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Mouse TAPBPR functions as an MHC-I peptide exchange catalyst

ABSTRACT: Human TAPBPR is known to function as a Major Histocompatibility Complex class I (MHC-I) peptide exchange catalyst which shapes the peptide repertoire presented to immune cells. Never14theless, investigations characterizing TAPBPR from other species are limited. Here, we characterize mouse TAPBPR, exploring its association partners in mouse cell lines and comparing its function to human TAPBPR. We find that mouse TAPBPR binds MHC-I and calnexin, with a notably sustained interaction with H2-Db compared to H2-Kb. We reveal mouse TAPBPR mediates peptide exchange on both H2-Db and H2-Kb, restricting the peptide repertoire presented on MC-38 cells. Intriguingly, mouse TAPBPR promotes the selection of peptides with a C-terminal methionine on H2-Kb. Together, our findings establish that mouse TAPBPR plays an important role in shaping the MHC-I immunopeptidome by functioning as a peptide editor, like its human counterpart.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Melanocyte, Epithelial Cell, Cell Culture

DISEASE(S): Colorectal Adenocarcinoma,Skin Melanoma

SUBMITTER: Marcel Wacker

LAB HEAD: Dr. Juliane Sarah Walz

PROVIDER: PXD069965 | Pride | 2026-03-23

REPOSITORIES: Pride

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			Action	DRS
	230821_MW_MC38_CL3_DB_Y3B22_17share_DDA_1_400-650mz_msms45.msf	Msf
	230821_MW_MC38_CL3_DB_Y3B22_17share_DDA_1_400-650mz_msms45.raw	Raw
	230821_MW_MC38_CL3_DB_Y3B22_17share_DDA_2_400-650mz_msms46.msf	Msf
	230821_MW_MC38_CL3_DB_Y3B22_17share_DDA_2_400-650mz_msms46.raw	Raw
	230821_MW_MC38_CL3_DB_Y3B22_17share_DDA_3_400-650mz_msms47.msf	Msf

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Mouse TAPBPR functions as an MHC-I peptide exchange catalyst

Project description:Human TAPBPR is known to function as a Major Histocompatibility Complex class I (MHC-I) peptide exchange catalyst which shapes the peptide repertoire presented to immune cells. Never14theless, investigations characterizing TAPBPR from other species are limited. Here, we characterize mouse TAPBPR, exploring its association partners in mouse cell lines and comparing its function to human TAPBPR. We find that mouse TAPBPR binds MHC-I and calnexin, with a notably sustained interaction with H2-Db compared to H2-Kb. We reveal mouse TAPBPR mediates peptide exchange on both H2-Db and H2-Kb, restricting the peptide repertoire presented on MC-38 cells. Intriguingly, mouse TAPBPR promotes the selection of peptides with a C-terminal methionine on H2-Kb. Together, our findings establish that mouse TAPBPR plays an important role in shaping the MHC-I immunopeptidome by functioning as a peptide editor, like its human counterpart.

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