Linked Life Data

21575136

Source:http://linkedlifedata.com/resource/pubmed/id/21575136

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2011-7-1
pubmed:abstractText
Glutaredoxins (Grxs) have been shown to be critical in maintaining redox homeostasis in living cells. Recently, an emerging subgroup of Grxs with one cysteine residue in the putative active motif (monothiol Grxs) has been identified. However, the biological and physiological functions of this group of proteins have not been well characterized. Here, we characterize a mammalian monothiol Grx (Grx3, also termed TXNL2/PICOT) with high similarity to yeast ScGrx3/ScGrx4. In yeast expression assays, mammalian Grx3s were localized to the nuclei and able to rescue growth defects of grx3grx4 cells. Furthermore, Grx3 inhibited iron accumulation in yeast grx3gxr4 cells and suppressed the sensitivity of mutant cells to exogenous oxidants. In mice, Grx3 mRNA was ubiquitously expressed in developing embryos, adult tissues and organs, and was induced during oxidative stress. Mouse embryos absent of Grx3 grew smaller with morphological defects and eventually died at 12.5 days of gestation. Analysis in mouse embryonic fibroblasts revealed that Grx3(-/-) cells had impaired growth and cell cycle progression at the G(2) /M phase, whereas the DNA replication during the S phase was not affected by Grx3 deletion. Furthermore, Grx3-knockdown HeLa cells displayed a significant delay in mitotic exit and had a higher percentage of binucleated cells. Therefore, our findings suggest that the mammalian Grx3 has conserved functions in protecting cells against oxidative stress and deletion of Grx3 in mice causes early embryonic lethality which could be due to defective cell cycle progression during late mitosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1742-4658
pubmed:author
pubmed:copyrightInfo
© 2011 The Authors Journal compilation © 2011 FEBS.
pubmed:issnType
Electronic
pubmed:volume
278
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2525-39
pubmed:meshHeading
pubmed-meshheading:21575136-Animals, pubmed-meshheading:21575136-Carrier Proteins, pubmed-meshheading:21575136-Cell Cycle, pubmed-meshheading:21575136-Cell Line, pubmed-meshheading:21575136-Embryo, Mammalian, pubmed-meshheading:21575136-Embryonic Development, pubmed-meshheading:21575136-Female, pubmed-meshheading:21575136-Gene Expression Regulation, Enzymologic, pubmed-meshheading:21575136-Gene Silencing, pubmed-meshheading:21575136-Genes, Lethal, pubmed-meshheading:21575136-Glutaredoxins, pubmed-meshheading:21575136-Humans, pubmed-meshheading:21575136-Isoenzymes, pubmed-meshheading:21575136-Male, pubmed-meshheading:21575136-Mice, pubmed-meshheading:21575136-Mice, Inbred C57BL, pubmed-meshheading:21575136-Mice, Transgenic, pubmed-meshheading:21575136-Myoblasts, pubmed-meshheading:21575136-Oxidative Stress, pubmed-meshheading:21575136-RNA, Messenger, pubmed-meshheading:21575136-Recombinant Fusion Proteins
pubmed:year
2011
pubmed:articleTitle
A mammalian monothiol glutaredoxin, Grx3, is critical for cell cycle progression during embryogenesis.
pubmed:affiliation
United States Department of Agriculture/Agricultural Research Service Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA. ncheng@bcm.tmc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't