Nix (gene): Difference between revisions

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Nix is a pro-apoptotic gene that is regulated by hypoxia. It expresses a signaling protein related to the BH3-only family. This protein induces autophagy, an intracellular function by which cytoplasmic components are delivered to the lysosome to be broken down and used elsewhere or excreted from the cell. <ref>Zhang, Ji, and Paul A. Ney. “ROLE OF BNIP3 AND NIX IN CELL DEATH, AUTOPHAGY, AND MITOPHAGY.” Cell death and differentiation 16.7 (2009): 939–946. PMC. Web. 15 Apr. 2015.</ref> This protein is important in development because it allows cells to have a consistent store of cellular components. <ref>Mizushima, Noboru, and Beth Levine. "Autophagy in Mammalian Development and Differentiation." Nature Cell Biology 12.9 (2010): 823-30. Nature Publishing Group. Web. 15 Apr. 2015. <http://www.nature.com/ncb/journal/v12/n9/full/ncb0910-823.html>.</ref> It also holds an important role in the differentiation and maturation of erythrocytes and lymphocytes by the process of mitophagy with the help of its regulator BNIP3. <ref>Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.</ref> Using a gene knock out technique in mice, scientists have been able to attribute this pruning of mitochondria and induction of cellular necrosis to the expression of the Nix gene. <ref>Zhang, Ji, and Paul A. Ney. “ROLE OF BNIP3 AND NIX IN CELL DEATH, AUTOPHAGY, AND MITOPHAGY.” Cell death and differentiation 16.7 (2009): 939–946. PMC. Web. 15 Apr. 2015.</ref>

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Not only does it hold a role in the differentiation of these immune and oxygen-carrying cells, but it also affects the development and maintenance of heart tissue. It has been found to be a cause of pathologic hypertrophy and cardiomyocyte apoptosis involved in congenital heart disease. <ref>Dorn, Gerald W. "Physiologic Growth and Pathologic Genes in Cardiac Development and Cardiomyopathy." Trends in Cardiovascular Medicine 15.5 (2015): 185-89. ScienceDirect. Web. 15 Apr. 2015. <http://www.sciencedirect.com/science/article/pii/S1050173805000630>.</ref> The effects of Nix are amplified in the neonatal heart compared to the adult heart. Overexpression of Nix in the fetal mouse has been found to cause severe growth retardation and massive cardiomyocyte apoptosis often followed by lethality. These early interactions between the fetal heart and Nix expression are thought to have a role in the development of adult heart disease. <ref>Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.</ref>


{{AFC comment|1=Please introduce appropriate [[WP:LINK]]s and [[WP:SECTION]]s. &mdash;&nbsp;'''[[User:Yash!|<span style="color:black">Yash!</span>]]&nbsp;<sup>[[User Talk:Yash!|<span style="color:black">[talk]</span>]]</sup>''' 05:48, 25 April 2015 (UTC)}}


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Nix is a pro-apoptotic gene that is regulated by hypoxia. It expresses a signaling protein related to the BH3-only family. This protein induces autophagy, an intracellular function by which cytoplasmic components are delivered to the lysosome to be broken down and used elsewhere or excreted from the cell.<ref>Zhang, Ji, and Paul A. Ney. “ROLE OF BNIP3 AND NIX IN CELL DEATH, AUTOPHAGY, AND MITOPHAGY.” Cell death and differentiation 16.7 (2009): 939–946. PMC. Web. 15 Apr. 2015.</ref> This protein is important in development because it allows cells to have a consistent store of cellular components. <ref>Mizushima, Noboru, and Beth Levine. "Autophagy in Mammalian Development and Differentiation." Nature Cell Biology 12.9 (2010): 823-30. Nature Publishing Group. Web. 15 Apr. 2015. <http://www.nature.com/ncb/journal/v12/n9/full/ncb0910-823.html>.</ref> It also holds an important role in the differentiation and maturation of erythrocytes and lymphocytes by the process of mitophagy with the help of its regulator BNIP3. <ref>Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.</ref> Using a gene knock out technique in mice, scientists have been able to attribute this pruning of mitochondria and induction of cellular necrosis to the expression of the Nix gene. <ref>Zhang, Ji, and Paul A. Ney. “ROLE OF BNIP3 AND NIX IN CELL DEATH, AUTOPHAGY, AND MITOPHAGY.” Cell death and differentiation 16.7 (2009): 939–946. PMC. Web. 15 Apr. 2015.</ref>


⚫
Not only does it hold a role in the differentiation of these immune and oxygen-carrying cells, but it also affects the development and maintenance of heart tissue. It has been found to be a cause of pathologic hypertrophy and cardiomyocyte apoptosis involved in congenital heart disease.<ref>Dorn, Gerald W. "Physiologic Growth and Pathologic Genes in Cardiac Development and Cardiomyopathy." Trends in Cardiovascular Medicine 15.5 (2015): 185-89. ScienceDirect. Web. 15 Apr. 2015. <http://www.sciencedirect.com/science/article/pii/S1050173805000630>.</ref> The effects of Nix are amplified in the neonatal heart compared to the adult heart. Overexpression of Nix in the fetal mouse has been found to cause severe growth retardation and massive cardiomyocyte apoptosis often followed by lethality. These early interactions between the fetal heart and Nix expression are thought to have a role in the development of adult heart disease. <ref>Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.</ref>


==References==
==References==
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*Dorn, Gerald W. "Physiologic Growth and Pathologic Genes in Cardiac Development and Cardiomyopathy." Trends in Cardiovascular Medicine 15.5 (2015): 185-89. ScienceDirect. Web. 15 Apr. 2015. <http://www.sciencedirect.com/science/article/pii/S1050173805000630>.
*Dorn, Gerald W. "Physiologic Growth and Pathologic Genes in Cardiac Development and Cardiomyopathy." Trends in Cardiovascular Medicine 15.5 (2015): 185-89. ScienceDirect. Web. 15 Apr. 2015. <http://www.sciencedirect.com/science/article/pii/S1050173805000630>.
*Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.
*Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.

{{AFC submission|||ts=20150415180320|u=Angiewatts|ns=118}}

Revision as of 05:48, 25 April 2015

Nix is a pro-apoptotic gene that is regulated by hypoxia. It expresses a signaling protein related to the BH3-only family. This protein induces autophagy, an intracellular function by which cytoplasmic components are delivered to the lysosome to be broken down and used elsewhere or excreted from the cell.[1] This protein is important in development because it allows cells to have a consistent store of cellular components. [2] It also holds an important role in the differentiation and maturation of erythrocytes and lymphocytes by the process of mitophagy with the help of its regulator BNIP3. [3] Using a gene knock out technique in mice, scientists have been able to attribute this pruning of mitochondria and induction of cellular necrosis to the expression of the Nix gene. [4]

Not only does it hold a role in the differentiation of these immune and oxygen-carrying cells, but it also affects the development and maintenance of heart tissue. It has been found to be a cause of pathologic hypertrophy and cardiomyocyte apoptosis involved in congenital heart disease.[5] The effects of Nix are amplified in the neonatal heart compared to the adult heart. Overexpression of Nix in the fetal mouse has been found to cause severe growth retardation and massive cardiomyocyte apoptosis often followed by lethality. These early interactions between the fetal heart and Nix expression are thought to have a role in the development of adult heart disease. [6]

References

  1. ^ Zhang, Ji, and Paul A. Ney. “ROLE OF BNIP3 AND NIX IN CELL DEATH, AUTOPHAGY, AND MITOPHAGY.” Cell death and differentiation 16.7 (2009): 939–946. PMC. Web. 15 Apr. 2015.
  2. ^ Mizushima, Noboru, and Beth Levine. "Autophagy in Mammalian Development and Differentiation." Nature Cell Biology 12.9 (2010): 823-30. Nature Publishing Group. Web. 15 Apr. 2015. <http://www.nature.com/ncb/journal/v12/n9/full/ncb0910-823.html>.
  3. ^ Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.
  4. ^ Zhang, Ji, and Paul A. Ney. “ROLE OF BNIP3 AND NIX IN CELL DEATH, AUTOPHAGY, AND MITOPHAGY.” Cell death and differentiation 16.7 (2009): 939–946. PMC. Web. 15 Apr. 2015.
  5. ^ Dorn, Gerald W. "Physiologic Growth and Pathologic Genes in Cardiac Development and Cardiomyopathy." Trends in Cardiovascular Medicine 15.5 (2015): 185-89. ScienceDirect. Web. 15 Apr. 2015. <http://www.sciencedirect.com/science/article/pii/S1050173805000630>.
  6. ^ Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.
  • Zhang, Ji, and Paul A. Ney. “ROLE OF BNIP3 AND NIX IN CELL DEATH, AUTOPHAGY, AND MITOPHAGY.” Cell death and differentiation 16.7 (2009): 939–946. PMC. Web. 15 Apr. 2015.
  • Mizushima, Noboru, and Beth Levine. "Autophagy in Mammalian Development and Differentiation." Nature Cell Biology 12.9 (2010): 823-30. Nature Publishing Group. Web. 15 Apr. 2015. <http://www.nature.com/ncb/journal/v12/n9/full/ncb0910-823.html>.
  • Dorn, Gerald W. "Physiologic Growth and Pathologic Genes in Cardiac Development and Cardiomyopathy." Trends in Cardiovascular Medicine 15.5 (2015): 185-89. ScienceDirect. Web. 15 Apr. 2015. <http://www.sciencedirect.com/science/article/pii/S1050173805000630>.
  • Dorn, Gerald W. “Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors.” Journal of cardiovascular translational research 3.4 (2010): 374–383. PMC. Web. 15 Apr. 2015.
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