sirolimus and ethylene-diurea

sirolimus has been researched along with ethylene-diurea* in 1 studies

Other Studies

1 other study(ies) available for sirolimus and ethylene-diurea

Article	Year
Lkb1/Stk11 regulation of mTOR signaling controls the transition of chondrocyte fates and suppresses skeletal tumor formation. Proceedings of the National Academy of Sciences of the United States of America, 2013, Nov-26, Volume: 110, Issue:48 Liver kinase b1 (Lkb1) protein kinase activity regulates cell growth and cell polarity. Here, we show Lkb1 is essential for maintaining a balance between mitotic and postmitotic cell fates in development of the mammalian skeleton. In this process, Lkb1 activity controls the progression of mitotic chondrocytes to a mature, postmitotic hypertrophic fate. Loss of this Lkb1-dependent switch leads to a dramatic expansion of immature chondrocytes and formation of enchondroma-like tumors. Pathway analysis points to a mammalian target of rapamycin complex 1-dependent mechanism that can be partially suppressed by rapamycin treatment. These findings highlight a critical requirement for integration of mammalian target of rapamycin activity into developmental decision-making during mammalian skeletogenesis. Topics: AMP-Activated Protein Kinases; Analysis of Variance; Animals; Bromodeoxyuridine; Cell Differentiation; Chondrocytes; Histological Techniques; In Situ Hybridization; Mechanistic Target of Rapamycin Complex 1; Mice; Multiprotein Complexes; Phenylurea Compounds; Protein Serine-Threonine Kinases; Signal Transduction; Sirolimus; TOR Serine-Threonine Kinases	2013

Article

Year

Lkb1/Stk11 regulation of mTOR signaling controls the transition of chondrocyte fates and suppresses skeletal tumor formation.

Proceedings of the National Academy of Sciences of the United States of America, 2013, Nov-26, Volume: 110, Issue:48

Liver kinase b1 (Lkb1) protein kinase activity regulates cell growth and cell polarity. Here, we show Lkb1 is essential for maintaining a balance between mitotic and postmitotic cell fates in development of the mammalian skeleton. In this process, Lkb1 activity controls the progression of mitotic chondrocytes to a mature, postmitotic hypertrophic fate. Loss of this Lkb1-dependent switch leads to a dramatic expansion of immature chondrocytes and formation of enchondroma-like tumors. Pathway analysis points to a mammalian target of rapamycin complex 1-dependent mechanism that can be partially suppressed by rapamycin treatment. These findings highlight a critical requirement for integration of mammalian target of rapamycin activity into developmental decision-making during mammalian skeletogenesis.

Topics: AMP-Activated Protein Kinases; Analysis of Variance; Animals; Bromodeoxyuridine; Cell Differentiation; Chondrocytes; Histological Techniques; In Situ Hybridization; Mechanistic Target of Rapamycin Complex 1; Mice; Multiprotein Complexes; Phenylurea Compounds; Protein Serine-Threonine Kinases; Signal Transduction; Sirolimus; TOR Serine-Threonine Kinases

2013