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Minor histocompatibility protein

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GTPase activator for the Rho-type GTPases.

Below are the list of possible Minor histocompatibility protein products. If you cannot find the target and/or product is not available in our catalog, please click here to contact us and request the product or submit your request for custom elisa kit production, custom recombinant protein production or custom antibody production. Custom ELISA Kits, Recombinant Proteins and Antibodies can be designed, manufactured and produced according to the researcher's specifications.
 

Minor histocompatibility protein HA-1

 Minor histocompatibility protein HA-1 ELISA Kit
 Minor histocompatibility protein HA-1 Recombinant
 Minor histocompatibility protein HA-1 Antibody
HMHA1: GTPase activator for the Rho-type GTPases (Potential).

Protein type: Cell surface; GAPs; GAPs, Rac/Rho

Cellular Component: membrane
 Hmha1 ELISA Kit
 Hmha1 Recombinant
 Hmha1 Antibody
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Minor histocompatibility protein HB-1

 Minor histocompatibility protein HB-1 ELISA Kit
 Minor histocompatibility protein HB-1 Recombinant
 Minor histocompatibility protein HB-1 Antibody
HMHB1: Precursor of the histocomplatibility antigen HB-1. More generally, minor histocomplatibility 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 pept
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ides 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 histocomplatibility antigen in HLA-matched sibling marrow transplants. HB-1 is presented on the cell surface by MHC class I HLA-B44. This complex specifically elicits donor-cytotoxic T lymphocyte (CTL) reactivity in B-cell acute lymphoblastic leukemia (B-ALL) after treatment by HLA-identical allogenic bone marrow transplantation (BMT). It induces cell recognition and lysis by CTL. However, HB-1 restricted expression in B-ALL cells and not in normal tissues may allow a specific CTL reactivity against B-ALL without the risk of evoking graft-versus-host disease.

Chromosomal Location of Human Ortholog: 5q31.3
 HMHB1 ELISA Kit
 HMHB1 Recombinant
 HMHB1 Antibody
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Minor histocompatibility protein HMSD variant form

 Minor histocompatibility protein HMSD variant form ELISA Kit
 Minor histocompatibility protein HMSD variant form Recombinant
 Minor histocompatibility protein HMSD variant form Antibody
Also known as Minor histocompatibility protein HMSD variant form (HSMD-v).
HMSD-v: This allelic splice variant of HMSD is the precursor of the histocompatibility antigen ACC-6. 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
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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. However, associated with GVHD, a favorable graft-versus-leukemia (GVL) can be induced by donor-recipient disparities in mHags. ACC-6 is presented to the cell surface by MHC HLA-B*4403. 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. Immunogenicity of most autosomal mHags results from single- nucleotide polymorphisms that cause amino-acid substitutions within epitopes, leading to the differential recognition of peptides between donor and recipient. 2 isoforms of the human protein are produced by alternative splicing.

Chromosomal Location of Human Ortholog: 18q22.1
 HMSD ELISA Kit
 HMSD Recombinant
 HMSD Antibody
 C18orf53 ELISA Kit
 C18orf53 Recombinant
 C18orf53 Antibody
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