Nanopublications

Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAQ42j5e-PN8JHfcTAx5X7Tpz9iUA14J05By_SYQ3HFwY#provenance>. }

Showing items 1 to 11 of 11 with 100 items per page.

_7 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "1.4" provenance.
large_corpus.bel authoredBy _7 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _6 provenance.
assertion hadPrimarySource 17118707 provenance.
_6 wasQuotedFrom 17118707 provenance.
_6 value "Several studies have further suggested that the upregulation of STAT3 directly confers a drug-resistance phenotype. For example, overexpression of this transcription factor protects epidermal keratinocytes or cervical carcinoma cells from ultraviolet radiation (UV)-induced apoptosis [74,75]. In addition, STAT3 deficiency sensitizes keratinocytes to UV-induced apoptosis. Interestingly, a simple application of a naked STAT3 plasmid on the skin is sufficient to prevent the effect of irradiation. This protective effect was also confirmed in colorectal cancer cell lines where STAT3 inactivation also enhances UV-induced cell death [57]. In multiple myeloma, the aberrant activation of STAT3 has also been shown to confer resistance to FASmediated apoptosis [28]. The inhibition of STAT3 signaling downregulates the expression of survival proteins and restores the sensitivity to cell-death receptors. Furthermore, a constitutively activated form of STAT3 has been shown in vivo to protect liver cells from FAS-mediated apoptosis and necrosis [76]. This has been related to an enhanced expression of anti-apoptotic proteins such as FLICE-inhibitory protein (FLIP), BCL2, or BCL-XL and a downregulation of FADD-like interleukin-1 b-converting enzyme (FLICE) and caspase 3." provenance.