Mouse Anti-TAP2 Recombinant Antibody (CBYJT-1964) (CBMAB-T1051-YJ)

Transporter 2, ATP-Binding Cassette, Sub-Family B (MDR/TAP)

TAP2 is a member of the superfamily of ATP-binding cassette (ABC) transporters. ABC proteins transport various molecules across extra- and intra-cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). It is a member of the MDR/TAP subfamily. Members of the MDR/TAP subfamily are involved in multidrug resistance. This gene is located 7 kb telomeric to gene family member ABCB2. TAP2 is involved in antigen presentation. This protein forms a heterodimer with ABCB2 in order to transport peptides from the cytoplasm to the endoplasmic reticulum. Mutations in TAP2 may be associated with ankylosing spondylitis, insulin-dependent diabetes mellitus, and celiac disease.

Transporter 2, ATP Binding Cassette Subfamily B Member; Transporter 2, ATP-Binding Cassette, Sub-Family B (MDR/TAP); Peptide Transporter Involved In Antigen Processing 2; Really Interesting New Gene 11 Protein; Peptide Transporter PSF2; Peptide Supply Factor 2; RING11; ABCB3; PSF-2; PSF2; APT2

ABC transporter associated with antigen processing. In complex with TAP1 mediates unidirectional translocation of peptide antigens from cytosol to endoplasmic reticulum (ER) for loading onto MHC class I (MHCI) molecules (PubMed:25656091, PubMed:25377891).
Uses the chemical energy of ATP to export peptides against the concentration gradient (PubMed:25377891).
During the transport cycle alternates between 'inward-facing' state with peptide binding site facing the cytosol to 'outward-facing' state with peptide binding site facing the ER lumen. Peptide antigen binding to ATP-loaded TAP1-TAP2 induces a switch to hydrolysis-competent 'outward-facing' conformation ready for peptide loading onto nascent MHCI molecules. Subsequently ATP hydrolysis resets the transporter to the 'inward facing' state for a new cycle (PubMed:25377891, PubMed:25656091, PubMed:11274390).
Typically transports intracellular peptide antigens of 8 to 13 amino acids that arise from cytosolic proteolysis via IFNG-induced immunoproteasome. Binds peptides with free N- and C-termini, the first three and the C-terminal residues being critical. Preferentially selects peptides having a highly hydrophobic residue at position 3 and hydrophobic or charged residues at the C-terminal anchor. Proline at position 2 has the most destabilizing effect (PubMed:7500034, PubMed:9256420, PubMed:11274390).
As a component of the peptide loading complex (PLC), acts as a molecular scaffold essential for peptide-MHCI assembly and antigen presentation (PubMed:26611325, PubMed:1538751, PubMed:25377891).

Biological Process antigen processing and presentation of endogenous peptide antigen via MHC class IIDA:UniProtKB1 Publication
Biological Process antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-dependentIEA:Ensembl
Biological Process antigen processing and presentation of endogenous peptide antigen via MHC class Ib via ER pathway, TAP-dependentIMP:UniProtKB1 Publication
Biological Process antigen processing and presentation of exogenous protein antigen via MHC class Ib, TAP-dependentIEA:Ensembl
Biological Process cytosol to endoplasmic reticulum transportIMP:UniProtKB1 Publication
Biological Process peptide antigen transportIDA:UniProtKB1 Publication
Biological Process peptide transportIBA:GO_Central1 Publication
Biological Process positive regulation of T cell mediated cytotoxicityIEA:Ensembl
Biological Process protein transportIEA:UniProtKB-KW
Biological Process response to molecule of bacterial originIEA:Ensembl
Biological Process T cell mediated cytotoxicityIEA:Ensembl
Biological Process transmembrane transportIBA:GO_Central1 Publication

Endoplasmic reticulum membrane
The transmembrane segments seem to form a pore in the membrane.

Bare lymphocyte syndrome 1 (BLS1):
A HLA class I deficiency. Contrary to bare lymphocyte syndromes type 2 and type 3, which are characterized by early-onset severe combined immunodeficiency, class I antigen deficiencies are not accompanied by particular pathologic manifestations during the first years of life. Systemic infections have not been described. Chronic bacterial infections, often beginning in the first decade of life, are restricted to the respiratory tract.

Lumenal: 1-6 aa
Helical: 7-27 aa
Cytoplasmic: 28-56 aa
Helical: 57-77 aa
Lumenal: 78-98 aa
Helical: 99-119 aa
Cytoplasmic: 120-148 aa
Helical: 149-169 aa
Lumenal: 170-187 aa
Helical: 188-208 aa
Cytoplasmic: 209-266 aa
Helical: 267-287 aa
Lumenal: 288-293 aa
Helical: 294-314 aa
Cytoplasmic: 315-374 aa
Helical: 375-395 aa
Lumenal: 396-408 aa
Helical: 409-429 aa
Cytoplasmic: 430-686 aa