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We are analyzing https://link.springer.com/article/10.1007/s10495-006-0022-z.

Title:
Caspase-12 compensates for lack of caspase-2 and caspase-3 in female germ cells | Apoptosis
Description:
Previously, we analyzed mice lacking either caspase-2 or caspase-3 and documented a role for caspase-2 in developmental and chemotherapy-induced apoptosis of oocytes. Those data also revealed dispensability of caspase-3, although we found this caspase critical for ovarian granulosa cell death. Because of the mutual interdependence of germ cells and granulosa cells, herein we generated caspase-2 and -3 double-mutant (DKO) mice to evaluate how these two caspases functionally relate to each other in orchestrating oocyte apoptosis. No difference was observed in the rate of spontaneous oocyte apoptosis between DKO and wildtype (WT) females. In contrast, the oocytes from DKO females were more susceptible to apoptosis induced by DNA damaging agents, compared with oocytes from WT females. This increased sensitivity to death of DKO oocytes appears to be a specific response to DNA damage, and it was associated with a compensatory upregulation of caspase-12. Interestingly, DKO oocytes were more resistant to apoptosis induced by methotrexate (MTX) than WT oocytes. These results revealed that in female germ cells, insults that directly interfere with their metabolic status (e.g. MTX) require caspase-2 and caspase-3 as obligatory executioners of the ensuing cell death cascade. However, when DNA damage is involved, and in the absence of caspase-2 and -3, caspase-12 becomes upregulated and mediates apoptosis in oocytes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Telecommunications

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {πŸ“ˆ}

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


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Keywords {πŸ”}

article, google, scholar, cas, pubmed, caspase, cell, apoptosis, death, tilly, cells, oocytes, germ, perez, research, jurisicova, human, department, flavell, access, differ, mol, university, matikainen, yuan, dko, reed, bcl, nature, usa, privacy, cookies, content, takai, mice, endoplasmic, reticulum, korsmeyer, family, bax, nat, gene, biology, data, information, publish, search, momoi, role, ovarian,

Topics {βœ’οΈ}

month download article/chapter parental age-related aneuploidy female germ cells human germ cells aß-induced cell death full article pdf endoplasmic reticulum stress harvard medical school article apoptosis aims germ cells tunicamycin-treated cells privacy choices/manage cookies bcl-2 gene family chemotherapy-induced apoptosis related subjects massachusetts general hospital vincent research funds age-related decline doxorubicin-mediated death orchestrating oocyte apoptosis spontaneous oocyte apoptosis acid sphingomyelinase gene harakiri gene product mount sinai hospital caspase-3 activation correlates dna damaging agents granulosa cell apoptosis caspases functionally relate check access instant access critical control points ovarian cancer models apoptosis-related genes yale university school michigan state university apoptosis-based therapies european economic area scope submit manuscript basic biological phenomenon wide-ranging implications prenatal oogenesis advanced chronological age sphingosine-1-phosphate therapy porter ga jr acquired deleterious mutations investigator salary award ontario cancer institute conditions privacy policy granulosa cells analyzed mice lacking

Questions {❓}

  • Lim AST, Tsakok MFH (1997) Age-related decline in fertility: a link to degenerative oocytes?

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Caspase-12 compensates for lack of caspase-2 and caspase-3 in female germ cells
         description:Previously, we analyzed mice lacking either caspase-2 or caspase-3 and documented a role for caspase-2 in developmental and chemotherapy-induced apoptosis of oocytes. Those data also revealed dispensability of caspase-3, although we found this caspase critical for ovarian granulosa cell death. Because of the mutual interdependence of germ cells and granulosa cells, herein we generated caspase-2 and -3 double-mutant (DKO) mice to evaluate how these two caspases functionally relate to each other in orchestrating oocyte apoptosis. No difference was observed in the rate of spontaneous oocyte apoptosis between DKO and wildtype (WT) females. In contrast, the oocytes from DKO females were more susceptible to apoptosis induced by DNA damaging agents, compared with oocytes from WT females. This increased sensitivity to death of DKO oocytes appears to be a specific response to DNA damage, and it was associated with a compensatory upregulation of caspase-12. Interestingly, DKO oocytes were more resistant to apoptosis induced by methotrexate (MTX) than WT oocytes. These results revealed that in female germ cells, insults that directly interfere with their metabolic status (e.g. MTX) require caspase-2 and caspase-3 as obligatory executioners of the ensuing cell death cascade. However, when DNA damage is involved, and in the absence of caspase-2 and -3, caspase-12 becomes upregulated and mediates apoptosis in oocytes.
         datePublished:2007-01-24T00:00:00Z
         dateModified:2007-01-24T00:00:00Z
         pageStart:791
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            Chemotherapy
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            Cancer Research
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            Oncology
            Biochemistry
            general
            Virology
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      headline:Caspase-12 compensates for lack of caspase-2 and caspase-3 in female germ cells
      description:Previously, we analyzed mice lacking either caspase-2 or caspase-3 and documented a role for caspase-2 in developmental and chemotherapy-induced apoptosis of oocytes. Those data also revealed dispensability of caspase-3, although we found this caspase critical for ovarian granulosa cell death. Because of the mutual interdependence of germ cells and granulosa cells, herein we generated caspase-2 and -3 double-mutant (DKO) mice to evaluate how these two caspases functionally relate to each other in orchestrating oocyte apoptosis. No difference was observed in the rate of spontaneous oocyte apoptosis between DKO and wildtype (WT) females. In contrast, the oocytes from DKO females were more susceptible to apoptosis induced by DNA damaging agents, compared with oocytes from WT females. This increased sensitivity to death of DKO oocytes appears to be a specific response to DNA damage, and it was associated with a compensatory upregulation of caspase-12. Interestingly, DKO oocytes were more resistant to apoptosis induced by methotrexate (MTX) than WT oocytes. These results revealed that in female germ cells, insults that directly interfere with their metabolic status (e.g. MTX) require caspase-2 and caspase-3 as obligatory executioners of the ensuing cell death cascade. However, when DNA damage is involved, and in the absence of caspase-2 and -3, caspase-12 becomes upregulated and mediates apoptosis in oocytes.
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      dateModified:2007-01-24T00:00:00Z
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         Oocyte
         Apoptosis
         Chemotherapy
         Caspases
         DNA damage
         Cancer Research
         Cell Biology
         Oncology
         Biochemistry
         general
         Virology
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            name:T. Matikainen
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                  name:Massachusetts General Hospital/Harvard Medical School
                  address:
                     name:Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital/Harvard Medical School, Boston, USA
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                     name:Samuel Lunenfeld Research Institute, Mount Sinai Hospital, and Department of Obstetrics and Gynecology, University of Toronto, Toronto, Canada
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                  name:Massachusetts General Hospital/Harvard Medical School
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                     name:Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital/Harvard Medical School, Boston, USA
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                  name:National Institute of Neuroscience, NCNP
                  address:
                     name:Divisions of Development and Differentiation, National Institute of Neuroscience, NCNP, Kodaira, Japan
                     type:PostalAddress
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            type:Person
            name:T. Nakagawa
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                  name:Department of Cell Biology, Harvard Medical School
                  address:
                     name:Department of Cell Biology, Harvard Medical School, Boston, USA
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            name:B. Lemmers
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            name:G. I. Perez
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               name:Divisions of Development and Differentiation, National Institute of Neuroscience, NCNP, Kodaira, Japan
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               type:PostalAddress
            type:Organization
      name:R. Hakem
      affiliation:
            name:University of Toronto
            address:
               name:Division of Cellular and Molecular Biology, Department of Medical Biophysics, Ontario Cancer Institute, University of Toronto, Ontario, Canada
               type:PostalAddress
            type:Organization
      name:T. Momoi
      affiliation:
            name:National Institute of Neuroscience, NCNP
            address:
               name:Divisions of Development and Differentiation, National Institute of Neuroscience, NCNP, Kodaira, Japan
               type:PostalAddress
            type:Organization
      name:J. Yuan
      affiliation:
            name:Department of Cell Biology, Harvard Medical School
            address:
               name:Department of Cell Biology, Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      name:J. L. Tilly
      affiliation:
            name:Massachusetts General Hospital/Harvard Medical School
            address:
               name:Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital/Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      name:G. I. Perez
      affiliation:
            name:Michigan State University
            address:
               name:Department of Physiology, Michigan State University, Michigan, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital/Harvard Medical School, Boston, USA
      name:Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital/Harvard Medical School, Boston, USA
      name:Samuel Lunenfeld Research Institute, Mount Sinai Hospital, and Department of Obstetrics and Gynecology, University of Toronto, Toronto, Canada
      name:Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital/Harvard Medical School, Boston, USA
      name:Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital/Harvard Medical School, Boston, USA
      name:Divisions of Development and Differentiation, National Institute of Neuroscience, NCNP, Kodaira, Japan
      name:Department of Cell Biology, Harvard Medical School, Boston, USA
      name:Division of Cellular and Molecular Biology, Department of Medical Biophysics, Ontario Cancer Institute, University of Toronto, Ontario, Canada
      name:Section of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, USA
      name:Division of Cellular and Molecular Biology, Department of Medical Biophysics, Ontario Cancer Institute, University of Toronto, Ontario, Canada
      name:Divisions of Development and Differentiation, National Institute of Neuroscience, NCNP, Kodaira, Japan
      name:Department of Cell Biology, Harvard Medical School, Boston, USA
      name:Vincent Center for Reproductive Biology, Department of Obstetrics and Gynecology, Massachusetts General Hospital/Harvard Medical School, Boston, USA
      name:Department of Physiology, Michigan State University, Michigan, USA
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