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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RATt4tuaTAQr4c6yP_DwM-T7ThdrFRvfXgrVvBRdb9c1c#_6 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RATt4tuaTAQr4c6yP_DwM-T7ThdrFRvfXgrVvBRdb9c1c#_5 http://www.w3.org/ns/prov#value HBP1 levels have been investigated for differentiation, in which there is an increase in many cell types (Parker et al., 1995 and Tevosian et al., 1997). Similarly, p38 MAPK activity is also linked with differentiation and recently, with senescence and tumor suppression (reviewed in Kyriakis and Avruch, 2001 and see below). The involvement of HBP1 in senescence is not known and under investigation. Conceivably, p38 MAPK, p21, and HBP1 may share similar pathways for differentiation, G1 progression, and possibly senescence. The identification of p21 as a substrate for the p38 MAPK was delineated through a systematic investigation of TGFb-induced cell cycle arrest for relevant kinases and substrates. Initially, these investigators found that p21 protein levels increased by a post-transcriptional mechanism and concluded that the SAPKs p38 MAPK and JNK were involved in stabilizing the p21 protein. 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