• Rac2 (Ras-related C3 botulinum toxin substrate 2) is a small (~21 kDa) signaling G protein (to be specific, a GTPase), and is a member of the Rac subfamily of the family Rho family of GTPases. (wikipedia.org)
  • Rac2 GTPase deficiency depletes BCR-ABL+ leukemic stem cells and progenitors in vivo. (alexslemonade.org)
  • The present invention relates generally to improved methods and pharmaceutical compositions for mobilizing hematopoietic stem and progenitor cell from bone marrow into peripheral blood by administration of at least one inhibitor of a GTPase, such as Rac1 and/or Rac2 GTPase. (justia.com)
  • Hyperactivation of p21(ras) and the hematopoietic-specific Rho GTPase, Rac2, cooperate to alter the proliferation of neurofibromin-deficient mast cells in vivo and in vitro. (nih.gov)
  • Immunohistochemistry: Rac1 Antibody [NB100-91266] - Rat spinal cord using Rabbit antibody to RAC1, RAC2 (100-150) at 1:1000 dilution. (novusbio.com)
  • Detects both RAC1 (Gene ID: 5879, UniProt: P63000) and RAC2 (Gene ID: 5880, UniProt: P15153). (novusbio.com)
  • Improved methods and pharmaceutical compositions are provided herein for mobilizing hematopoietic progenitor cells from bone marrow into peripheral blood, comprising the administration of an effective amount of an inhibitor of GTPases, such as Rac1 and Rac2 alone or in combination. (justia.com)
  • In particular, embodiments of the method involve inhibition of both Rac1 and Rac2 GTPases to increase the numbers of hematopoietic stem cells into a subject's peripheral blood of a subject. (justia.com)
  • To investigate this possibility, we established TRIP6 shRNA expressing cell lines with overexpressing Rac2, and examined the proliferation ability of these cells-derived tumorspheres. (ntnu.edu.tw)
  • We found that the Rac2 may act downstream of TRIP6 and mediate TRIP6-regulated proliferation of GBM tumorsphere. (ntnu.edu.tw)
  • Here, we report a novel heterozygous missense mutation in RAC2 with incomplete penetrance, and the associated phenotypes, in a Chinese family. (cqmu.edu.cn)
  • A mutation in RAC2 resulting in a p.G15D substitution. (cqmu.edu.cn)
  • A Novel RAC2 Variant Presenting as Severe Combined Immunodeficiency. (nih.gov)
  • A gain-of-function RAC2 mutation is associated with bone-marrow hypoplasia and an autosomal dominant form of severe combined immunodeficiency. (nih.gov)
  • Defects in RAC2 are the cause of neutrophil immunodeficiency syndrome, that clinically resembles LAD1. (lu.se)
  • A monoallelic activating mutation in RAC2 resulting in a combined immunodeficiency. (harvard.edu)
  • Not too little, not too much: the impact of mutation types in Wiskott-Aldrich syndrome and RAC2 patients. (nih.gov)
  • The disease is due to a point dominant negative mutation in the RAC2 gene causing decreased Rac2 protein expression and a defect in a signaling pathway controlling shape change/motility of neutrophils as well as assembly and activation of NADPH oxidase. (cdc.gov)
  • It is encoded by the gene RAC2. (wikipedia.org)
  • 32 disease terms (MeSH) has been reported with RAC2 gene. (cdc.gov)
  • Rac2 (Ras-related C3 botulinum toxin substrate 2) is a small (~21 kDa) signaling G protein (to be specific, a GTPase), and is a member of the Rac subfamily of the family Rho family of GTPases. (wikipedia.org)
  • Other studies address the function of Rho GTPases, particularly Rac2, which she showed is expressed in endothelial cells and regulates both normal fluid flux and edema formation during injury. (unc.edu)
  • Lastly, the interferon-induced transmembrane protein (IFITM3), interferon alpha inducible protein (IFI6), cysteine rich protein-1 (CRIP1), and the RAC family small GTPase2 (RAC2) were notably upregulated in AA patients. (nih.gov)
  • A quantitative model of resurgence, Resurgence as Choice in Context (RaC2), provided a poor fit to the data (r2 = .52). (abainternational.org)
  • FBRs to such elevated extrinsic forces in the mice were also mediated by the activation of Rac2 signalling in a subpopulation of mechanoresponsive myeloid cells, which could be substantially reduced via the pharmacological or genetic inhibition of Rac2. (stanford.edu)
  • We found that the human FBR is mediated by immune-cell-specific RAC2 mechanotransduction signalling, independently of the chemistry and mechanical properties of the implant, and that a pathological FBR that is human-like at the molecular, cellular and tissue levels can be induced in mice via the application of human-tissue-scale forces through a vibrating silicone implant. (stanford.edu)