table Methods from Inhibiting PI3Kβ with AZD8186 Regulates Key Metabolic Pathways in PTEN-Null Tumors Open
Supplementary Table Methods
View article: Indazole-6-phenylcyclopropylcarboxylic Acids as Selective GPR120 Agonists with in Vivo Efficacy
Indazole-6-phenylcyclopropylcarboxylic Acids as Selective GPR120 Agonists with in Vivo Efficacy Open
GPR120 agonists have therapeutic potential for the treatment of diabetes, but few selective agonists have been reported. We identified an indazole-6-phenylcyclopropylcarboxylic acid series of GPR120 agonists and conducted SAR studies to op…
View article: CCDC 1530875: Experimental Crystal Structure Determination
CCDC 1530875: Experimental Crystal Structure Determination Open
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available …
View article: Lipid derivatives activate GPR119 and trigger GLP-1 secretion in primary murine L-cells
Lipid derivatives activate GPR119 and trigger GLP-1 secretion in primary murine L-cells Open
GPR119 ligands strongly enhanced GLP-1 release from colonic cultures, reflecting the high proportion of colonic L-cells that exhibited cAMP responses to GPR119 agonists. Less GPR119-dependence could be demonstrated in the upper small intes…