IL1RAP
An Error has occured retrieving Wikidata item for infobox IL1RAP (Interleukin-1 receptor accessory protein) هوَ بروتين يُشَفر بواسطة جين IL1RAP في الإنسان.[1][2][2][3]
الوظيفة
هذا القسم فارغ أو غير مكتمل. ساهم في توسيعه. (يوليو 2018) |
الأهمية السريرية
هذا القسم فارغ أو غير مكتمل. ساهم في توسيعه. (يوليو 2018) |
المراجع
- ^ Dale M، Hammond DW، Cox A، Nicklin MJ (أبريل 1998). "The human gene encoding the interleukin-1 receptor accessory protein (IL1RAP) maps to chromosome 3q28 by fluorescence in situ hybridization and radiation hybrid mapping". Genomics. ج. 47 ع. 2: 325–6. DOI:10.1006/geno.1997.5113. PMID:9479509.
- ^ أ ب "Entrez Gene: IL1RAP interleukin 1 receptor accessory protein". مؤرشف من الأصل في 2010-12-05.
- ^ Wesche H، Korherr C، Kracht M، Falk W، Resch K، Martin MU (أبريل 1997). "The interleukin-1 receptor accessory protein (IL-1RAcP) is essential for IL-1-induced activation of interleukin-1 receptor-associated kinase (IRAK) and stress-activated protein kinases (SAP kinases)". J Biol Chem. ج. 272 ع. 12: 7727–31. DOI:10.1074/jbc.272.12.7727. PMID:9065432.
قراءة متعمقة
- Greenfeder SA، Nunes P، Kwee L، وآخرون (1995). "Molecular cloning and characterization of a second subunit of the interleukin 1 receptor complex". J. Biol. Chem. ج. 270 ع. 23: 13757–65. DOI:10.1074/jbc.270.23.13757. PMID:7775431.
- Parnet P، Garka KE، Bonnert TP، وآخرون (1996). "IL-1Rrp is a novel receptor-like molecule similar to the type I interleukin-1 receptor and its homologues T1/ST2 and IL-1R AcP". J. Biol. Chem. ج. 271 ع. 8: 3967–70. DOI:10.1074/jbc.271.8.3967. PMID:8626725.
- Huang J، Gao X، Li S، Cao Z (1998). "Recruitment of IRAK to the interleukin 1 receptor complex requires interleukin 1 receptor accessory protein". Proc. Natl. Acad. Sci. U.S.A. ج. 94 ع. 24: 12829–32. Bibcode:1997PNAS...9412829H. DOI:10.1073/pnas.94.24.12829. PMC:24223. PMID:9371760.
- Cullinan EB، Kwee L، Nunes P، وآخرون (1998). "IL-1 receptor accessory protein is an essential component of the IL-1 receptor". J. Immunol. ج. 161 ع. 10: 5614–20. PMID:9820540.
- Lang D، Knop J، Wesche H، وآخرون (1999). "The type II IL-1 receptor interacts with the IL-1 receptor accessory protein: a novel mechanism of regulation of IL-1 responsiveness". J. Immunol. ج. 161 ع. 12: 6871–7. PMID:9862719.
- Morton NM، de Groot RP، Cawthorne MA، Emilsson V (1999). "Interleukin-1beta activates a short STAT-3 isoform in clonal insulin-secreting cells". FEBS Lett. ج. 442 ع. 1: 57–60. DOI:10.1016/S0014-5793(98)01623-8. PMID:9923604.
- Sizemore N، Leung S، Stark GR (1999). "Activation of phosphatidylinositol 3-kinase in response to interleukin-1 leads to phosphorylation and activation of the NF-kappaB p65/RelA subunit". Mol. Cell. Biol. ج. 19 ع. 7: 4798–805. PMC:84278. PMID:10373529.
- Jensen LE، Muzio M، Mantovani A، Whitehead AS (2000). "IL-1 signaling cascade in liver cells and the involvement of a soluble form of the IL-1 receptor accessory protein". J. Immunol. ج. 164 ع. 10: 5277–86. DOI:10.4049/jimmunol.164.10.5277. PMID:10799889.
- Burns K، Clatworthy J، Martin L، وآخرون (2000). "Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor". Nat. Cell Biol. ج. 2 ع. 6: 346–51. DOI:10.1038/35014038. PMID:10854325.
- Bigonnesse F، Marois M، Maheux R، Akoum A (2001). "Interleukin-1 receptor accessory protein is constitutively expressed in human endometrium throughout the menstrual cycle". Mol. Hum. Reprod. ج. 7 ع. 4: 333–9. DOI:10.1093/molehr/7.4.333. PMID:11279295.
- Jefferies C، Bowie A، Brady G، وآخرون (2001). "Transactivation by the p65 subunit of NF-kappaB in response to interleukin-1 (IL-1) involves MyD88, IL-1 receptor-associated kinase 1, TRAF-6, and Rac1". Mol. Cell. Biol. ج. 21 ع. 14: 4544–52. DOI:10.1128/MCB.21.14.4544-4552.2001. PMC:87113. PMID:11416133.
- Radons J، Gabler S، Wesche H، وآخرون (2002). "Identification of essential regions in the cytoplasmic tail of interleukin-1 receptor accessory protein critical for interleukin-1 signaling". J. Biol. Chem. ج. 277 ع. 19: 16456–63. DOI:10.1074/jbc.M201000200. PMID:11880380.
- Strausberg RL، Feingold EA، Grouse LH، وآخرون (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. ج. 99 ع. 26: 16899–903. Bibcode:2002PNAS...9916899M. DOI:10.1073/pnas.242603899. PMC:139241. PMID:12477932.
- Ruhul Amin AR، Machida K، Oshima K، وآخرون (2003). "A role for SHPS-1/SIRPalpha1 in IL-1beta- and TNFalpha-dependent signaling". Oncogene. ج. 21 ع. 57: 8871–8. DOI:10.1038/sj.onc.1206018. PMID:12483539.
- Smith DE؛ Hanna R؛ Della Friend؛ وآخرون (2003). "The soluble form of IL-1 receptor accessory protein enhances the ability of soluble type II IL-1 receptor to inhibit IL-1 action". Immunity. ج. 18 ع. 1: 87–96. DOI:10.1016/S1074-7613(02)00514-9. PMID:12530978.
- Boch JA، Yoshida Y، Koyama Y، وآخرون (2003). "Characterization of a cascade of protein interactions initiated at the IL-1 receptor". Biochem. Biophys. Res. Commun. ج. 303 ع. 2: 525–31. DOI:10.1016/S0006-291X(03)00385-1. PMID:12659850.
- Bin LH، Xu LG، Shu HB (2003). "TIRP, a novel Toll/interleukin-1 receptor (TIR) domain-containing adapter protein involved in TIR signaling". J. Biol. Chem. ج. 278 ع. 27: 24526–32. DOI:10.1074/jbc.M303451200. PMID:12721283.
- Jensen LE، Whitehead AS (2004). "Expression of alternatively spliced interleukin-1 receptor accessory protein mRNAs is differentially regulated during inflammation and apoptosis". Cell. Signal. ج. 15 ع. 8: 793–802. DOI:10.1016/S0898-6568(03)00039-1. PMID:12781872.