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PMID:17570218

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Citation

Abal, M, Obrador-Hevia, A, Janssen, KP, Casadome, L, Menendez, M, Carpentier, S, Barillot, E, Wagner, M, Ansorge, W, Moeslein, G, Fsihi, H, Bezrookove, V, Reventos, J, Louvard, D, Capella, G and Robine, S (2007) APC inactivation associates with abnormal mitosis completion and concomitant BUB1B/MAD2L1 up-regulation. Gastroenterology 132:2448-58

Abstract

Chromosomal instability, a hallmark of most colorectal cancers, has been related to altered chromosome segregation and the consequent deficit in genetic integrity. A role for the tumor suppressor gene APC has been proposed in colorectal cancer that leads to compromised chromosome segregation even though the molecular mechanism is not yet understood. Here, we tackled the genetic basis for the contribution of APC to chromosomal instability in familial adenomatous polyposis and sporadic colorectal cancer.

Links

PubMed Online version:10.1053/j.gastro.2007.03.027

Keywords

Adenomatous Polyposis Coli/genetics; Adenomatous Polyposis Coli/metabolism; Adenomatous Polyposis Coli/pathology; Animals; Cell Cycle; Chromosomal Instability; Colorectal Neoplasms/genetics; Colorectal Neoplasms/metabolism; Colorectal Neoplasms/pathology; Cytokinesis; Gene Expression; Gene Silencing; Genes, APC; Humans; Mice; Mice, Inbred Strains; Mitosis/genetics; Mutation; Protein Kinases/genetics; Protein Kinases/metabolism; Protein-Serine-Threonine Kinases; Stathmin/genetics; Stathmin/metabolism; Transcription, Genetic; Up-Regulation

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


See also

References

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