Decoy receptor 2: Difference between revisions

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'''Decoy receptor 2''' ('''DCR2'''), also known as '''TRAIL receptor 4''' ('''TRAILR4''') and '''tumor necrosis factor receptor superfamily member 10D''' ('''TNFRSF10D'''), is a human [[cell surface receptor]] of the [[TNF-receptor]] superfamily.<ref name="pmid9382840">{{cite journal | vauthors = Marsters SA, Sheridan JP, Pitti RM, Huang A, Skubatch M, Baldwin D, Yuan J, Gurney A, Goddard AD, Godowski P, Ashkenazi A | title = A novel receptor for Apo2L/TRAIL contains a truncated death domain | journal = Curr Biol | volume = 7 | issue = 12 | pages = 1003–6 |date=Feb 1998 | pmid = 9382840 | pmc =  | doi =10.1016/S0960-9822(06)00422-2  }}</ref><ref name="pmid9537512">{{cite journal | vauthors = Pan G, Ni J, Yu G, Wei YF, Dixit VM | title = TRUNDD, a new member of the TRAIL receptor family that antagonizes TRAIL signalling | journal = FEBS Lett | volume = 424 | issue = 1-2 | pages = 41–5 |date=Apr 1998 | pmid = 9537512 | pmc =  | doi =10.1016/S0014-5793(98)00135-5  }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: TNFRSF10D tumor necrosis factor receptor superfamily, member 10d, decoy with truncated death domain| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=8793| accessdate = }}</ref>
'''Decoy receptor 2''' ('''DCR2'''), also known as '''TRAIL receptor 4''' ('''TRAILR4''') and '''tumor necrosis factor receptor superfamily member 10D''' ('''TNFRSF10D'''), is a human [[cell surface receptor]] of the [[TNF-receptor]] superfamily.<ref name="pmid9382840">{{cite journal | vauthors = Marsters SA, Sheridan JP, Pitti RM, Huang A, Skubatch M, Baldwin D, Yuan J, Gurney A, Goddard AD, Godowski P, Ashkenazi A | title = A novel receptor for Apo2L/TRAIL contains a truncated death domain | journal = Curr Biol | volume = 7 | issue = 12 | pages = 1003–6 |date=Feb 1998 | pmid = 9382840 | pmc =  | doi =10.1016/S0960-9822(06)00422-2  }}</ref><ref name="pmid9537512">{{cite journal | vauthors = Pan G, Ni J, Yu G, Wei YF, Dixit VM | title = TRUNDD, a new member of the TRAIL receptor family that antagonizes TRAIL signalling | journal = FEBS Lett | volume = 424 | issue = 1-2 | pages = 41–5 |date=Apr 1998 | pmid = 9537512 | pmc =  | doi =10.1016/S0014-5793(98)00135-5  | url =https://deepblue.lib.umich.edu/bitstream/2027.42/116376/1/feb2s0014579398001355.pdf }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: TNFRSF10D tumor necrosis factor receptor superfamily, member 10d, decoy with truncated death domain| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=8793| accessdate = }}</ref>


==Function==
==Function==

Revision as of 12:15, 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
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Wikidata
View/Edit Human

Decoy receptor 2 (DCR2), also known as TRAIL receptor 4 (TRAILR4) and tumor necrosis factor receptor superfamily member 10D (TNFRSF10D), is a human cell surface receptor of the TNF-receptor superfamily.[1][2][3]

Function

The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains an extracellular TRAIL-binding domain, a transmembrane domain, and a truncated cytoplasmic death domain. This receptor does not induce apoptosis, and has been shown to play an inhibitory role in TRAIL-induced cell apoptosis.[3]

References

  1. Marsters SA, Sheridan JP, Pitti RM, Huang A, Skubatch M, Baldwin D, Yuan J, Gurney A, Goddard AD, Godowski P, Ashkenazi A (Feb 1998). "A novel receptor for Apo2L/TRAIL contains a truncated death domain". Curr Biol. 7 (12): 1003–6. doi:10.1016/S0960-9822(06)00422-2. PMID 9382840.
  2. Pan G, Ni J, Yu G, Wei YF, Dixit VM (Apr 1998). "TRUNDD, a new member of the TRAIL receptor family that antagonizes TRAIL signalling" (PDF). FEBS Lett. 424 (1–2): 41–5. doi:10.1016/S0014-5793(98)00135-5. PMID 9537512.
  3. 3.0 3.1 "Entrez Gene: TNFRSF10D tumor necrosis factor receptor superfamily, member 10d, decoy with truncated death domain".

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.