## Abstract Cdk9/Cyclin T1 complex is very important in controlling specific differentiative pathways of several cell types. Limited data are available regarding the expression of Cdk9/Cyclin T1 in hematopoietic and lymphoid tissues. Cdk9/Cyclin T1 expression seems to be related to particular stage
The role of the Cdk9/Cyclin T1 complex in T cell differentiation
✍ Scribed by Eleonora Leucci; Giulia De Falco; Anna Onnis; Giovanna Cerino; Mario Cocco; Anna Luzzi; Domenica Crupi; Chiara Tigli; Cristiana Bellan; Piero Tosi; Lorenzo Leoncini; Antonio Giordano
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 217 KB
- Volume
- 212
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
The Cdk9/Cyclin T1 complex is very important in controlling specific differentiative pathways of several cell types, including muscle cells and neurons. We recently demonstrated the involvement of this complex in B cell activation/differentiation. To check whether the Cdk9/Cyclin T1 complex is also involved in the T cell activation/differentiation process, we isolated different T cell populations by magnetic separation, based on their surface antigens. We observed that the expression level of Cdk9/Cyclin T1 increases in effector T cells (CD27^+^), as well as in activated T cells (CD25^+^) and memory T cells (CD45RA^−^), thus suggesting a specific upregulation of the Cdk9/Cyclin T1 complex following antigen encounter. We have previously demonstrated that in B cells, Cdk9 interacts in vivo with the E2A gene products E12/E47 (members of the basic helix‐loop‐helix family) which are involved in differentiation. In this article, we show that this interaction also occurs in T cells. This suggests an active role for the Cdk9/Cyclin T1 complex during lymphoid differentiation, through physical binding with E12 and E47. These preliminary results suggest that the Cdk9/Cyclin T1 complex may be important in the activation and differentiation program of lymphoid cells and that its upregulation, which is due to still unknown mechanisms, may contribute to malignant transformation. J. Cell. Physiol. 212: 411–415, 2007. © 2007 Wiley‐Liss, Inc.
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