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We began analyzing https://link.springer.com/article/10.1007/s10495-008-0216-7, but it redirected us to https://link.springer.com/article/10.1007/s10495-008-0216-7. The analysis below is for the second page.

Title[redir]:
Involvement of oxidative stress and caspase 2-mediated intrinsic pathway signaling in age-related increase in muscle cell apoptosis in mice | Apoptosis
Description:
Apoptosis has been implicated as a mechanism of loss of muscle cells in normal aging and plays an important role in age-related sarcopenia. To test the hypothesis that caspase 2 and c-Jun NH2-terminal kinase (JNK)-mediated intrinsic pathway signaling contribute to skeletal muscle cell apoptosis in aging, we compared activation of caspase 2 and JNK and the in vivo expression of 4-hydroxynonenal protein adducts (4-HNE), inducible nitric oxide synthase (iNOS), glucose-6-phosphate dehydrogenase (G6PDH), B-cell lymphoma-2 (BCL-2), BAX, and phospho-BCL-2 in gastrocnemius muscles of young (5 months old) and old (25 months old) mice. A distinct age-related increase in 4-HNE and iNOS expression was readily detected in mice. Increased oxidative stress and iNOS induction were further accompanied by a decrease in G6PDH expression, activation of caspase 2 and JNK, and inactivation of BCL-2 through phosphorylation at serine 70, and caspase 9 activation. Regression analysis further revealed that increased muscle cell death in aging was significantly correlated with changes in the levels of these molecules. Taken together, our data indicate that caspase 2 and JNK-mediated intrinsic pathway signaling is one of the mechanisms involved in age-related increase in muscle cell apoptosis.

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

Content Management System {📝}

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Custom-built

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Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


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How Does Doi.org Make Money? {💸}

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Keywords {🔍}

article, google, scholar, cas, pubmed, apoptosis, caspase, cell, muscle, activation, oxidative, cells, death, biol, kinase, aging, stress, nitric, signaling, bcl, sinha, hikim, phosphorylation, rat, research, agerelated, mice, role, skeletal, pathway, cjun, jnk, expression, protein, access, mitochondrial, factor, privacy, cookies, content, involvement, mediated, intrinsic, gonzalezcadavid, sinhahikim, sarcopenia, inducible, oxide, synthase, exp,

Topics {✒️}

c-jun nh2-terminal kinase ccaat/enhancer-binding protein-beta inducible nitric-oxide synthase β-carotene-induced apoptosis nitric oxide-induced apoptosis month download article/chapter oxidative stress-induced apoptosis raf-1/mek/erk cascade heat shock-induced apoptosis drug-induced bcl-2 phosphorylation glucose-6-phosphate dehydrogenase activity c-jun nh indrani sinha-hikim lipopolysaccharide-induced cell death protein kinase cδ life-long calorie restriction harbor-ucla medical center 2-methoxyestradiol-induced p53 induction p38 map kinase 4-hydroxynonenal protein adducts gonzalez-cadavid nf nitric oxide signaling distinct age-related increase map kinase pathways sinha hikim ap mitochondrial membrane depolarization full article pdf article apoptosis aims apoptosis-inducing factor skeletal muscle apoptosis terminal kinase activating transcription factor-2 rat skeletal muscle increased oxidative stress stress-induced apoptosis vinblastine-induced phosphorylation nuclear factor kappa p38 mapk signaling privacy choices/manage cookies neuronal death induced camkii-mediated phosphorylation gonzalez-cadavid mitochondrial dna mutations muscle cell apoptosis glucose-6-phosphate dehydrogenase stretch-induced apoptosis docetaxel-induced apoptosis cultured astrocytes induced subsequent bcl-2 phosphorylation oocyte cell death

Schema {🗺️}

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      headline:Involvement of oxidative stress and caspase 2-mediated intrinsic pathway signaling in age-related increase in muscle cell apoptosis in mice
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      name:Division of Endocrinology, Metabolism, and Molecular Medicine (I.S.-H;M.B; R.S), Charles R. Drew University, Los Angeles, USA
      name:Division of Endocrinology, Metabolism, and Molecular Medicine (I.S.-H;M.B; R.S), Charles R. Drew University, Los Angeles, USA
      name:Division of Endocrinology, Metabolism, and Molecular Medicine (I.S.-H;M.B; R.S), Charles R. Drew University, Los Angeles, USA
      name:Division of Endocrinology, Metabolism, and Molecular Medicine (I.S.-H;M.B; R.S), Charles R. Drew University, Los Angeles, USA
      name:Division of Endocrinology, Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA and Los Angeles Biomedical Research Institute, Torrance, USA
      name:Los Angeles Biomedical Research Institute, Torrance, USA
      name:Division of Endocrinology, Metabolism, and Molecular Medicine (I.S.-H;M.B; R.S), Charles R. Drew University, Los Angeles, USA
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