Linked Life Data

15104675

Source:http://linkedlifedata.com/resource/pubmed/id/15104675

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-4-23
pubmed:abstractText
The promyelocytic leukemia (PML) protein is the product of the PML gene that fuses with the retinoic acid receptor-alpha (RARalpha) gene in acute promyelocytic leukemia (APL) and produces disruption of PML bodies. Wild-type PML localizes in the nucleus with a typical speckled pattern. PML bodies accumulate several proteins involved in multiple cellular pathways such as apoptosis, transcriptional regulation, and proteasomal degradation of ubiquitinated proteins. The ubiquitin-proteasome pathway at PML bodies is dependent on proteasome component recruitment. Proteasome components such as low-molecular weight proteins (LMPs) are frequently downregulated in different tumor tissues that present impaired major histocompatibility complex (MHC) class I expression. We have recently documented LMP7 downregulation in colorectal tumors with total loss of MHC class I antigen. An immunohistochemical study of PML protein in these tumors revealed a disrupted pattern of PML bodies in a nuclear diffuse form, as observed in APL cells. Therefore, the disruption of the PML bodies was clearly associated with LMP7 downregulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0001-2815
pubmed:author
pubmed:issnType
Print
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
446-52
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Promyelocytic leukemia (PML) nuclear bodies are disorganized in colorectal tumors with total loss of major histocompatibility complex class I expression and LMP7 downregulation.
pubmed:affiliation
Departamento de Análisis Clínicos, Hospital Universitario Virgen de las Nieves, Avd. Fuerzas Armadas 2, 18014 Granada, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't