Document Detail

The intracellular tyrosine kinase Brk sensitizes non-transformed cells to inducers of apoptosis.
MedLine Citation:
PMID:  16082217     Owner:  NLM     Status:  MEDLINE    
The intracellular tyrosine kinase Brk is expressed in regenerating epithelial tissues with highest levels in the gastrointestinal tract and skin. In these tissues, Brk is restricted to epithelial cells that are exiting the cell cycle and undergoing terminal differentiation. While not expressed in mammary gland, Brk expression is often induced in primary breast tumors and breast tumor cell lines. To identify potential oncogenic functions of Brk, we utilized the immortalized Rat1a rat fibroblast cell line that is highly sensitive to transformation. We generated Rat1a cell lines that stably overexpress wild-type and activated Brk, and we analyzed their growth properties and ability to undergo apoptosis in response to stress and DNA damage. Overexpression of Brk did not induce anchorage-independent growth, and no changes in cell morphology or cell cycle progression were observed. However, when constitutively expressed, Brk sensitized Rat1a cells to a variety of apoptotic stimuli including serum deprivation and a combination of UV irradiation and serum starvation. These findings indicate that Brk does not promote proliferation of non-transformed cells, but plays a positive role in the regulation of the apoptotic response to DNA-damage and stress.
Andrea Haegebarth; Rafael Nunez; Angela L Tyner
Related Documents :
8050577 - Metastatic potential of transformed rat 3y1 cell lines is inversely correlated with lys...
10703737 - Dual effect of pseudorabies virus growth factor (prgf) displayed on actin cytoskeleton.
2539697 - Human papovavirus bk early gene regulation in nonpermissive cells.
17650227 - Effects of extracellular signal-regulated kinase on rat cultured hepatic stellate cells...
22704207 - Chlorination-induced cellular damage and recovery in marine microalga, chlorella salina.
17702767 - Avoiding false-positive signals with nuclease-vulnerable molecular beacons in single li...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2005-09-23
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  4     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2005 Sep 
Date Detail:
Created Date:  2005-09-22     Completed Date:  2006-06-12     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1239-46     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cell Differentiation
Cell Line
Cell Proliferation
Cell Transformation, Neoplastic
Cells, Cultured
Cytoplasm / metabolism
DNA Damage
Fibroblasts / metabolism
Flow Cytometry
Microscopy, Fluorescence
Myristic Acid / chemistry
Neoplasm Proteins / metabolism,  physiology*
Protein Binding
Protein Structure, Tertiary
Protein-Tyrosine Kinases / chemistry,  metabolism,  physiology*
Retroviridae / genetics
Time Factors
Tyrosine / chemistry
Ultraviolet Rays
src Homology Domains
Grant Support
Reg. No./Substance:
0/Neoplasm Proteins; 0I3V7S25AW/Myristic Acid; 42HK56048U/Tyrosine; EC Kinases; EC protein, human

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Death-from-cancer signatures and stem cell contribution to metastatic cancer.
Next Document:  New and old functions of STAT3: a pivotal target for individualized treatment of cancer.