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Tuesday, October 13, 2020 | History

2 edition of Identifying the roles of Rac1 and Rac2 in osteoclastogenesis --in vitro found in the catalog.

Identifying the roles of Rac1 and Rac2 in osteoclastogenesis --in vitro

Dina P. Lebowitz

Identifying the roles of Rac1 and Rac2 in osteoclastogenesis --in vitro

by Dina P. Lebowitz

  • 385 Want to read
  • 28 Currently reading

Published in 2007 .
Written in English


Edition Notes

Thesis (M.Sc.)--University of Toronto, 2007.

Statementby Dina P. Lebowitz.
The Physical Object
Paginationv, 79 leaves :
Number of Pages79
ID Numbers
Open LibraryOL19397236M


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Identifying the roles of Rac1 and Rac2 in osteoclastogenesis --in vitro by Dina P. Lebowitz Download PDF EPUB FB2

Identifying the roles of Rac1 and Rac2 in osteoclastogenesis --in vitro by Dina P. Lebowitz 1 edition - first published in Not in Library.

SBDS is required for Rac2-mediated monocyte migration and signaling downstream of RANK during osteoclastogenesis Article (PDF Available) in Blood (6) November with 28 Reads. To elucidate the specific roles of the Rac1 and Rac2 isoforms during osteoclastogenesis, we used mice deficient in Rac1, Rac2, or both Rac1 and Rac2 in monocyte/osteoclast precursors.

The number of osteoclast precursors on the bone surface is finely determined by the balance between the trafficking of osteoclast precursors to and from the circulation.

This is a novel point of control for osteoclastogenesis in vivo. S1P-dependent migratory control of osteoclast precursors is an attractive target for treating : Junichi Kikuta, Erin Nevius, Masaru Ishii, João P. Pereira. Recently Rac1 and Rac2, the isoforms in osteoclasts, were deleted and the resulting mice have osteopetrosis.

Similarly, genetic manipulation of mice to create animals lacking cdc42 in osteoclasts or having a basally hyperactive form of the same GTPase, yielded reciprocal osteopetrotic and osteopenic phenotypes respectively [].

The mission of the Vanderbilt University Medical Center's Center for Matrix Biology is to foster cohesive interactions among Vanderbilt University scientists who work, directly or indirectly, on extracellular matrix biology in order to facilitate collaborations, promote excellence and acquire funding support.

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The first mouse knockout was Rac2 in (75), which has primarily been studied for defects in the haematopoietic system. Global deletion of Rac1 or Cdc42 is lethal at a very early stage of development (76, 77), and so far global RhoA deletion has not been reported, but.

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