SCUBA

ARHGAP45 — Rho GTPase activating protein 45

ARHGAP45 belongs to a gene co-expression module in 3 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

ARHGAP45's module in each cell type

Cell typeModuleShares the module with
Gamma-delta T cellsImmune Synapse Cytoskeleton
Cytoskeletal
ARHGAP4, ATP2A3, CD48, DDOST, ICAM3, IL32, LAPTM5, LTB4R2 +8 more
MacrophagesRetromer Endosomal Sorting
Vesicular traficking
ABHD15, ARHGAP9, CNPY3, CRBN, CTSO, DAB2, DRAM2, FAM217B +20 moreView in SCUBA
Mucosal-associated invariant T cellT cell Activation Signaling
TCR Signaling
AGAP2, CDK5RAP3, DNMT1, IL10RA, ITGAL, JADE2, NBR1, PLCB2 +6 more

About the gene

SynonymsHA-1, HMHA1, KIAA0223
Chromosome19: 1065923-1086628
Predicted locationIntracellular
Essential geneNo
Protein classPlasma proteins, Predicted intracellular proteins
Molecular functionGTPase activation

Function

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.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.