Correction for “ Interleukin 1 receptor - associated kinase 1 ( IRAK 1 )
نویسندگان
چکیده
MICROBIOLOGY Correction for “Interleukin 1 receptor-associated kinase 1 (IRAK1) mutation is a common, essential driver for Kaposi sarcoma herpesvirus lymphoma,” by Dongmei Yang, Wuguo Chen, Jie Xiong, Carly J. Sherrod, David H. Henry, and Dirk P. Dittmer, which appeared in issue 44, November 4, 2014, of Proc Natl Acad Sci USA (111:E4762–E4768; first published October 23, 2014; 10.1073/ pnas.1405423111). The authors note that on page E4765, left column, third full paragraph, the text should instead appear as “From a statistical point of view, all the PEL-specific SNVs represent candidate driver mutations and deserve experimental follow-up, most notably VBP1 and WDR13, which are abundantly transcribed in PEL. We prioritized IRAK1 because IRAK inhibitors have entered phase I human clinical trials. Fifty-five previously identified, noncoding SNVs in the IRAK1 locus were not conserved among PEL; only the IRAK1 mutation was. The IRAK1 mutation is a common polymorphism, as recorded in various SNV databases. The odds ratio for association of this SNV with PEL is estimated at 8.4. . .686.5 (95% CI). Because we only had two matched normal and tumor samples, we cannot claim that any of the PEL-specific SNVs represent somatic events in addition to PEL-defining polymorphisms.”
منابع مشابه
IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) family.
The interleukin-1 receptor-associated kinase (IRAK) was first described as a signal transducer for interleukin-1 (IL-1) and has later been implicated in signal transduction of other members of the Toll/IL-1 receptor family. We now report the identification and characterization of a novel IRAK-like molecule. In contrast to the ubiquitously expressed IRAK and IRAK-2, this new IRAK-like molecule i...
متن کاملMutant cells that do not respond to interleukin-1 (IL-1) reveal a novel role for IL-1 receptor-associated kinase.
Mutagenized human 293 cells containing an interleukin-1 (IL-1)-regulated herpes thymidine kinase gene, selected in IL-1 and gancyclovir, have yielded many independent clones that are unresponsive to IL-1. The four clones analyzed here carry recessive mutations and represent three complementation groups. Mutant A in complementation group I1 lacks IL-1 receptor-associated kinase (IRAK), while the...
متن کاملInterleukin (IL)-1 Receptor–associated Kinase (IRAK) Requirement for Optimal Induction of Multiple IL-1 Signaling Pathways and IL-6 Production
Interleukin (IL)-1 is a proinflammatory cytokine with pleiotropic effects in inflammation. IL-1 binding to its receptor triggers a cascade of signaling events, including activation of the stress-activated mitogen-activated protein (MAP) kinases, c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase, as well as transcription factor nuclear factor kappaB (NF-kappaB). IL-1 signaling results in cellul...
متن کاملIRAK-4 Inhibitors for Inflammation
Interleukin-1 receptor-associated kinases (IRAKs) are key components in the signal transduction pathways utilized by interleukin-1 receptor (IL-1R), interleukin-18 receptor (IL-18R), and Toll-like receptors (TLRs). Out of four members in the mammalian IRAK family, IRAK-4 is considered to be the "master IRAK", the only family member indispensable for IL-1R/TLR signaling. In humans, mutations res...
متن کاملInterleukin-1 (IL-1) receptor-associated kinase-dependent IL-1-induced signaling complexes phosphorylate TAK1 and TAB2 at the plasma membrane and activate TAK1 in the cytosol.
Interleukin-1 (IL-1) receptor-associated kinase (IRAK) plays an important role in the sequential formation and activation of IL-1-induced signaling complexes. Previous studies showed that IRAK is recruited to the IL-1-receptor complex, where it is hyperphosphorylated. We now find that the phosphorylated IRAK in turn recruits TRAF6 to the receptor complex (complex I), which differs from the prev...
متن کاملIncreased IRAK-4 Kinase Activity in Alzheimer’s Disease; IRAK-1/4 Inhibitor I Prevents Pro-inflammatory Cytokine Secretion but not the Uptake of Amyloid Beta by Primary Human Glia
Alzheimer’s disease (AD) is characterized by the deposition of amyloid-β (Aβ), which is associated with a neuroinflammatory response involving microglia and astrocytes. This neuroinflammatory response has detrimental effects on disease progression but also has a beneficial function on removal of excess Aβ. Microglia and astrocytes are involved in the clearance of Aβ from the brain, but neuroinf...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2015