Show simple item record

dc.contributor.authorKim, Peter Geon
dc.contributor.authorAlbacker, Colleen E.
dc.contributor.authorLu, Yi-fen
dc.contributor.authorJang, Il-ho
dc.contributor.authorLim, Yoowon
dc.contributor.authorHeffner, Garrett C.
dc.contributor.authorArora, Natasha
dc.contributor.authorBowman, Teresa V.
dc.contributor.authorLin, Michelle I.
dc.contributor.authorLensch, M. William
dc.contributor.authorAngeles, Alejandro Los
dc.contributor.authorZon, Leonard I.
dc.contributor.authorLoewer, Sabine
dc.contributor.authorDaley, George Q.
dc.date.accessioned2019-10-14T16:31:54Z
dc.date.issued2013
dc.identifier.citationKim, P. G., C. E. Albacker, Y.-f. Lu, I.-h. Jang, Y. Lim, G. C. Heffner, N. Arora, et al. 2013. “Signaling Axis Involving Hedgehog, Notch, and Scl Promotes the Embryonic Endothelial-to-Hematopoietic Transition.” Proceedings of the National Academy of Sciences 110 (2): E141–50. doi:10.1073/pnas.1214361110.
dc.identifier.issn0027-8424
dc.identifier.issn0744-2831
dc.identifier.issn1091-6490
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:41543107*
dc.description.abstractDuring development, the hematopoietic lineage transits through hemogenic endothelium, but the signaling pathways effecting this transition are incompletely characterized. Although the Hedgehog (Hh) pathway is hypothesized to play a role in patterning blood formation, early embryonic lethality of mice lacking Hh signaling precludes such analysis. To determine a role for Hh signaling in patterning of hemogenic endothelium, we assessed the effect of altered Hh signaling in differentiating mouse ES cells, cultured mouse embryos, and developing zebrafish embryos. In differentiating mouse ES cells and mouse yolk sac cultures, addition of Indian Hh ligand increased hematopoietic progenitors, whereas chemical inhibition of Hh signaling reduced hematopoietic progenitors without affecting primitive streak mesoderm formation. In the setting of Hh inhibition, induction of either Notch signaling or overexpression of Stem cell leukemia (Scl)/T-cell acute lymphocytic leukemia protein 1 rescued hemogenic vascular-endothelial cadherin(+) cells and hematopoietic progenitor formation. Together, our results reveal that Scl overexpression is sufficient to rescue the developmental defects caused by blocking the Hh and Notch pathways, and inform our understanding of the embryonic endothelial-to-hematopoietic transition.
dc.language.isoen_US
dc.publisherNational Academy of Sciences
dash.licenseLAA
dc.titleSignaling axis involving Hedgehog, Notch, and Scl promotes the embryonic endothelial-to-hematopoietic transition
dc.typeJournal Article
dc.description.versionVersion of Record
dc.relation.journalProceedings of the National Academy of Sciences of the United States of America
dash.depositing.authorZon, Leonard::81a6e88fe074c911e300de7359c46d7d::600
dc.date.available2019-10-14T16:31:54Z
dash.workflow.comments1Science Serial ID 91094
dc.identifier.doi10.1073/pnas.1214361110
dash.source.volume110;2
dash.source.pageE141


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record