DCC specifications

Information


Unique identifier OMICS_23068
Name DCC
Alternative name Deleted in Colorectal Carcinoma
Restrictions to use None
Community driven No
Data access Browse
User data submission Allowed
Maintained Yes

Taxon


  • Primates
    • Homo sapiens

Maintainer


  • person_outline Ashley Marsh

Publication for Deleted in Colorectal Carcinoma

DCC citations

 (2)
library_books

Maslinic Acid Enriched Diet Decreases Intestinal Tumorigenesis in ApcMin/+ Mice through Transcriptomic and Metabolomic Reprogramming

2013
PLoS One
PMCID: 3601079
PMID: 23527181
DOI: 10.1371/journal.pone.0059392

[…] lism, and DNA repair; the Msh6 gene (), involved in the post-replicative DNA mismatch repair system (MMR) and the Tgfb1 gene and its receptor (Tgfb1r1) ().On the other hand, MA caused upregulation of deleted in colorectal carcinoma (Dcc) gene (), encoding the pro-apoptotic protein DCC. However, MA also downregulated DIP13α (Appl1), a mediator of the DCC apoptotic pathway (). Furthermore, MA reduce […]

library_books

Comprehensive Genomic Analysis of a BRCA2 Deficient Human Pancreatic Cancer

2011
PLoS One
PMCID: 3130048
PMID: 21750719
DOI: 10.1371/journal.pone.0021639

[…] ulated in primary colorectal tumours , and Wnt-beta Catenin signalling is known to be aberrant in some pancreatic adenocarcinomas .Three homozygous variants were present in the tumour suppressor DCC (Deleted in Colorectal Carcinoma), which encodes a netrin receptor required for cell differentiation , and also the induction of apoptosis in the absence of ligand . Mutations and loss of DCC have prev […]

DCC institution(s)
Bruce Lefroy Centre for Genetic Health Research, Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, VIC, Australia; Department of Paediatrics, University of Melbourne, Parkville, VIC, Australia; The University of Queensland, Queensland Brain Institute, St Lucia, Brisbane, VIC, Australia; The University of Queensland, Faculty of Medicine, Herston, Brisbane, VIC, Australia; Drug Delivery, Disposition and Dynamics (D4), Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC, Australia; Division of Genetics and Genomics, Boston Children’s Hospital, Boston, MA, USA
DCC funding source(s)
Supported by the National Health and Medical Research Council (NHMRC) Australia Project Grants (GNT1059666 and GNT1126153), the Campbell Edwards Trust, the Victorian Government's Operational Infrastructure Support Program, the Australian Government NHMRC IRIISS, the Repository Core for Neurological Disorders, the Department of Neurology, Boston Children’s Hospital, NIH IDDRC 1U54 HD090255, an Australian Postgraduate Award, foundation Desmarest, an NHMRC Principal Research Fellowship and NHMRC Career Development Fellowship (GNT1032364).

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