{'fraction_non_alphanumeric': 0.03640776699029126, 'fraction_numerical': 0.015776699029126214, 'mean_word_length': 6.568807339449541, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
CREB transcription factor modulates Bcl2 transcription in response to C5a in HL‐60‐derived neutrophils

Background  Complement fragment C5a and neutrophils have been implicated in the pathogenesis of renal disease and C5a has also been shown to delay apoptosis of human neutrophils via a transcription‐independent pathway. However, transcription‐dependent pathways have not been well described. The present study examined whether activation of HL‐60‐derived neutrophils by C5a modulates the transcription of two members of the Bcl2 family, Bax (pro‐apoptotic) and Bcl2 (anti‐apoptotic) molecules, and whether the cAMP‐response element‐binding protein (CREB) transcription factor mediates these effects through the phosphatidylinositol 3‐kinase (PI3K)/Akt and extra‐cellular signal‐regulated kinase (ERK) signalling pathways.