Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by S Tani ichi
Total Records ( 2 ) for S Tani ichi
  S Tani ichi , M Satake and K. Ikuta

The IL-7R controls local accessibility of joining (J) gene segments in the mouse TCR locus by recruiting signal transducers and activators of transcription (STAT) 5 and transcriptional coactivators to the J germ line promoters and inducing histone acetylation and germ line transcription. Because STAT consensus motifs are conserved not only in the J promoters but also in the TCR 3' enhancer (E) elements, it is possible that STAT5 interacts with and activates E. To address this question, we first showed that the lysine 4 residue of histone H3 is substantially methylated at E1 and E4 elements in wild-type early thymocytes and that the levels of the methylation are reduced in IL-7R chain-deficient mice. We also showed that STAT5 has potential to elevate histone acetylation of the E elements in a cytokine-dependent cell line by cytokine stimulation. Next, we demonstrated that STAT5 is recruited to the STAT consensus motifs in the E elements after cytokine stimulation and that transcription factors Runt-related (Runx) and c-Myb are constitutively recruited to E. Furthermore, we showed that STAT5 augments basal E activity controlled by Runx and c-Myb. These results suggest that STAT5 is recruited to the consensus motifs in the E elements by cytokine stimulation and augments basal E activity independent of Runx and c-Myb. Therefore, this study implies that the E elements might be activated in two successive steps, first by Runx and c-Myb and next by STAT5.

  S Tani ichi , H. C Lee , S. K Ye and K. Ikuta

The signal of the IL-7R and signal transducers and activators of transcription (STAT) 5 plays an essential role in T-cell development by inducing V–J recombination in the TCR locus. Previously, we have shown that STAT5 binds to the J promoters and controls chromatin accessibility by histone acetylation. However, little is known on control mechanism of V region by the IL-7R. To elucidate the regulation by STAT5, we first analyzed the chromatin status of V region in primary thymocytes. The levels of histone H3 acetylation are high at V5, HsA element and V2 in Rag2–/– thymocytes but low in IL-7R -chain (IL-7R)-deficient early thymocytes, suggesting that IL-7R signaling controls the accessibility of the V region. In addition, high levels of histone H3 acetylation and germ line transcription were induced at V5 and HsA by cytokine and STAT5 in cytokine-dependent Ba/F3 and other hematopoietic cell lines. Importantly, the chromatin accessibility of V5 gene is increased by cytokine signal. Furthermore, STAT5 was not recruited to a non-canonical STAT-binding motif in the endogenous chromatin of the V5 promoter by cytokine stimulation, while STAT5 binds to a consensus motif in the HsA element. In accordance with this result, STAT5 does not directly activate the V5 promoter by reporter assay. These results suggested that while STAT5 directly binds to HsA element and induces its histone acetylation, STAT5 indirectly activates the V5 promoter. Thus, this study implies a potential role of STAT5 in accessibility control of V region, especially at V5 and HsA.

Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility