CIDEA: Difference between revisions

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'''Cell death activator CIDE-A''' is a [[protein]] that in humans is encoded by the ''CIDEA'' [[gene]].<ref name="pmid9564035">{{cite journal | vauthors = Inohara N, Koseki T, Chen S, Wu X, Nunez G | title = CIDE, a novel family of cell death activators with homology to the 45 kDa subunit of the DNA fragmentation factor | journal = EMBO J | volume = 17 | issue = 9 | pages = 2526–33 |date=Jun 1998 | pmid = 9564035 | pmc = 1170594 | doi = 10.1093/emboj/17.9.2526 }}</ref><ref name="pmid18509062">{{cite journal | vauthors = Puri V, Ranjit S, Konda S, Nicoloro SM, Straubhaar J, Chawla A, Chouinard M, Lin C, Burkart A, Corvera S, Perugini RA, Czech MP | title = Cidea is associated with lipid droplets and insulin sensitivity in humans | journal = Proc Natl Acad Sci U S A | volume = 105 | issue = 22 | pages = 7833–8 |date=Jun 2008 | pmid = 18509062 | pmc = 2409392 | doi = 10.1073/pnas.0802063105 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: CIDEA cell death-inducing DFFA-like effector a| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=1149| accessdate = }}</ref> Cidea is an essential transcriptional coactivator regulating mammary gland secretion of milk lipids.<ref>[http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.2614.html Cidea is an essential transcriptional coactivator regulating mammary gland secretion of milk lipids]</ref>
'''Cell death activator CIDE-A''' is a [[protein]] that in humans is encoded by the ''CIDEA'' [[gene]].<ref name="pmid9564035">{{cite journal | vauthors = Inohara N, Koseki T, Chen S, Wu X, Nunez G | title = CIDE, a novel family of cell death activators with homology to the 45 kDa subunit of the DNA fragmentation factor | journal = EMBO J | volume = 17 | issue = 9 | pages = 2526–33 |date=Jun 1998 | pmid = 9564035 | pmc = 1170594 | doi = 10.1093/emboj/17.9.2526 | url = https://deepblue.lib.umich.edu/bitstream/2027.42/102041/1/emboj7590961.pdf }}</ref><ref name="pmid18509062">{{cite journal | vauthors = Puri V, Ranjit S, Konda S, Nicoloro SM, Straubhaar J, Chawla A, Chouinard M, Lin C, Burkart A, Corvera S, Perugini RA, Czech MP | title = Cidea is associated with lipid droplets and insulin sensitivity in humans | journal = Proc Natl Acad Sci U S A | volume = 105 | issue = 22 | pages = 7833–8 |date=Jun 2008 | pmid = 18509062 | pmc = 2409392 | doi = 10.1073/pnas.0802063105 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: CIDEA cell death-inducing DFFA-like effector a| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=1149| accessdate = }}</ref> Cidea is an essential transcriptional [[Coactivator (genetics)|coactivator]] regulating [[mammary gland]] secretion of milk lipids.<ref>[http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.2614.html Cidea is an essential transcriptional coactivator regulating mammary gland secretion of milk lipids]</ref>


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| summary_text = This gene encodes the homolog of the mouse protein Cidea that has been shown to activate apoptosis. This activation of apoptosis is inhibited by the DNA fragmentation factor DFF45 but not by caspase inhibitors. Mice that lack functional Cidea have higher metabolic rates, higher lipolysis in brown adipose tissue and higher core body temperatures when subjected to cold. These mice are also resistant to diet-induced obesity and diabetes. This suggests that in mice this gene product plays a role in thermogenesis and lipolysis. Two alternative transcripts encoding different isoforms have been identified.<ref name="entrez" />
| summary_text = This gene encodes the [[homolog]] of the mouse protein Cidea that has been shown to activate [[apoptosis]]. This activation of apoptosis is inhibited by the DNA fragmentation factor DFF45 but not by [[caspase]] inhibitors. Mice that lack functional Cidea have higher [[metabolic rate|metabolic rates]], higher [[lipolysis]] in [[brown adipose tissue]] and higher core body temperatures when subjected to cold. These mice are also resistant to diet-induced [[obesity]] and [[diabetes]]. This suggests that in mice this gene product plays a role in [[thermogenesis]] and lipolysis. Two alternative transcripts encoding different [[isoforms]] have been identified.<ref name="entrez" />
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Revision as of 13:04, 4 November 2018

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Cell death activator CIDE-A is a protein that in humans is encoded by the CIDEA gene.[1][2][3] Cidea is an essential transcriptional coactivator regulating mammary gland secretion of milk lipids.[4]

This gene encodes the homolog of the mouse protein Cidea that has been shown to activate apoptosis. This activation of apoptosis is inhibited by the DNA fragmentation factor DFF45 but not by caspase inhibitors. Mice that lack functional Cidea have higher metabolic rates, higher lipolysis in brown adipose tissue and higher core body temperatures when subjected to cold. These mice are also resistant to diet-induced obesity and diabetes. This suggests that in mice this gene product plays a role in thermogenesis and lipolysis. Two alternative transcripts encoding different isoforms have been identified.[3]

References

  1. Inohara N, Koseki T, Chen S, Wu X, Nunez G (Jun 1998). "CIDE, a novel family of cell death activators with homology to the 45 kDa subunit of the DNA fragmentation factor" (PDF). EMBO J. 17 (9): 2526–33. doi:10.1093/emboj/17.9.2526. PMC 1170594. PMID 9564035.
  2. Puri V, Ranjit S, Konda S, Nicoloro SM, Straubhaar J, Chawla A, Chouinard M, Lin C, Burkart A, Corvera S, Perugini RA, Czech MP (Jun 2008). "Cidea is associated with lipid droplets and insulin sensitivity in humans". Proc Natl Acad Sci U S A. 105 (22): 7833–8. doi:10.1073/pnas.0802063105. PMC 2409392. PMID 18509062.
  3. 3.0 3.1 "Entrez Gene: CIDEA cell death-inducing DFFA-like effector a".
  4. Cidea is an essential transcriptional coactivator regulating mammary gland secretion of milk lipids

External links

Further reading