@article {8068,
	title = {MID2 can substitute for MID1 and control exocytosis of lytic granules in cytotoxic T cells.},
	journal = {APMIS},
	volume = {123},
	year = {2015},
	month = {2015 Aug},
	pages = {682-7},
	abstract = {<p>We have recently shown that the E3 ubiquitin ligase midline 1 (MID1) is upregulated in murine cytotoxic lymphocytes (CTL), where it controls exocytosis of lytic granules and the killing capacity. Accordingly, CTL from MID1 knock-out (MID1(-/-)) mice have a 25-30\% reduction in exocytosis of lytic granules and cytotoxicity compared to CTL from wild-type (WT) mice. We wondered why the MID1 gene knock-out did not affect exocytosis and cytotoxicity more severely and speculated whether MID2, a close homologue of MID1, might partially compensate for the loss of MID1 in MID1(-/-) CTL. Here, we showed that MID2, like MID1, is upregulated in activated murine T cells. Furthermore, MID1(-/-) CTL upregulated MID2 two-twenty-fold stronger than CTL from WT mice, suggesting that MID2 might compensate for MID1. In agreement, transfection of MID2 into MID1(-/-) CTL completely rescued exocytosis of lytic granules in MID1(-/-) CTL, and vice versa, knock-down of MID2 inhibited exocytosis of lytic granules in both WT and MID1(-/-) CTL, demonstrating that both MID1 and MID2 play a central role in the regulation of granule exocytosis and that functional redundancy exists between MID1 and MID2 in CTL.</p>},
	keywords = {Animals, Cytoplasmic Granules, Exocytosis, Interferon-gamma, Mice, Mice, Inbred C57BL, Mice, Knockout, Microtubule-Associated Proteins, Proteins, T-Lymphocytes, Cytotoxic, Transcription Factors, Up-Regulation},
	issn = {1600-0463},
	doi = {10.1111/apm.12402},
	author = {Boding, Lasse and Hansen, Ann K and Meroni, Germana and Levring, Trine B and Woetmann, Anders and {\O}dum, Niels and Bonefeld, Charlotte M and Geisler, Carsten}
}
