Linked Life Data

16707437

Source:http://linkedlifedata.com/resource/pubmed/id/16707437

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2006-5-18
pubmed:abstractText
Rhabdomyosarcoma is the most common sarcoma in children and is difficult to treat if the primary tumor is nonresectable or if the disease presents with metastases. The function of the serine/threonine kinase Mirk was investigated in this cancer. Mirk has both growth arrest and survival functions in terminally differentiating skeletal myoblasts. Maintenance of Mirk growth arrest properties would cause down-regulation of Mirk in transformed myoblasts. Alternatively, Mirk expression would be retained if rhabdomyosarcoma cells used Mirk survival capability. Mirk expression was significant in 12 of 16 clinical cases of rhabdomyosarcoma. Mirk was detected in each rhabdomyosarcoma cell line examined. Mirk was a functional kinase in each of three rhabdomyosarcoma cell lines, where it proved to be more active than in C2C12 skeletal myoblasts. Mirk mediated survival of the majority of clonogenic rhabdomyosarcoma cells. Knockdown of Mirk by RNA interference reduced the fraction of RD and of Rh30 rhabdomyosarcoma cells capable of colony formation 3- to 4-fold in multiple experiments. Depletion of Mirk induced cell death by apoptosis, as shown by increased numbers of terminal deoxynucleotidyl transferase-mediated nick-end labeling-positive cells and by increased binding of Annexin V. Mirk is a stress-activated kinase that mediates expression of contractile proteins in differentiating myoblasts, but Mirk is not essential for muscle formation in the embryo. It is likely that Mirk also facilitates survival of satellite cell-derived rhabdomyoblasts in regenerating skeletal muscle and aids their differentiation. This survival function is maintained in rhabdomyosarcoma, where Mirk may be a novel therapeutic target.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5143-50
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16707437-Adolescent, pubmed-meshheading:16707437-Adult, pubmed-meshheading:16707437-Aged, pubmed-meshheading:16707437-Aged, 80 and over, pubmed-meshheading:16707437-Animals, pubmed-meshheading:16707437-Apoptosis, pubmed-meshheading:16707437-Cell Line, Tumor, pubmed-meshheading:16707437-Cell Survival, pubmed-meshheading:16707437-Child, pubmed-meshheading:16707437-Child, Preschool, pubmed-meshheading:16707437-Cytoplasm, pubmed-meshheading:16707437-Female, pubmed-meshheading:16707437-Humans, pubmed-meshheading:16707437-Immunohistochemistry, pubmed-meshheading:16707437-Male, pubmed-meshheading:16707437-Mice, pubmed-meshheading:16707437-Middle Aged, pubmed-meshheading:16707437-Mitogen-Activated Protein Kinases, pubmed-meshheading:16707437-Myoblasts, pubmed-meshheading:16707437-Protein-Serine-Threonine Kinases, pubmed-meshheading:16707437-Protein-Tyrosine Kinases, pubmed-meshheading:16707437-Rhabdomyosarcoma, Alveolar, pubmed-meshheading:16707437-Rhabdomyosarcoma, Embryonal, pubmed-meshheading:16707437-Transcription Factors
pubmed:year
2006
pubmed:articleTitle
Mirk/Dyrk1b mediates cell survival in rhabdomyosarcomas.
pubmed:affiliation
Department of Pathology, Upstate Medical University, State University of New York, Syracuse, New York 13210, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural