Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2007-9-10
pubmed:abstractText
SMARCB1/INI1, which negatively regulates cell cycle progression from G0/G1 into the S-phase via the p16INK4a-RB-E2F pathway, has been reported to be inactivated homozygously by deletion and/or mutations in malignant rhabdoid tumor (MRT). In the current study, we investigated the alteration of the SMARCB1/INI1 gene using simple methods, and its gene product at the protein level. Moreover, we investigated the status of hyperphosphorylation in RB protein, known as a key cell cycle molecule.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0171-5216
pubmed:author
pubmed:issnType
Print
pubmed:volume
133
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
817-24
pubmed:meshHeading
pubmed-meshheading:17486366-Child, Preschool, pubmed-meshheading:17486366-Chromosomal Proteins, Non-Histone, pubmed-meshheading:17486366-DNA-Binding Proteins, pubmed-meshheading:17486366-Female, pubmed-meshheading:17486366-Gene Deletion, pubmed-meshheading:17486366-Gene Expression Regulation, Neoplastic, pubmed-meshheading:17486366-Humans, pubmed-meshheading:17486366-Immunoenzyme Techniques, pubmed-meshheading:17486366-Infant, pubmed-meshheading:17486366-Infant, Newborn, pubmed-meshheading:17486366-Male, pubmed-meshheading:17486366-Mutation, pubmed-meshheading:17486366-Phosphorylation, pubmed-meshheading:17486366-Retinoblastoma Protein, pubmed-meshheading:17486366-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:17486366-Rhabdoid Tumor, pubmed-meshheading:17486366-Transcription Factors
pubmed:year
2007
pubmed:articleTitle
Highly aggressive behavior of malignant rhabdoid tumor: a special reference to SMARCB1/INI1 gene alterations using molecular genetic analysis including quantitative real-time PCR.
pubmed:affiliation
Department of Anatomic Pathology, Pathological Sciences, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't