| First Author | Endo J | Year | 2000 |
| Journal | FEBS Lett | Volume | 468 |
| Issue | 2-3 | Pages | 234-8 |
| PubMed ID | 10692593 | Mgi Jnum | J:60738 |
| Mgi Id | MGI:1353849 | Doi | 10.1016/s0014-5793(00)01219-9 |
| Citation | Endo J, et al. (2000) Deficiency of a STE20/PAK family kinase LOK leads to the acceleration of LFA-1 clustering and cell adhesion of activated lymphocytes. FEBS Lett 468(2-3):234-8 |
| abstractText | Lymphocyte-oriented kinase (LOK) is a member of the STE20/p21-activated kinase (PAK) family and expressed predominantly in lymphoid organs. Generation of LOK-deficient mice revealed that the leukocyte-function-associated antigen (LFA-1)/intercellular adhesion molecules (ICAM)-mediated aggregation of mitogen-stimulated T cells was greatly enhanced in the absence of LOK. Though levels of total LFA-1 and ICAMs as well as the active form of LFA-1 on T cell blasts were comparable in the presence and absence of LOK, clustering of active LFA-1 detected by binding of soluble ICAM-1 was accelerated in the absence of LOK. These results suggest that LOK is potentially involved in the regulation of LFA-1-mediated lymphocyte adhesion. |
