RASSF1A interacts with and activates the mitotic kinase Aurora-A

The RAS association domain family 1A ( RASSF1A ) gene is located at chromosome 3p21.3 within a specific area of common heterozygous and homozygous deletions. RASSF1A frequently undergoes promoter methylation-associated inactivation in human cancers. Rassf1a −/− mice are prone to both spontaneous and...

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Veröffentlicht in:Oncogene 2008-10, Vol.27 (47), p.6175-6186
Hauptverfasser: Liu, L, Guo, C, Dammann, R, Tommasi, S, Pfeifer, G P
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container_end_page 6186
container_issue 47
container_start_page 6175
container_title Oncogene
container_volume 27
creator Liu, L
Guo, C
Dammann, R
Tommasi, S
Pfeifer, G P
description The RAS association domain family 1A ( RASSF1A ) gene is located at chromosome 3p21.3 within a specific area of common heterozygous and homozygous deletions. RASSF1A frequently undergoes promoter methylation-associated inactivation in human cancers. Rassf1a −/− mice are prone to both spontaneous and carcinogen-induced tumorigenesis, supporting the notion that RASSF1A is a tumor suppressor. However, it is not fully understood how RASSF1A is involved in tumor suppression pathways. Here we show that overexpression of RASSF1A inhibits centrosome separation. RASSF1A interacts with Aurora-A, a mitotic kinase. Surprisingly, knockdown of RASSF1A by siRNA led to reduced activation of Aurora-A, whereas overexpression of RASSF1A resulted in increased activation of Aurora-A, suggesting that RASSF1A is involved in Aurora-A activation. Like other Aurora-A activators, RASSF1A was also a substrate of Aurora-A in vitro . The failure of recombinant RASSF1A to activate recombinant Aurora-A indicates that RASSF1A may not activate Aurora-A directly and suggests that RASSF1A may function as a scaffold to bring together Aurora-A and its activator(s). Inhibition of centrosome separation by RASSF1A overexpression is most likely a consequence of hyperstabilization of microtubules by this protein.
doi_str_mv 10.1038/onc.2008.220
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Inhibition of centrosome separation by RASSF1A overexpression is most likely a consequence of hyperstabilization of microtubules by this protein.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>18641684</pmid><doi>10.1038/onc.2008.220</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Nature; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings
subjects Animals
Apoptosis
Aurora Kinase A
Aurora Kinases
Biological and medical sciences
Carcinogens
Cell Biology
Cell cycle, cell proliferation
Cell division
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Centrosome - chemistry
Cercopithecus aethiops
Chromosome 3
Chromosomes
COS Cells
DNA methylation
Enzyme Activation
Fundamental and applied biological sciences. Psychology
Genetics
HeLa Cells
Human Genetics
Humans
Internal Medicine
Kinases
Medicine
Medicine & Public Health
Microtubules
Molecular and cellular biology
Oncology
original-article
Protein-Serine-Threonine Kinases - chemistry
Protein-Serine-Threonine Kinases - metabolism
RNA, Small Interfering - pharmacology
Rodents
siRNA
Tumor suppressor genes
Tumor Suppressor Proteins - antagonists & inhibitors
Tumor Suppressor Proteins - physiology
Tumorigenesis
title RASSF1A interacts with and activates the mitotic kinase Aurora-A
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