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Literature summary for 2.7.10.2 extracted from

  • Kim, R.K.; Yoon, C.H.; Hyun, K.H.; Lee, H.; An, S.; Park, M.J.; Kim, M.J.; Lee, S.J.
    Role of lymphocyte-specific protein tyrosine kinase (LCK) in the expansion of glioma-initiating cells by fractionated radiation (2010), Biochem. Biophys. Res. Commun., 402, 631-636.
    View publication on PubMed
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Application

Application Comment Organism
medicine lymphocyte-specific protein tyrosine kinase LCK is involved in the fractionated radiation-induced expansion of the glioma-initiating cell population and acquisition of resistance to anticancer treatments. Fractionated radiation causes a selective increase in the activity of LCK. The activities of other Src family kinases Src, Fyn, and Lyn are not significantly increased. Knockdown of LCK expression with siRNA effectively block fractionated radiation-induced expansion of the CD133+ cell population. siRNA targeting of LCK also suppresses fractionated radiation-induced expression of the glioma stem cell marker proteins CD133, Nestin, and Musashi. Expression of the proteins Notch2 and Sox2 in glioma cells treated with fractionated radiation is also downregulated by LCK inhibition. siRNA-mediated knockdown of LCK effectively restores the sensitivity of glioma cells to cisplatin and etoposide Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
glioma cell
-
 Homo sapiens
-
U-373MG cell
-
 Homo sapiens
-
U-87MG cell
-
 Homo sapiens
-

Synonyms

Synonyms Comment Organism
Lck
-
 Homo sapiens
lymphocyte-specific protein tyrosine kinase
-
 Homo sapiens

General Information

General Information Comment Organism
physiological function lymphocyte-specific protein tyrosine kinase LCK is involved in the fractionated radiation-induced expansion of the glioma-initiating cell population and acquisition of resistance to anticancer treatments. Fractionated radiation causes a selective increase in the activity of LCK. The activities of other Src family kinases Src, Fyn, and Lyn are not significantly increased. Knockdown of LCK expression with siRNA effectively block fractionated radiation-induced expansion of the CD133+ cell population. siRNA targeting of LCK also suppresses fractionated radiation-induced expression of the glioma stem cell marker proteins CD133, Nestin, and Musashi. Expression of the proteins Notch2 and Sox2 in glioma cells treated with fractionated radiation is also downregulated by LCK inhibition. siRNA-mediated knockdown of LCK effectively restores the sensitivity of glioma cells to cisplatin and etoposide Homo sapiens