Matches in Nanopublications for { ?s ?p "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " ?g. }
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- _3 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _4 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _3 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _3 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _3 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _3 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _4 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _3 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _4 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.
- _4 value "Shear stress, atorvastatin, and adiponectin all increased AMPK Thr172 (activating phosphorylation found at Thr183 on the Uniprot sequence Q5EG47) and eNOS Ser633 phosphorylations (Ser632 from sequence Uniprot P70313), which were abolished if AMPK was pharmacologically inhibited or genetically ablated. The constitutively active form of AMPK or an AMPK agonist caused a sustained Ser633 phosphorylation. " provenance.