American Association for Cancer Research
Browse
00085472can070922-sup-supplemental_figure_2.pdf (75.92 kB)

Supplementary Figure 2 from Traf1 Induction and Protection from Tumor Necrosis Factor by Nuclear Factor-κB p65 Is Independent of Serine 536 Phosphorylation

Download (75.92 kB)
journal contribution
posted on 2023-03-30, 17:44 authored by Carl Y. Sasaki, Colin F. Slemenda, Paritosh Ghosh, Theresa J. Barberi, Dan L. Longo
Supplementary Figure 2 from Traf1 Induction and Protection from Tumor Necrosis Factor by Nuclear Factor-κB p65 Is Independent of Serine 536 Phosphorylation

History

ARTICLE ABSTRACT

Abnormal nuclear factor-κB (NF-κB) signaling has been attributed to the initiation and progression of cancer. Posttranslational modification of p65 facilitates optimal NF-κB signaling after activation. Here, we show that the phosphorylation of serine 536 was required for p65-mediated transcription and IκBα expression in fibroblasts. Furthermore, tumor necrosis factor (TNF) treatment slightly induced p65 phosphorylation, and both unphosphorylated and phosphorylated p65 translocated into the nucleus. The phosphorylation of serine 536 was not required for p65-mediated protection from TNF cytotoxicity and Traf1 induction in fibroblasts. Also, the corecruitment of p65 and RNA polymerase II to the Traf1 enhancer region did not require p65 phosphorylation. However, the corecruitment of p65 and RNA polymerase II to the Csf2 promoter required the phosphorylation of serine 536. These findings suggested that the requirement of serine phosphorylation at residue 536 and the distance between the NF-κB response element and the start of transcription may influence which genes will be transcribed. [Cancer Res 2007;67(23):11218–25]

Usage metrics

    Cancer Research

    Categories

    Keywords

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC