SMAD proteins are involved in apoptosis induction in ventricular cardiomyocytes.
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Summary
AP-1/SMAD signaling has been identified as a common pathway in cardiomyocyte apoptosis and SMAD proteins are characterized as potential candidates for proteins that shift AP-1 signaling from hypertrophy to apoptosis.
- Type
- article
- Published
- 2005-07-01
- Cited by
- 62
- References
- 39
- Access
- Open access
- OpenAlex
- https://openalex.org/W15949472
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:9966164
Keywords
Photonics, Optoelectronics, Materials science, Diode, OLED
References
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- Increased JNK, AP-1 and NF-kappa B DNA binding activities in isoproterenol-induced cardiac remodeling.
- Transcription activator protein 1 (AP‐1) mediates NO‐induced apoptosis of adult cardiomyocytes
- Elevation of expression of Smads 2, 3, and 4, decorin and TGF-beta in the chronic phase of myocardial infarct scar healing.
- Role of JunB in Erythroid Differentiation*
- Hypertrophy-associated gene induction after beta-adrenergic stimulation in adult cardiomyocytes.
- Genetic redox preconditioning differentially modulates AP-1 and NF kappa B responses following cardiac ischemia/reperfusion injury and protects against necrosis and apoptosis.
- Transforming growth factor-beta-induced apoptosis is mediated by Smad-dependent expression of GADD45b through p38 activation.
- Oxidative stress induces DNA fragmentation and caspase activation via the c-Jun NH2-terminal kinase pathway in H9c2 cardiac muscle cells.
- Dual Blockade of Cyclic AMP Response Element- (CRE) and AP-1-directed Transcription by CRE-transcription Factor Decoy Oligonucleotide
- Critical Role of Smads and AP-1 Complex in Transforming Growth Factor-β-dependent Apoptosis*
- Differential regulation of Bcl‐2, AP‐1 and NF‐κB on cardiomyocyte apoptosis during myocardial ischemic stress adaptation
- Induction of cardiac fibrosis by transforming growth factor-beta(1).
- Smads bind directly to the Jun family of AP-1 transcription factors.
- Culturing of calcium stable adult cardiac myocytes.
- Nuclear factor of activated T cells contains Fos and Jun
- Smad3/AP-1 interactions control transcriptional responses to TGF-β in a promoter-specific manner
- Links between tumor suppressors: p53 is required for TGF-beta gene responses by cooperating with Smads.
- Dominant Negative Mutant of c-Jun Inhibits Cardiomyocyte Hypertrophy Induced by Endothelin 1 and Phenylephrine
- Variations in Jun and Fos protein expression and AP-1 activity in cycling, resting and stimulated fibroblasts
Cited by
- Computational Detection of Stage-Specific Transcription Factor Clusters during Heart Development
- Wound healing signals mediated by Rho/ROCK activation in response to radiotherapy and consequences fot treatmeny of late damage within normal tissues
- Good and bad sides of TGFβ-signaling in myocardial infarction
- Modulation of growth factors and cell cycle regulatory molecules in experimental cardiomyopathy
- Growth differentiation factor 15 acts anti‐apoptotic and pro‐hypertrophic in adult cardiomyocytes
- Renin and the IGFII/M6P Receptor System in Cardiac Biology
- Positive and Negative Transcriptional Regulation of the Foxp3 gene is Mediated by TGF-β Signal Transducer Smad3 Access and Binding to Enhancer I
- Desferrioxamine Attenuates Doxorubicin-Induced Acute Cardiotoxicity through TFG-β/Smad p53 Pathway in Rat Model
- Essential role of Smad4 in maintaining cardiomyocyte proliferation during murine embryonic heart development.
- Enhanced SERCA2A expression improves contractile performance of ventricular cardiomyocytes of rat under adrenergic stimulation
- Robinin modulates doxorubicin-induced cardiac apoptosis by TGF-β1 signaling pathway in Sprague Dawley rats.
- Inhibition of AP-1 signaling by JDP2 overexpression protects cardiomyocytes against hypertrophy and apoptosis induction.
- Transgenic overexpression of the adenine nucleotide translocase 1 protects cardiomyocytes against TGFβ1-induced apoptosis by stabilization of the mitochondrial permeability transition pore.
- Activin receptor-like kinase 7 mediates high glucose-induced H9c2 cardiomyoblast apoptosis through activation of Smad2/3.
- Contractile performance of adult ventricular rat cardiomyocytes is not directly jeopardized by NO/cGMP-dependent induction of pro-apoptotic pathways.
- SMAD‐proteins as a molecular switch from hypertrophy to apoptosis induction in adult ventricular cardiomyocytes
- Gata4 is required for maintenance of postnatal cardiac function and protection from pressure overload-induced heart failure
- Cardiac pathologies in relation to Smad-dependent pathways.
- Cardiac-specific mindin overexpression attenuates cardiac hypertrophy via blocking AKT/GSK3β and TGF-β1-Smad signalling.
- TGFβ receptor activation enhances cardiac apoptosis via SMAD activation and concomitant NO release
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