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The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans.

紀錄類型:	書目-語言資料,手稿 : Monograph/item
正題名/作者:	The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans./
作者:	Munkacsy, Erin Elizabeth.
面頁冊數:	1 online resource (105 pages)
附註:	Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.
Contained By:	Dissertation Abstracts International78-10B(E).
標題:	Cellular biology. -
電子資源:	click for full text (PQDT)
ISBN:	9781369813906

The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans.
Munkacsy, Erin Elizabeth.

The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans. - 1 online resource (105 pages)

Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.

Thesis (Ph.D.)

Includes bibliographical references

Mitochondrial dysfunction underlies numerous age-related pathologies. In an effort to discover how the detrimental effects of mitochondrial dysfunction might be alleviated, we examined how the nematode Caenorhabditis elegans not only adapts to disruption of the mitochondrial electron transport chain, but in many instances responds with extended lifespan.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2018

Mode of access: World Wide Web

ISBN: 9781369813906Subjects--Topical Terms:

1148666
Cellular biology.
Index Terms--Genre/Form:

554714
Electronic books.

The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans.
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100 1 $a Munkacsy, Erin Elizabeth. $3 1182387
245 1 4 $a The Role of Mitochondrial Retrograde Signaling in the Lifespan Extension of Caenorhabditis Elegans.
264 0 $c 2017
300 $a 1 online resource (105 pages)
336 $a text $b txt $2 rdacontent
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500 $a Source: Dissertation Abstracts International, Volume: 78-10(E), Section: B.
500 $a Adviser: Nicholas Musi.
502 $a Thesis (Ph.D.) $c The University of Texas Health Science Center at San Antonio $d 2017.
504 $a Includes bibliographical references
520 $a Mitochondrial dysfunction underlies numerous age-related pathologies. In an effort to discover how the detrimental effects of mitochondrial dysfunction might be alleviated, we examined how the nematode Caenorhabditis elegans not only adapts to disruption of the mitochondrial electron transport chain, but in many instances responds with extended lifespan.
520 $a Altering mitochondrial function changes the relative quantities of metabolites in the cell and may contribute to the resulting organismal phenotype. Some of these metabolites are uniquely enriched in long-lived Caenorhabditis elegans strains with mutations in nuclear-encoded mitochondrial proteins. Specifically, these worms generate elevated amounts of alpha-ketoacids, which are structurally related to alpha-ketoglutarate and may inhibit alpha-ketoglutarate dependent dehydrogenases. We found that provision of several alpha-ketoacids to wild-type worms is sufficient to extend their lifespan and at least one mode of action is through stabilization of hypoxia-inducible factor-1. We also found that an a-ketoglutarate mimetic, 2,4-pyridinedicarboxylic acid, is able to increase the lifespan of wild-type worms but not hypoxia-inducible factor-1 null mutants. Metabolites that build up following mitochondrial respiratory dysfunction may form a novel mode of cell signaling that acts to regulate lifespan.
520 $a In addition, we have identified a novel p38 mitogen-activated protein kinase signaling cascade that is induced by disruption of mitochondrial electron transport chain but independent of the mitochondrial unfolded protein response. This novel cascade is generally activated in counterpoint to the worm ortholog of mammalian nuclear factor-erythroid-related factor, which we show is under the control of the activating transcription factor associated with stress. Significantly, we show that those forms of mitochondrial disruption that activate this mitogen-activated protein kinase cascade induce life extension dependent upon this pathway.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2018
538 $a Mode of access: World Wide Web
650 4 $a Cellular biology. $3 1148666
650 4 $a Aging. $3 559847
655 7 $a Electronic books. $2 local $3 554714
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690 $a 0493
710 2 $a ProQuest Information and Learning Co. $3 1178819
710 2 $a The University of Texas Health Science Center at San Antonio. $b Cellular & Structural Biology. $3 1182388
773 0 $t Dissertation Abstracts International $g 78-10B(E).
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10253990 $z click for full text (PQDT)