000114847 001__ 114847
000114847 005__ 20190527135626.0
000114847 0247_ $$2doi$$a10.1074/jbc.270.18.10743
000114847 037__ $$aARTICLE
000114847 245__ $$aMouse interleukin-2 receptor alpha gene expression. Interleukin-1 and interleukin-2 control transcription via distinct cis-acting elements
000114847 269__ $$a1995
000114847 260__ $$c1995
000114847 336__ $$aJournal Articles
000114847 500__ $$aSwiss Institute for Experimental Cancer Research (ISREC), Epalinges.
000114847 520__ $$aWe have shown that interleukin-1 (IL-1) and IL-2 control IL-2 receptor alpha (IL-2R alpha) gene transcription in CD4-CD8- murine T lymphocyte precursors. Here we map the cis-acting elements that mediate interleukin responsiveness of the mouse IL-2R alpha gene using a thymic lymphoma-derived hybridoma (PC60). The transcriptional response of the IL-2R alpha gene to stimulation by IL-1 + IL-2 is biphasic. IL-1 induces a rapid, protein synthesis-independent appearance of IL-2R alpha mRNA that is blocked by inhibitors of NF-kappa B activation. It also primes cells to become IL-2 responsive and thereby prepares the second phase, in which IL-2 induces a 100-fold further increase in IL-2R alpha transcripts. Transient transfection experiments show that several elements in the promoter-proximal region of the IL-2R alpha gene contribute to IL-1 responsiveness, most importantly an NF-kappa B site conserved in the human and mouse gene. IL-2 responsiveness, on the other hand, depends on a 78-nucleotide segment 1.3 kilobases upstream of the major transcription start site. This segment functions as an IL-2-inducible enhancer and lies within a region that becomes DNase I hypersensitive in normal T cells in which IL-2R alpha expression has been induced. IL-2 responsiveness requires three distinct elements within the enhancer. Two of these are potential binding sites for STAT proteins.
000114847 700__ $$aSperisen, P.
000114847 700__ $$aWang, S. M.
000114847 700__ $$aSoldaini, E.
000114847 700__ $$aPla, M.
000114847 700__ $$aRusterholz, C.
000114847 700__ $$0244404$$g113607$$aBucher, P.
000114847 700__ $$aCorthesy, P.
000114847 700__ $$aReichenbach, P.
000114847 700__ $$aNabholz, M.
000114847 773__ $$j270$$tJournal of Biological Chemistry$$k18$$q10743-53
000114847 909C0 $$xU11780$$0252244$$pGR-BUCHER
000114847 909CO $$pSV$$particle$$ooai:infoscience.tind.io:114847
000114847 937__ $$aGR-BUCHER-ARTICLE-1995-004
000114847 973__ $$rREVIEWED$$sPUBLISHED$$aOTHER
000114847 980__ $$aARTICLE