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Rho GTP ases control specific cytoskeleton‐dependent functions of hematopoietic stem cells
Author(s) -
Nayak Ramesh C.,
Chang KyungHee,
Vaitinadin NatarajaSarma,
Cancelas Jose A.
Publication year - 2013
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12119
Subject(s) - gtpase , microbiology and biotechnology , biology , guanine nucleotide exchange factor , stem cell , rac gtp binding proteins , signal transduction , cytoskeleton , actin cytoskeleton , progenitor cell , gtp binding protein regulators , haematopoiesis , rac1 , g protein , cell , genetics
Summary The Rho family of guanosine triphosphatases ( GTP ases) is composed of members of the Ras superfamily of proteins. They are GTP ‐bound molecules with a modest intrinsic GTP ase activity that can be accelerated upon activation/localization of specialized guanine nucleotide exchange factors. Members of this family act as molecular switches and are required for coordinated cytoskeletal rearrangements that are crucial in a set of specialized functions of mammalian stem cells. These functions include self‐renewal, adhesion, and migration. Mouse gene‐targeting studies have provided convincing evidence of the indispensable and dispensable roles of individual members of the Rho GTP ase family and the putative upstream and downstream mediators in stem cell‐specific functions. The role of Rho GTP ases and related signaling pathways previously seen in other cell types and organisms have been confirmed in mammalian hematopoietic stem cells ( HSC s), and new signaling pathways and unexpected functions unique to HSC s have been identified and dissected. This review summarizes our current understanding of the role of Rho family of GTP ases on HSC and progenitor activity through cytoskeleton‐mediated signaling pathways, providing insight about relevant signaling pathways that regulate mammalian stem cell self‐renewal, adhesion, and migration.