Investigation of Rab35 and EPI64C continue to be important to our research objectives, given our finding that EPI64C and Rab35 regulate a recycling pathway in T-cells and contribute to IS formation, most likely by participating in TCR transport to the immunological synapse. Because of the singular usefulness of knockout mice in understanding key biological functions of gene, we have been expending much of our effort in this direction. Therefore, we have created conditional knockout mice for EPI64C and Rab35. We have finally obtained chimeric knockout mice and offspring that carry the knockout haplotypes. Breeding is in progress to create knockout mice carrying appropriate Cre genes to selectively express in hematopoietic cells. We demonstrated that recycling of the Ca2+-activated K+ channel, KCa2.3, is dependent upon Rab35/EPI64C. Roles of other molecules in T-cell recognition are being analyzed in their respective projects, ERM in BC 010995, and NHERF1 and Myo1G in BC 010993.
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| Gao, Yajuan; Balut, Corina M; Bailey, Mark A et al. (2010) Recycling of the Ca2+-activated K+ channel, KCa2.3, is dependent upon RME-1, Rab35/EPI64C, and an N-terminal domain. J Biol Chem 285:17938-53 |
| Liu, Yin; Belkina, Natalya V; Shaw, Stephen (2009) HIV infection of T cells: actin-in and actin-out. Sci Signal 2:pe23 |
| Horgan, Kevin; Shaw, Stephen; Boirivant, Monica (2009) Immunomagnetic purification of T cell subpopulations. Curr Protoc Immunol Chapter 7:Unit7.4 |
| Patino-Lopez, Genaro; Dong, Xiaoyun; Ben-Aissa, Khadija et al. (2008) Rab35 and its GAP EPI64C in T cells regulate receptor recycling and immunological synapse formation. J Biol Chem 283:18323-30 |
