Product Datasheet  
ARHGAP45 Antibody  
Catalog Number: 47786  
Technical:tech@swbio.com  
Information:info@swbio.com  
Description  
  • host_species:  
  • Rabbit
  • Amount:  
  • 100μgμg
  • Swiss-Prot No.:  
  • Swiss-Prot#:Q92619
    NCBI Gene ID:23526
    Gene Accssion:NP_036424
  • Form of Antibody:  
  • Rabbit IgG in pH7.4 PBS, 0.05% NaN3, 40% Glycerol.
  • Storage:  
  • Store at -20˚C
  • Immunogen:  
  • Synthetic peptide of human ARHGAP45
  • reactivity:  
  • Hu
  • appl_detail:  
  • IHC dilution:1: 10-50
  • other_names:  
  • HA-1; HMHA1; HLA-HA1
  • Purification:  
  • Antigen affinity purification
  • Specificity:  
  • The antibody detects endogenous levels of total ARHGAP45 protein.
  • Applications:  
  • IHC
  • Background:  
  • Contains a GTPase activator for the Rho-type GTPases (RhoGAP) domain that would be able to negatively regulate the actin cytoskeleton as well as cell spreading. However, also contains N-terminally a BAR-domin which is able to play an autoinhibitory effect on this RhoGAP activity. Precursor of the histocompatibility antigen HA-1. More generally, minor histocompatibility antigens (mHags) refer to immunogenic peptide which, when complexed with MHC, can generate an immune response after recognition by specific T-cells. The peptides are derived from polymorphic intracellular proteins, which are cleaved by normal pathways of antigen processing. The binding of these peptides to MHC class I or class II molecules and its expression on the cell surface can stimulate T-cell responses and thereby trigger graft rejection or graft-versus-host disease (GVHD) after hematopoietic stem cell transplantation from HLA-identical sibling donor. GVHD is a frequent complication after bone marrow transplantation (BMT), due to mismatch of minor histocompatibility antigen in HLA-matched sibling marrow transplants. Specifically, mismatching for mHag HA-1 which is recognized as immunodominant, is shown to be associated with the development of severe GVHD after HLA-identical BMT. HA-1 is presented to the cell surface by MHC class I HLA-A*0201, but also by other HLA-A alleles. This complex specifically elicits donor-cytotoxic T-lymphocyte (CTL) reactivity against hematologic malignancies after treatment by HLA-identical allogenic BMT. It induces cell recognition and lysis by CTL.



 
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