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As an alternative, previously, there was an established BPC 157-NO system interaction (4, 8, 25-27) as well as a particular potential in angiogenesis (28-30) especially evident in the advanced healing process of the various tissues (25, 31-38) including those that may be almost avascular ( i.e
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Thus, it is plausible that the aforementioned mechanism, whereby conflicts between slowed replisomes and head-on transcription complexes lead to R-loop formation and subsequent fork reversal, also underlies cyclin E1-induced replication stress (Fig
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