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Leader
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00000nz a2200037n 45 0 |
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001
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WKP|Q61651997
(VIAF cluster)
(Authority/Source Record)
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003
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WKP |
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005
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20241121000320.0 |
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008
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241121nneanz||abbn n and d |
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035
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‡a
(WKP)Q61651997
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024
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‡a
0000-0002-0080-3546
‡2
orcid
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035
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‡a
(OCoLC)Q61651997
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100
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0 |
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‡a
Laetitia Pereira
‡c
researcher ORCID ID = 0000-0002-0080-3546
‡9
en
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400
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0 |
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‡a
Laetitia Pereira
‡c
wetenschapper
‡9
nl
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670
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‡a
Author's 'Ca(2+)-induced Ca(2+) entry' or how the L-type Ca(2+) channel remodels its own signalling pathway in cardiac cells.
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670
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‡a
Author's Calcium signaling in diabetic cardiomyocytes.
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670
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‡a
Author's CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca
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670
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‡a
Author's CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca(2+) leak and the pathophysiological response to chronic β-adrenergic stimulation.
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670
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‡a
Author's Diabetic hyperglycaemia activates CaMKII and arrhythmias by O-linked glycosylation
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670
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‡a
Author's Divergent regulation of ryanodine receptor 2 calcium release channels by arrhythmogenic human calmodulin missense mutants.
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670
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‡a
Author's Epac enhances excitation-transcription coupling in cardiac myocytes
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670
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‡a
Author's Epac2 mediates cardiac β1-adrenergic-dependent sarcoplasmic reticulum Ca2+ leak and arrhythmia.
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670
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‡a
Author's Functional characterization of the cAMP-binding proteins Epac in cardiac myocytes
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670
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‡a
Author's Is Epac1 a good therapeutic strategy against cardiac remodelling?
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670
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‡a
Author's Mineralocorticoid modulation of cardiac ryanodine receptor activity is associated with downregulation of FK506-binding proteins.
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670
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‡a
Author's Neuropeptide Y rapidly enhances [Ca2+]i transients and Ca2+ sparks in adult rat ventricular myocytes through Y1 receptor and PLC activation
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670
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‡a
Author's Novel Epac fluorescent ligand reveals distinct Epac1 vs. Epac2 distribution and function in cardiomyocytes.
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670
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‡a
Author's Requirement for Ca2+/calmodulin-dependent kinase II in the transition from pressure overload-induced cardiac hypertrophy to heart failure in mice.
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670
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Author's Role of NOD1 in Heart Failure Progression via Regulation of Ca2+ Handling.
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670
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‡a
Author's The cAMP binding protein Epac modulates Ca2+ sparks by a Ca2+/calmodulin kinase signalling pathway in rat cardiac myocytes
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670
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‡a
Author's While systolic cardiomyocyte function is preserved, diastolic myocyte function and recovery from acidosis are impaired in CaMKIIδ-KO mice
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670
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‡a
Author's β-Adrenergic induced SR Ca2+ leak is mediated by an Epac-NOS pathway.
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909
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‡a
(orcid) 0000000200803546
‡9
1
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919
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‡a
campbindingproteinepacmodulatesca2+sparksbyaca2+calmodulinkinasesignallingpathwayinratcardiacmyocytes
‡A
The cAMP binding protein Epac modulates Ca2+ sparks by a Ca2+/calmodulin kinase signalling pathway in rat cardiac myocytes
‡9
1
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919
|
|
|
‡a
roleofnod1inheartfailureprogressionviaregulationofca2+handling
‡A
Role of NOD1 in Heart Failure Progression via Regulation of Ca2+ Handling.
‡9
1
|
|
919
|
|
|
‡a
requirementforca2+calmodulindependentkinase2inthetransitionfrompressureoverloadinducedcardiachypertrophytoheartfailureinmice
‡A
Requirement for Ca2+/calmodulin-dependent kinase II in the transition from pressure overload-induced cardiac hypertrophy to heart failure in mice.
‡9
1
|
|
919
|
|
|
‡a
novelepacfluorescentligandrevealsdistinctepac1vsepac2distributionandfunctionincardiomyocytes
‡A
Novel Epac fluorescent ligand reveals distinct Epac1 vs. Epac2 distribution and function in cardiomyocytes.
‡9
1
|
|
919
|
|
|
‡a
neuropeptideyrapidlyenhances1transientsandca2+sparksinadultratventricularmyocytesthroughy1receptorandplcactivation
‡A
Neuropeptide Y rapidly enhances [Ca2+]i transients and Ca2+ sparks in adult rat ventricular myocytes through Y1 receptor and PLC activation
‡9
1
|
|
919
|
|
|
‡a
mineralocorticoidmodulationofcardiacryanodinereceptoractivityisassociatedwithdownregulationoffk506bindingproteins
‡A
Mineralocorticoid modulation of cardiac ryanodine receptor activity is associated with downregulation of FK506-binding proteins.
‡9
1
|
|
919
|
|
|
‡a
isepac1agoodtherapeuticstrategyagainstcardiacremodelling
‡A
Is Epac1 a good therapeutic strategy against cardiac remodelling?
‡9
1
|
|
919
|
|
|
‡a
functionalcharacterizationofthecampbindingproteinsepacincardiacmyocytes
‡A
Functional characterization of the cAMP-binding proteins Epac in cardiac myocytes
‡9
1
|
|
919
|
|
|
‡a
epac2mediatescardiacβ1adrenergicdependentsarcoplasmicreticulumca2+leakandarrhythmia
‡A
Epac2 mediates cardiac β1-adrenergic-dependent sarcoplasmic reticulum Ca2+ leak and arrhythmia.
‡9
1
|
|
919
|
|
|
‡a
epacenhancesexcitationtranscriptioncouplingincardiacmyocytes
‡A
Epac enhances excitation-transcription coupling in cardiac myocytes
‡9
1
|
|
919
|
|
|
‡a
divergentregulationofryanodinereceptor2calciumreleasechannelsbyarrhythmogenichumancalmodulinmissensemutants
‡A
Divergent regulation of ryanodine receptor 2 calcium release channels by arrhythmogenic human calmodulin missense mutants.
‡9
1
|
|
919
|
|
|
‡a
diabetichyperglycaemiaactivatescamkiiandarrhythmiasbyolinkedglycosylation
‡A
Diabetic hyperglycaemia activates CaMKII and arrhythmias by O-linked glycosylation
‡9
1
|
|
919
|
|
|
‡a
camkiiδmediatesβadrenergiceffectsonryr2phosphorylationandsrca2+leakandthepathophysiologicalresponsetochronicβadrenergicstimulation
‡A
CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca(2+) leak and the pathophysiological response to chronic β-adrenergic stimulation.
‡9
1
|
|
919
|
|
|
‡a
camkiiδmediatesβadrenergiceffectsonryr2phosphorylationandsrca
‡A
CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca
‡9
1
|
|
919
|
|
|
‡a
calciumsignalingindiabeticcardiomyocytes
‡A
Calcium signaling in diabetic cardiomyocytes.
‡9
1
|
|
919
|
|
|
‡a
ca2+inducedca2+entryorhowthe50typeca2+channelremodelsitsownsignallingpathwayincardiaccells
‡A
'Ca(2+)-induced Ca(2+) entry' or how the L-type Ca(2+) channel remodels its own signalling pathway in cardiac cells.
‡9
1
|
|
919
|
|
|
‡a
βadrenergicinducedsrca2+leakismediatedbyanepacnospathway
‡A
β-Adrenergic induced SR Ca2+ leak is mediated by an Epac-NOS pathway.
‡9
1
|
|
919
|
|
|
‡a
whilesystoliccardiomyocytefunctionispreserveddiastolicmyocytefunctionandrecoveryfromacidosisareimpairedincamkiiδkomice
‡A
While systolic cardiomyocyte function is preserved, diastolic myocyte function and recovery from acidosis are impaired in CaMKIIδ-KO mice
‡9
1
|
|
996
|
|
|
‡2
PTBNP|225538
|
|
996
|
|
|
‡2
SUDOC|221268251
|
|
996
|
|
|
‡2
NTA|146709691
|
|
996
|
|
|
‡2
LC|n 99909131
|
|
996
|
|
|
‡2
ISNI|0000000069109267
|
|
996
|
|
|
‡2
BLBNB|000319664
|
|
996
|
|
|
‡2
SUDOC|122653726
|
|
996
|
|
|
‡2
ISNI|0000000069106103
|
|
996
|
|
|
‡2
ISNI|0000000451462328
|
|
996
|
|
|
‡2
CAOONL|ncf10908351
|
|
996
|
|
|
‡2
BIBSYS|90895505
|
|
996
|
|
|
‡2
B2Q|0000279690
|
|
996
|
|
|
‡2
ISNI|0000000034018146
|
|
996
|
|
|
‡2
SUDOC|175740461
|
|
996
|
|
|
‡2
PTBNP|197760
|
|
996
|
|
|
‡2
NII|DA10031452
|
|
997
|
|
|
‡a
0 0 lived 0 0
‡9
1
|
