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Group I p21-activated kinases facilitate Tax-mediated transcriptional activation of the human T-cell leukemia virus type 1 long terminal repeats

Ching-Ping Chan1, Yeung-Tung Siu1, Kin-Hang Kok1, Yick-Pang Ching2*, Hei-Man Vincent Tang1* and Dong-Yan Jin1*

Author Affiliations

1 Department of Biochemistry, The University of Hong Kong, 3/F Laboratory Block, 21 Sassoon Road, Pokfulam, Hong Kong

2 Department of Anatomy and State Key Laboratory of Brain and Cognitive Science, The University of Hong Kong, 1/F Laboratory Block, 21 Sassoon Road, Pokfulam, Hong Kong

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Retrovirology 2013, 10:47  doi:10.1186/1742-4690-10-47

Published: 26 April 2013



Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia and tropical spastic paraparesis. HTLV-1 encodes transactivator protein Tax that interacts with various cellular factors to modulate transcription and other biological functions. Additional cellular mediators of Tax-mediated transcriptional activation of HTLV-1 long terminal repeats (LTR) remain to be identified and characterized.


In this study, we investigated the regulatory role of group I p21-activated kinases (Paks) in Tax-induced LTR activation. Both wild-type and kinase-dead mutants of Pak3 were capable of potentiating the activity of Tax to activate LTR transcription. The effect of Paks on the LTR was attributed to the N-terminal regulatory domain and required the action of CREB, CREB-regulating transcriptional coactivators (CRTCs) and p300/CREB-binding protein. Paks physically associated with Tax and CRTCs. Paks were recruited to the LTR in the presence of Tax. siRNAs against either Pak1 or Pak3 prevented the interaction of Tax with CRTC1 and the recruitment of Tax to the LTR. These siRNAs also inhibited LTR-dependent transcription in HTLV-1-transformed MT4 cells and in cells transfected with an infectious clone of HTLV-1.


Group I Paks augment Tax-mediated transcriptional activation of HTLV-1 LTR in a kinase-independent manner.

HTLV-1; Tax; p21-activated kinases; CREB; CREB-regulating transcriptional activators