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Apoptosis and in vivo models to study the molecules related to this phenomenon

Bibliographic Details
Main Author: Luchs,Adriana
Publication Date: 2010
Other Authors: Pantaleão,Claudia
Format: Article
Language: eng
Source: Einstein (São Paulo)
Download full: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082010000400495
Summary: ABSTRACT Apoptosis or programmed cell death is a physiological process, essential for eliminating cells in excess or that are no longer necessary to the organism, acting on tissue homeostasis, although the phenomenon is also involved in pathological conditions. Apoptosis promotes activation of biochemical pathways inside cells called caspase pathway, of the proteins responsible for the cleavage of several cell substrates, leading to cell death. Antiapoptotic members of the Bcl-2 family (B cell CLL/lymphoma 2), that belong to the intrinsic route of the activation of caspases, such as Bcl-xL (extra-large B-cell lymphoma) and Bcl-w (Bcl-2-like 2), act predominantly to prevent that pro-apoptotic members, such as Bax (Bcl-2-associated X protein) and Bak (Bcl-2 relative bak) lead to cell death. Antiapoptotic molecules are considered potentially oncogenic. Murine models are known to be valuable systems for the experimental analysis of oncogenes in vivo, and for the identification of pharmacological targets for cancer and to assess antitumor therapies. Given the importance of tumorigenesis studies on the immune responses to cancer and the possibility of investigating the participation of antiapoptotic molecules in tumor progression in vivo, the development of new models may be platforms for studies on tumorigenesis, immune antitumor responses, investigation of the ectopic expression of antiapoptotic molecules and immunotherapies for tumors.
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spelling Apoptosis and in vivo models to study the molecules related to this phenomenonApoptosis/immunologyApoptosis/physiologyGenes, bcl-2/metabolismCaspasesCell deathNeoplasmsABSTRACT Apoptosis or programmed cell death is a physiological process, essential for eliminating cells in excess or that are no longer necessary to the organism, acting on tissue homeostasis, although the phenomenon is also involved in pathological conditions. Apoptosis promotes activation of biochemical pathways inside cells called caspase pathway, of the proteins responsible for the cleavage of several cell substrates, leading to cell death. Antiapoptotic members of the Bcl-2 family (B cell CLL/lymphoma 2), that belong to the intrinsic route of the activation of caspases, such as Bcl-xL (extra-large B-cell lymphoma) and Bcl-w (Bcl-2-like 2), act predominantly to prevent that pro-apoptotic members, such as Bax (Bcl-2-associated X protein) and Bak (Bcl-2 relative bak) lead to cell death. Antiapoptotic molecules are considered potentially oncogenic. Murine models are known to be valuable systems for the experimental analysis of oncogenes in vivo, and for the identification of pharmacological targets for cancer and to assess antitumor therapies. Given the importance of tumorigenesis studies on the immune responses to cancer and the possibility of investigating the participation of antiapoptotic molecules in tumor progression in vivo, the development of new models may be platforms for studies on tumorigenesis, immune antitumor responses, investigation of the ectopic expression of antiapoptotic molecules and immunotherapies for tumors.Instituto Israelita de Ensino e Pesquisa Albert Einstein2010-12-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082010000400495einstein (São Paulo) v.8 n.4 2010reponame:Einstein (São Paulo)instname:Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)instacron:IIEPAE10.1590/s1679-45082010rb1685info:eu-repo/semantics/openAccessLuchs,AdrianaPantaleão,Claudiaeng2017-03-14T00:00:00Zoai:scielo:S1679-45082010000400495Revistahttps://journal.einstein.br/pt-br/ONGhttps://old.scielo.br/oai/scielo-oai.php||revista@einstein.br2317-63851679-4508opendoar:2017-03-14T00:00Einstein (São Paulo) - Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)false
dc.title.none.fl_str_mv Apoptosis and in vivo models to study the molecules related to this phenomenon
title Apoptosis and in vivo models to study the molecules related to this phenomenon
spellingShingle Apoptosis and in vivo models to study the molecules related to this phenomenon
Luchs,Adriana
Apoptosis/immunology
Apoptosis/physiology
Genes, bcl-2/metabolism
Caspases
Cell death
Neoplasms
title_short Apoptosis and in vivo models to study the molecules related to this phenomenon
title_full Apoptosis and in vivo models to study the molecules related to this phenomenon
title_fullStr Apoptosis and in vivo models to study the molecules related to this phenomenon
title_full_unstemmed Apoptosis and in vivo models to study the molecules related to this phenomenon
title_sort Apoptosis and in vivo models to study the molecules related to this phenomenon
author Luchs,Adriana
author_facet Luchs,Adriana
Pantaleão,Claudia
author_role author
author2 Pantaleão,Claudia
author2_role author
dc.contributor.author.fl_str_mv Luchs,Adriana
Pantaleão,Claudia
dc.subject.por.fl_str_mv Apoptosis/immunology
Apoptosis/physiology
Genes, bcl-2/metabolism
Caspases
Cell death
Neoplasms
topic Apoptosis/immunology
Apoptosis/physiology
Genes, bcl-2/metabolism
Caspases
Cell death
Neoplasms
description ABSTRACT Apoptosis or programmed cell death is a physiological process, essential for eliminating cells in excess or that are no longer necessary to the organism, acting on tissue homeostasis, although the phenomenon is also involved in pathological conditions. Apoptosis promotes activation of biochemical pathways inside cells called caspase pathway, of the proteins responsible for the cleavage of several cell substrates, leading to cell death. Antiapoptotic members of the Bcl-2 family (B cell CLL/lymphoma 2), that belong to the intrinsic route of the activation of caspases, such as Bcl-xL (extra-large B-cell lymphoma) and Bcl-w (Bcl-2-like 2), act predominantly to prevent that pro-apoptotic members, such as Bax (Bcl-2-associated X protein) and Bak (Bcl-2 relative bak) lead to cell death. Antiapoptotic molecules are considered potentially oncogenic. Murine models are known to be valuable systems for the experimental analysis of oncogenes in vivo, and for the identification of pharmacological targets for cancer and to assess antitumor therapies. Given the importance of tumorigenesis studies on the immune responses to cancer and the possibility of investigating the participation of antiapoptotic molecules in tumor progression in vivo, the development of new models may be platforms for studies on tumorigenesis, immune antitumor responses, investigation of the ectopic expression of antiapoptotic molecules and immunotherapies for tumors.
publishDate 2010
dc.date.none.fl_str_mv 2010-12-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082010000400495
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082010000400495
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/s1679-45082010rb1685
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Instituto Israelita de Ensino e Pesquisa Albert Einstein
publisher.none.fl_str_mv Instituto Israelita de Ensino e Pesquisa Albert Einstein
dc.source.none.fl_str_mv einstein (São Paulo) v.8 n.4 2010
reponame:Einstein (São Paulo)
instname:Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)
instacron:IIEPAE
instname_str Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)
instacron_str IIEPAE
institution IIEPAE
reponame_str Einstein (São Paulo)
collection Einstein (São Paulo)
repository.name.fl_str_mv Einstein (São Paulo) - Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)
repository.mail.fl_str_mv ||revista@einstein.br
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