Dataset Information

MHC class I-mediated antigen presentation is independent of calreticulin

ABSTRACT: TMT-MS analysis of the proteome in whole cell lysates from primary murine neutrophil granulocytes and CD8+ T cells obtained from mice carrying a calreticulin knock out or oncogenic mutation (CALRdel52)

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): T Cell, Neutrophil

SUBMITTER: Klaus Kratochwill

LAB HEAD: Dr Klaus Kratochwill

PROVIDER: PXD062085 | Pride | 2025-11-17

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	241101_IP_MHo_041-V0057-X0335_Tcells.msf	Msf
	241102_IP_MHo_041-V0056-X0334_Neutrophils.msf	Msf
	IP_MHo_041-V0056-A01-F030-X0334-1.raw	Raw
	IP_MHo_041-V0056-A02-F030-X0334-1.raw	Raw
	IP_MHo_041-V0056-A03-F030-X0334-1.raw	Raw

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Publications

AQP7 deficiency drives adipose tissue remodeling and disrupts homeostasis.

Costa Ines Pd IP Schiano Guglielmo G Sacnun Juan Manuel JM Herzog Rebecca R Kerr Alastair A Dahlman Ingrid I Delporte Christine C Kratochwill Klaus K Devuyst Olivier O

npj metabolic health and disease 20251107 1

The aquaporin-7 (AQP7) channel mediates glycerol release from adipocytes. Genetic variants decreasing AQP7 expression are associated with adiposity and metabolic complications in humans. Using human data, mouse models, and cellular systems, we investigated how AQP7 influences adipose tissue maturation and homeostasis. Negative correlations between methylation on the AQP7 locus, expression of AQP7 in the adipose tissue and BMI were observed in humans. Mice lacking Aqp7 had increased body weight a ...[more]

PMID: 41203811

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