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All Rights Reserved. http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Small Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/dc/terms/license Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RA_4LeVcrgrcoeiCSXkRbRI4I8iUk5mRYs_CTIq1dLyV8#_6 http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/pav/version 1.6 http://www.tkuhn.ch/bel2nanopub/RA_4LeVcrgrcoeiCSXkRbRI4I8iUk5mRYs_CTIq1dLyV8#_5 http://www.w3.org/ns/prov#value In contrast, tissues treated with TNFR1 antibody, although hyperplastic, retained BMZ structure and proper desmoglein-3 expression, indicating intact tissue polarity (Fig. 5A and B). Blockade of TNFR1 signaling was accompanied by the absence of detectable pJNK in the tissues treated by the TNFR1 antibody (Supplementary Fig. S7). In addition, TNFR1 blockade reduced the mitotic index and limited mitotic cells to the basal layer, whereas proliferating cells were widespread and abundant in the control tumor tissue (Fig. 5C and D). 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