Linked Life Data

12507559

Source:http://linkedlifedata.com/resource/pubmed/id/12507559

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-12-31
pubmed:abstractText
Fanconi anemia (FA) is an autosomal recessive cancer susceptibility syndrome characterized by multiple congenital anomalies, bone marrow failure, and cellular sensitivity to mitomycin C (MMC). To date, six FA genes have been cloned, and the encoded proteins function in a novel pathway. The FA pathway is required for the normal cellular response to DNA damage. Following DNA damage, the pathway is activated, leading to monoubiquitination of the FA protein, FANCD2, and its targeting to subnuclear foci. Disruption of the FA pathway results in the absence of FANCD2 nuclear foci, leading to the cellular and clinical abnormalities of FA. Here, we review the recent studies describing the regulated monoubiquitination of the FANCD2 protein and discuss the interaction of the FA pathway with other DNA damage response pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1044-579X
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Elsevier Science Ltd.
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
77-82
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Regulation of the Fanconi anemia pathway by monoubiquitination.
pubmed:affiliation
Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Mayer 640, 44 Binney Street, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review