Total Synthesis of Lucilactaene, A Cell Cycle Inhibitor Active in p53-Inactive Cells

2005 ◽  
Vol 127 (46) ◽  
pp. 16038-16039 ◽  
Author(s):  
Robert S. Coleman ◽  
Matthew C. Walczak ◽  
Erica L. Campbell
Keyword(s):  
Cell Cycle ◽  
Total Synthesis ◽  
Cell Cycle Inhibitor ◽  
A Cell

Determination by Asymmetric Total Synthesis of the Absolute Configuration of Lucilactaene, a Cell-Cycle Inhibitor in p53-Transfected Cancer Cells

2005 ◽  
Vol 117 (20) ◽  
pp. 3170-3175 ◽  
Author(s):  
Junichiro Yamaguchi ◽  
Hideaki Kakeya ◽  
Takao Uno ◽  
Mitsuru Shoji ◽  
Hiroyuki Osada ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Total Synthesis ◽  
Cancer Cells ◽  
Absolute Configuration ◽  
Asymmetric Total Synthesis ◽  
Cell Cycle Inhibitor ◽  
A Cell ◽  
The Absolute

scholarly journals Total Synthesis of Lucilactaene, a Cell Cycle Inhibitor Active in p53-Inactive Cells.

ChemInform ◽  
2006 ◽  
Vol 37 (14) ◽  
Author(s):  
Robert S. Coleman ◽  
Matthew C. Walczak ◽  
Erica L. Campbell
Keyword(s):  
Cell Cycle ◽  
Total Synthesis ◽  
Cell Cycle Inhibitor ◽  
A Cell

Determination of the Absolute Configuration of Lucilactaene, a Cell-Cycle Inhibitor in p53-Transfected Cancer Cells, by Asymmetric Total Synthesis.

ChemInform ◽  
2005 ◽  
Vol 36 (38) ◽  
Author(s):  
Junichiro Yamaguchi ◽  
Hideaki Kakeya ◽  
Takao Uno ◽  
Mitsuru Shoji ◽  
Hiroyuki Osada ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Total Synthesis ◽  
Cancer Cells ◽  
Absolute Configuration ◽  
Asymmetric Total Synthesis ◽  
Cell Cycle Inhibitor ◽  
A Cell ◽  
The Absolute

Brief Total Synthesis of the Cell Cycle Inhibitor Tryprostatin B and Related Preparation of Its Alanine Analogue

2003 ◽  
Vol 68 (18) ◽  
pp. 6944-6951 ◽  
Author(s):  
Esmeralda Caballero ◽  
Carmen Avendaño ◽  
J. Carlos Menéndez
Keyword(s):  
Cell Cycle ◽  
Total Synthesis ◽  
Cell Cycle Inhibitor

scholarly journals Cell cycle progression in confining microenvironments is regulated by a growth-responsive TRPV4-PI3K/Akt-p27Kip1 signaling axis

2019 ◽  
Vol 5 (8) ◽  
pp. eaaw6171 ◽  
Author(s):  
Sungmin Nam ◽  
Vivek Kumar Gupta ◽  
Hong-pyo Lee ◽  
Joanna Y. Lee ◽  
Katrina M. Wisdom ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stress Relaxation ◽  
Cell Cycle Progression ◽  
Phosphatidylinositol 3 Kinase ◽  
Cycle Progression ◽  
Cell Cycle Inhibitor ◽  
Signaling Axis ◽  
A Cell ◽  
Stretch Activated Channels ◽  
Phase Entry

In tissues, cells reside in confining microenvironments, which may mechanically restrict the ability of a cell to double in size as it prepares to divide. How confinement affects cell cycle progression remains unclear. We show that cells progressed through the cell cycle and proliferated when cultured in hydrogels exhibiting fast stress relaxation but were mostly arrested in the G0/G1 phase of the cell cycle when cultured in hydrogels that exhibit slow stress relaxation. In fast-relaxing gels, activity of stretch-activated channels (SACs), including TRPV4, promotes activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, which in turn drives cytoplasmic localization of the cell cycle inhibitor p27Kip1, thereby allowing S phase entry and proliferation. Cell growth during G1 activated the TRPV4-PI3K/Akt-p27Kip1 signaling axis, but growth is inhibited in the confining slow-relaxing hydrogels. Thus, in confining microenvironments, cells sense when growth is sufficient for division to proceed through a growth-responsive signaling axis mediated by SACs.

scholarly journals p21 in Cancer Research

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1178 ◽  
Author(s):  
Shamloo ◽  
Usluer
Keyword(s):  
Cell Cycle ◽  
Cancer Research ◽  
Tumor Suppressor Function ◽  
Therapeutic Approaches ◽  
Cell Cycle Inhibitor ◽  
Cycle Arrest ◽  
Cancer Field ◽  
A Cell ◽  
P53 Status

p21 functions as a cell cycle inhibitor and anti-proliferative effector in normal cells, and is dysregulated in some cancers. Earlier observations on p21 knockout models emphasized the role of this protein in cell cycle arrest under the p53 transcription factor activity. Although tumor-suppressor function of p21 is the most studied aspect of this protein in cancer, the role of p21 in phenotypic plasticity and its oncogenic/anti-apoptotic function, depending on p21 subcellular localization and p53 status, have been under scrutiny recently. Basic science and translational studies use precision gene editing to manipulate p21 itself, and proteins that interact with it; these studies have led to regulatory/functional/drug sensitivity discoveries as well as therapeutic approaches in cancer field. In this review, we will focus on targeting p21 in cancer research and its potential in providing novel therapies.

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