FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3175182185> ?p ?o ?g. }

• W3175182185 abstract "Ischemic preconditioning, an endogenous protective mechanism to salvage ischemic myocardium, was described nearly 25 years ago; however, there has been little to no clinical translation. Further, there has been a critical lack of knowledge to understand the molecular mechanisms that bring about the protection. Nuclear factor-kappa B (NF-κB) and protein kinase A (PKA) are key regulators of gene transcription in the heart and have contradictory roles in cell death and survival. Activation of NF-κB and PKA has been shown to be protective as well as promote cardiac cell death in the setting of ischemia or oxidant stress. The answer as to why these two important regulators of gene transcription and cardiac physiology produce such a dichotomous response upon stress induction may provide insights into how protective signaling in the heart is integrated. We have discovered a novel scaffolding protein known as A-kinase interacting protein 1 (AKIP1) that is expressed at low levels in the heart and is induced by stress. Our data shows that AKIP1 binds to and regulates nuclear localization of PKA catalytic subunit (PKAc) and increases nuclear PKAc activity. Further, AKIP1 interacts with and enhances NF-κB nuclear localization in a PKAc dependent manner where disruption of AKIP1 binding to PKAc enhances nuclear NF-κB. In cardiomyocytes and in the heart, oxidant/ischemic stress caused an increase of AKIP1 levels. Further, our data suggests that overexpression of AKIP1 was protective to the heart. Therefore, we infer that AKIP1 may be a key molecular regulator/scaffold that assembles PKAc and NF-κB signaling complexes to alter the physiologic response of the heart in the basal and stressed states. Understanding the dynamics and physiologic implications of the interaction of PKAc and NF-κB with AKIP1 may provide a novel therapeutic control point for limiting cardiac injury associated with ischemic stress." @default.
• W3175182185 created "2021-07-05" @default.
• W3175182185 creator A5013168829 @default.
• W3175182185 creator A5014165479 @default.
• W3175182185 creator A5022592413 @default.
• W3175182185 creator A5030386911 @default.
• W3175182185 creator A5048203630 @default.
• W3175182185 creator A5048363770 @default.
• W3175182185 creator A5061985779 @default.
• W3175182185 date "2012-04-01" @default.
• W3175182185 modified "2023-10-16" @default.
• W3175182185 title "AKIP1 regulation of PKA and NF‐κB in the heart" @default.
• W3175182185 doi "https://doi.org/10.1096/fasebj.26.1_supplement.798.11" @default.
• W3175182185 hasPublicationYear "2012" @default.
• W3175182185 type Work @default.
• W3175182185 sameAs 3175182185 @default.
• W3175182185 citedByCount "0" @default.
• W3175182185 crossrefType "journal-article" @default.
• W3175182185 hasAuthorship W3175182185A5013168829 @default.
• W3175182185 hasAuthorship W3175182185A5014165479 @default.
• W3175182185 hasAuthorship W3175182185A5022592413 @default.
• W3175182185 hasAuthorship W3175182185A5030386911 @default.
• W3175182185 hasAuthorship W3175182185A5048203630 @default.
• W3175182185 hasAuthorship W3175182185A5048363770 @default.
• W3175182185 hasAuthorship W3175182185A5061985779 @default.
• W3175182185 hasConcept C126322002 @default.
• W3175182185 hasConcept C185592680 @default.
• W3175182185 hasConcept C2776914184 @default.
• W3175182185 hasConcept C2777730290 @default.
• W3175182185 hasConcept C71924100 @default.
• W3175182185 hasConcept C86803240 @default.
• W3175182185 hasConcept C95444343 @default.
• W3175182185 hasConceptScore W3175182185C126322002 @default.
• W3175182185 hasConceptScore W3175182185C185592680 @default.
• W3175182185 hasConceptScore W3175182185C2776914184 @default.
• W3175182185 hasConceptScore W3175182185C2777730290 @default.
• W3175182185 hasConceptScore W3175182185C71924100 @default.
• W3175182185 hasConceptScore W3175182185C86803240 @default.
• W3175182185 hasConceptScore W3175182185C95444343 @default.
• W3175182185 hasIssue "S1" @default.
• W3175182185 hasLocation W31751821851 @default.
• W3175182185 hasOpenAccess W3175182185 @default.
• W3175182185 hasPrimaryLocation W31751821851 @default.
• W3175182185 hasRelatedWork W1996155681 @default.
• W3175182185 hasRelatedWork W2365541820 @default.
• W3175182185 hasRelatedWork W2606375388 @default.
• W3175182185 hasRelatedWork W2782180291 @default.
• W3175182185 hasRelatedWork W2894581131 @default.
• W3175182185 hasRelatedWork W3203653663 @default.
• W3175182185 hasRelatedWork W4229446363 @default.
• W3175182185 hasRelatedWork W4283394682 @default.
• W3175182185 hasRelatedWork W4297261086 @default.
• W3175182185 hasRelatedWork W4300003206 @default.
• W3175182185 hasVolume "26" @default.
• W3175182185 isParatext "false" @default.
• W3175182185 isRetracted "false" @default.
• W3175182185 magId "3175182185" @default.
• W3175182185 workType "article" @default.