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Heather L. Szabo-Rogers

Researcher at King's College London

Publications -  9
Citations -  4279

Heather L. Szabo-Rogers is an academic researcher from King's College London. The author has contributed to research in topics: Stem cell & Haematopoiesis. The author has an hindex of 8, co-authored 8 publications receiving 3924 citations.

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Journal ArticleDOI

A Lineage of Myeloid Cells Independent of Myb and Hematopoietic Stem Cells

TL;DR: It is found that the transcription factor Myb was required for development of HSCs and all CD11bhigh monocytes and macrophages, but was dispensable for yolk sac (YS)macrophages and for the development of YS-derived F4/80bright macrophage populations in several tissues.
Journal Article

A lineage of myeloid cells independent of Myb and hematopoietic stem cells

TL;DR: Schulz et al. as discussed by the authors investigated whether adult macrophages all share a common developmental origin and found that a population of yolk-sac-derived, tissue-resident macophages was able to develop and persist in adult mice in the absence of hematopoietic stem cells.
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Neural crest origin of olfactory ensheathing glia

TL;DR: It is shown that OECs in fact originate from the neural crest and hence share a common developmental heritage with Schwann cells, which overturns the existing dogma on the developmental origin of O ECs.
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The planar cell polarity effector Fuz is essential for targeted membrane trafficking, ciliogenesis and mouse embryonic development.

TL;DR: It is reported here that Fuz mutant mice show neural tube defects, skeletal dysmorphologies and Hedgehog signalling defects stemming from disrupted ciliogenesis, and a central role for Fuz in membrane trafficking is established, showing thatFuz is essential for trafficking of cargo to basal bodies and to the apical tips of cilia.
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New directions in craniofacial morphogenesis.

TL;DR: A number of recent embryological studies, using chicken, frog, zebrafish and mouse, which have identified crucial signaling centers in the embryonic face are highlighted, demonstrating how small variations in growth factor signaling can lead to a diversity of phenotypic outcomes.