20 results on '"Raven, Jennifer F."'
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2. The Canadian Institutes of Health Research Institute of Infection and Immunity response to the threat of antimicrobial resistance
3. Next Generation Vaccine Biomarkers workshop October 30–31, 2014 – Ottawa, Canada
4. Stat1 is a suppressor of ErbB2/Neu-mediated cellular transformation and mouse mammary gland tumor formation
5. STAT1 Represses Skp2 Gene Transcription to Promote p27Kip1 Stabilization in Ras-Transformed Cells
6. The level and compartmentalization of phosphatidate phosphatase-1 (lipin-1) control the assembly and secretion of hepatic VLDL
7. Stat1 Phosphorylation Determines Ras Oncogenicity by Regulating p27Kip1
8. IRES-mediated translational control of AMAP1 expression during differentiation of monocyte U937 cells
9. PERK and PKR: Old kinases learn new tricks
10. PKR and PKR-like Endoplasmic Reticulum Kinase Induce the Proteasome-dependent Degradation of Cyclin D1 via a Mechanism Requiring Eukaryotic Initiation Factor 2α Phosphorylation
11. A Novel Function of eIF2α Kinases as Inducers of the Phosphoinositide-3 Kinase Signaling Pathway
12. Interferons induce tyrosine phosphorylation of the eIF2α kinase PKR through activation of Jak1 and Tyk2
13. The Catalytic Activity of the Eukaryotic Initiation Factor-2α Kinase PKR Is Required to Negatively Regulate Stat1 and Stat3 via Activation of the T-cell Protein-tyrosine Phosphatase
14. Stat1 Phosphorylation Determines Ras Oncogenicity by Regulating p27Kip1.
15. Stat1 Phosphorylation Determines Ras Oncogenicity by Regulating p27Kip1.
16. The eIF2α kinases inhibit vesicular stomatitis virus replication independently of eIF2α phosphorylation.
17. PERK and PKR.
18. The Catalytic Activity of the Eukaryotic Initiation Factor-2α Kinase PKR Is Required to Negatively Regulate Stat1 and Stat3 via Activation of the T-cell Protein-tyrosine Phosphatase.
19. The Second Canadian Symposium on hepatitis C virus: a call to action.
20. The level and compartmentalization of phosphatidate phosphatase-1 (lipin-1) control the assembly and secretion of hepatic VLDL.
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