000117377 001__ 117377
000117377 005__ 20180317092339.0
000117377 0247_ $$2doi$$a10.1038/ni1387
000117377 02470 $$2DAR$$a9463
000117377 02470 $$2ISI$$a000241437100009
000117377 037__ $$aARTICLE
000117377 245__ $$aHematopoietic stem cell and multilineage defects generated by constitutive beta-catenin activation
000117377 269__ $$a2006
000117377 260__ $$c2006
000117377 336__ $$aJournal Articles
000117377 500__ $$aMax-Delbruck Center for Molecular Medicine, 13125 Berlin, Germany.
000117377 520__ $$aGain of Wnt signaling through beta-catenin has been ascribed a critical function in the stimulation of hematopoietic stem cell self-renewal, whereas loss of beta-catenin is reportedly dispensable for hematopoiesis. Here we have used conditional mouse genetics and transplantation assays to demonstrate that constitutive activation of beta-catenin blocked multilineage differentiation, leading to the death of mice. Blood cell depletion was accompanied by failure of hematopoietic stem cells to repopulate irradiated hosts and to differentiate into mature cells. Activation of beta-catenin enforced cell cycle entry of hematopoietic stem cells, thus leading to exhaustion of the long-term stem cell pool. Our data suggest that fine-tuned Wnt stimulation is essential for hematopoiesis and is thus critical for therapeutic hematopoietic stem cell population expansion.
000117377 700__ $$aScheller, M.
000117377 700__ $$0240230$$aHuelsken, J.$$g171552
000117377 700__ $$aRosenbauer, F.
000117377 700__ $$aTaketo, M. M.
000117377 700__ $$aBirchmeier, W.
000117377 700__ $$aTenen, D. G.
000117377 700__ $$aLeutz, A.
000117377 773__ $$j7$$k10$$q1037-47$$tNat Immunol
000117377 909CO $$ooai:infoscience.tind.io:117377$$particle$$pSV
000117377 909C0 $$0252084$$pUPHUELSKEN$$xU11259
000117377 937__ $$aCDTSO-ARTICLE-2006-001
000117377 973__ $$aOTHER$$rREVIEWED$$sPUBLISHED
000117377 980__ $$aARTICLE