| First Author | Markotić A | Year | 2002 |
| Journal | Clin Exp Immunol | Volume | 128 |
| Issue | 1 | Pages | 27-35 |
| PubMed ID | 11982587 | Mgi Jnum | J:115565 |
| Mgi Id | MGI:3691933 | Doi | 10.1046/j.1365-2249.2002.01802.x |
| Citation | Markotic A, et al. (2002) Ganglioside expression in tissues of mice lacking beta2-microglobulin. Clin Exp Immunol 128(1):27-35 |
| abstractText | This study presents a comparative analysis of gangliosides from lymphoid (spleen and thymus) and other (brain, liver, lungs and muscle) tissues of C57BL/6 mice lacking the gene for beta2-microglobulin (beta2M), a constitutive component of the MHC class I molecule. Ganglioside fractions in the tissues of mice homozygous (beta2M-/-) and heterozygous (beta2M-/+) for the gene deletion were determined by high performance thin-layer chromatography (HPTLC), followed by immunostaining with specific polyclonal antibodies. Ubiquitous gangliosides GM3(Neu5Ac) and GM3(Neu5Gc) were the dominant gangliosides in the lungs of the control beta2M-/+ mice, whereas the homozygous knockout mice had substantially decreased expression of these structures. The lungs of the beta2M-/- mice also had reduced expression of T-lymphocyte-specific GM1b-type gangliosides (GM1b and GalNAc-GM1b). beta2M-deficient mice also had more GM1a and GD1a gangliosides in the liver, and several neolacto-series gangliosides were increased in the brain and lungs. This study provides in vivo evidence that the beta2M molecule can influence the acquisition of a distinct ganglioside assembly in different mouse organs, implicating its non-immunological functions. |
