https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:31299 Wed 23 Feb 2022 16:01:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20455 Wed 11 Apr 2018 16:49:10 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14353 Wed 11 Apr 2018 11:50:58 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16805 Wed 11 Apr 2018 11:29:15 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:9196 Wed 11 Apr 2018 10:54:31 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49273 Wed 10 May 2023 12:10:31 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52222 Thu 05 Oct 2023 10:30:50 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:20838 Sat 24 Mar 2018 08:05:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18969 Sat 24 Mar 2018 07:58:53 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19159 Sat 24 Mar 2018 07:52:20 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:19310 Sat 24 Mar 2018 07:52:15 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22827 Sat 24 Mar 2018 07:16:09 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39042 Mon 29 Jan 2024 17:54:16 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38689 FAT1 gene was cloned over 20 years ago, but there has only been an incremental understanding of its functional role in cancer and developmental disorders. FAT1 is highly expressed in a large proportion of cases of T-cell acute lymphoblastic leukemia (T-ALL) and B-cell ALL compared to their normal counterparts suggesting an oncogenic function. Conversely, the FAT1 gene is also recurrently mutated in a small subset of TALL cases and also in chronic lymphocytic leukemia. Functionally, the FAT1 cadherin has been implicated in Wnt signaling, hippo signaling and more recently mitochondrial function which together suggests a role outside the classical cadherin function in regulating cell-cell adhesion. Here we show that T-ALL cell lines and clinical samples express a unique N-terminal truncated FAT1 mRNA transcript that generates a protein from a novel transcriptional start site within a retained intronic sequence. This novel transcript is regulated independently of full-length FAT1 and results in the expression of a truncated protein lacking almost the entire extracellular domain of FAT1. Significantly, this truncated protein is a novel biomarker for T-ALL and was found to cooperate with NOTCH in driving T-ALL in vivo, suggesting that in the context of T-ALL, this truncated protein may act as an oncogene.]]> Fri 12 Aug 2022 13:35:10 AEST ]]>