C1 - Nucleotide signalling in the heart

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Nucleotide Signalling Experiments (1)

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Metni eşleştir

Zacollo & Pozzan aims

Zacollo & Pozzan methods

Zacollo & Pozzan results

Lygren aims

Lygren methods

Lygren results

Mongillo aims

Mongillo methods

Mongillo results

Beca aims

Beca methods

Beca results

Tıkla ve sürükle

PDE3A predominant enzyme, associates with the AKAP18d complex described by Lygren et al

[cAMP] measured w/ FRET (as above), PDE3 & PDE4 inhibitors applied at rest and after iso.

SR depletion with SERCA inhibitor BHQ, Ca added to EC compartment. siRNA AKAP18d knockdown -> attenuates reuptake.

Studied the spatio-temporal changes in cAMP following B-AR activation

cAMP localised to microdomains @ T-tubules/SR membrane, ~1um. IBMX disrupts localisation of signalling.

Isolated lagendorff hearts, contractility & relaxation enhanced in PDE3A KO mice but not PDE4A KO mice. Co-immunoprecipitation showed that PDE3A colocalises with SERCA2, PLN, AKAP18d, & PP2A

Determine the effects of AKAP18d siRNA knockdown on SR Ca uptake/release.

Studied roles of PDE3&4 in cAMP signalling at rest and after B-AR activation.

PDE4 inhibitor disrupted cAMP signalling at rest & after B-AR activation significantly more than did PDE3 inhibition.

Neonatal rat cardiac myocytes. [cAMP] assessed by FRET from cyan->yellow GFP. effects of PDE inhibitor IBMX also assessed.

AKAP18d facilitates formation of signalling complex, disruption prevents PLN from being phosphorylated & dissociating from SERCA.

Investigated the roles of PDE3A&B in regulating basal contractility and SR Ca content.


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