We are analyzing https://link.springer.com/article/10.1186/1750-1326-6-2.

Title:
6-OHDA generated ROS induces DNA damage and p53- and PUMA-dependent cell death | Molecular Neurodegeneration
Description:
Background Parkinson
Website Age:
28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

puma, ohda, cell, article, upr, death, cultures, figure, pubmed, neurons, google, scholar, treatment, cas, dopaminergic, loss, cells, analyzed, data, levels, apoptosis, dna, protein, atf, ohdainduced, activation, thpositive, damage, response, hours, chop, anova, stress, mice, genotype, caspase, pathway, treated, upregulation, results, induced, western, model, rna, twoway, required, animals, stained, authors, disease,

Topics {✒️}

hrp-linked anti-rabbit antibodies hrp-linked anti-mouse antibody 6-ohda-generated ros induces stress-induced {beta}-cell apoptosis open access article induces ros-dependent apoptosis ros-mediated dna damage mouse monoclonal anti-chop/gadd153 high-pressure liquid chromatography full size image article download pdf wild-type c57/bl6 mice md-tm mobile phase 6-ohda-induced dna damage semi-quantitative rt-pcr tyrosine hydroxylase n-acetyl-l-cysteine cy3-conjugated secondary antibodies 6-ohda-triggered cell death dna damage-induced phosphorylation mouse monoclonal anti-p53 quantitative real-time pcr mouse monoclonal α-neun 6-ohda-mediated cell death 6-ohda-induced protein damage rabbit polyclonal anti-puma puma-dependent cell death mouse monoclonal α-chop 6-ohda-induced cell death mouse monoclonal α-poly rabbit polyclonal anti-atf3 6-ohda-induced ros production 6-ohda-induced caspase-3 cleavage mouse monoclonal α-cytochrome separate p53-dependent pathway puma-cell death pathway dissociated da neuron prevent 6-ohda-mediated upregulation endoplasmic reticulum stress puma-dependent apoptotic cascade er stress-induced apoptosis rad53-related kinase ros-dependent manner mouse monoclonal anti sybr safe dna 6-ohda-induced cell loss mediate cell death ros-dependent upregulation sheep polyclonal anti 6-ohda-induced caspase activation

Questions {❓}

Conforti L, Adalbert R, Coleman MP: Neuronal death: where does the end begin?
Malhotra JD, Kaufman RJ: Endoplasmic reticulum stress and oxidative stress: a vicious cycle or a double-edged sword?

Schema {🗺️}

WebPage:
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         headline:6-OHDA generated ROS induces DNA damage and p53- and PUMA-dependent cell death
         description:Parkinson's disease (PD) is characterized by the selective loss of dopaminergic neurons in the substantia nigra (SN), resulting in tremor, rigidity, and bradykinesia. Although the etiology is unknown, insight into the disease process comes from the dopamine (DA) derivative, 6-hydroxydopamine (6-OHDA), which produces PD-like symptoms. Studies show that 6-OHDA activates stress pathways, such as the unfolded protein response (UPR), triggers mitochondrial release of cytochrome-c, and activates caspases, such as caspase-3. Because the BH3-only protein, Puma (p53-upregulated mediator of apoptosis), is activated in response to UPR, it is thought to be a link between cell stress and apoptosis. To test the hypothesis that Puma serves such a role in 6-OHDA-mediated cell death, we compared the response of dopaminergic neurons from wild-type and Puma-null mice to 6-OHDA. Results indicate that Puma is required for 6-OHDA-induced cell death, in primary dissociated midbrain cultures as well as in vivo. In these cultures, 6-OHDA-induced DNA damage and p53 were required for 6-OHDA-induced cell death. In contrast, while 6-OHDA led to upregulation of UPR markers, loss of ATF3 did not protect against 6-OHDA. Together, our results indicate that 6-OHDA-induced upregulation of Puma and cell death are independent of UPR. Instead, p53 and DNA damage repair pathways mediate 6-OHDA-induced toxicity.
         datePublished:2011-01-06T00:00:00Z
         dateModified:2011-01-06T00:00:00Z
         pageStart:1
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            Tyrosine Hydroxylase
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            Dopaminergic Neuron
            Unfold Protein Response
            Neurosciences
            Neurology
            Molecular Medicine
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ScholarlyArticle:
      headline:6-OHDA generated ROS induces DNA damage and p53- and PUMA-dependent cell death
      description:Parkinson's disease (PD) is characterized by the selective loss of dopaminergic neurons in the substantia nigra (SN), resulting in tremor, rigidity, and bradykinesia. Although the etiology is unknown, insight into the disease process comes from the dopamine (DA) derivative, 6-hydroxydopamine (6-OHDA), which produces PD-like symptoms. Studies show that 6-OHDA activates stress pathways, such as the unfolded protein response (UPR), triggers mitochondrial release of cytochrome-c, and activates caspases, such as caspase-3. Because the BH3-only protein, Puma (p53-upregulated mediator of apoptosis), is activated in response to UPR, it is thought to be a link between cell stress and apoptosis. To test the hypothesis that Puma serves such a role in 6-OHDA-mediated cell death, we compared the response of dopaminergic neurons from wild-type and Puma-null mice to 6-OHDA. Results indicate that Puma is required for 6-OHDA-induced cell death, in primary dissociated midbrain cultures as well as in vivo. In these cultures, 6-OHDA-induced DNA damage and p53 were required for 6-OHDA-induced cell death. In contrast, while 6-OHDA led to upregulation of UPR markers, loss of ATF3 did not protect against 6-OHDA. Together, our results indicate that 6-OHDA-induced upregulation of Puma and cell death are independent of UPR. Instead, p53 and DNA damage repair pathways mediate 6-OHDA-induced toxicity.
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      dateModified:2011-01-06T00:00:00Z
      pageStart:1
      pageEnd:13
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         Endoplasmic Reticulum Stress
         Tyrosine Hydroxylase
         Substantia Nigra
         Dopaminergic Neuron
         Unfold Protein Response
         Neurosciences
         Neurology
         Molecular Medicine
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               type:PostalAddress
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      name:Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, USA
      name:Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, USA

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