https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17021 Wed 11 Apr 2018 17:14:33 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53392 Thu 23 Nov 2023 13:37:24 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38357 Thu 09 Sep 2021 12:21:31 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:10760 Sat 24 Mar 2018 08:13:54 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17459 V600E is known to promote the stabilizing phosphorylation of the anti-apoptotic protein Mcl-1, implicated in melanoma survival and chemoresistance. We now show that B-RAF^V600E signaling also induces the transcription of Mcl-1 in melanocytes and melanoma. We demonstrate that activation of STAT3 serine-727 and tyrosine-705 phosphorylations is promoted by B-RAF^V600E activity and that the Mcl-1 promoter is dependent on a STAT consensus-site for B-RAF-mediated activation. Consequently, suppression of STAT3 activity disrupted B-RAF^V600E-mediated induction of Mcl-1 and reduced melanoma cell survival. We propose that STAT3 has a central role in the survival and contributes to chemoresistance of B-RAF^V600E melanoma.]]> Sat 24 Mar 2018 08:04:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18436 Sat 24 Mar 2018 07:59:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24136 Sat 24 Mar 2018 07:16:32 AEDT ]]>