AI Article Synopsis

  • - Polyinosinic:polycytidylic acid (poly (I:C)) is recognized for inducing interferons, but its mechanism became clearer with the discovery of Toll-like receptors (TLRs), which play a key role in the immune response.
  • - TLR3, which recognizes double-stranded RNA like poly (I:C), activates key transcription factors that can trigger multiple cellular processes, although its target genes are not well understood.
  • - In this study, 15 proteins connected to metabolism were identified as differentially expressed after poly (I:C) treatment, including calreticulin and profilin-1, suggesting that calreticulin's expression is TLR3-dependent while profilin-1's is not

Article Abstract

Polyinosinic:polycytidylic acid (poly (I:C)) has been formerly known to be an interferon inducer but the mechanism of its action was not revealed until the discovery of Toll-like receptors (TLRs). TLRs are members of transmembrane proteins that recognize conserved molecular motifs of viral and bacterial origin and initiate innate immune response. Recent studies have shown that they are also expressed on tumor cells, but their role in these cells is still not clear. TLR3 recognizes double-stranded RNA (poly (I:C)) and is primarily involved in the defense against viruses. TLR3 ligand binding initiates the activation of transcription factors NF-κB, IRF family members, and AP-1, which can induce wide cascading effect on the cell and consequently activate many cellular processes. Since little is known about TLR3 target genes, we have used the proteomic approach to widen the current knowledge. In this study, we have discovered 15 differentially expressed proteins, mostly connected with protein metabolic processes. Furthermore, we have confirmed by Western blot that calreticulin and profilin-1, proteins which have been shown previously to be involved in processes connected with tumor progression, are differentially expressed after poly(I:C) treatment. By using TLR3 small interfering RNA, we showed that calreticulin expression might be TLR3 dependent, unlike profilin-1.

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Source
http://dx.doi.org/10.1007/s13277-012-0366-7DOI Listing

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