scholarly journals Securin Is Not Required for Chromosomal Stability in Human Cells

PLoS Biology ◽  
2005 ◽  
Vol 3 (12) ◽  
pp. e416 ◽  
Author(s):  
Katrin Pfleghaar ◽  
Simone Heubes ◽  
Jürgen Cox ◽  
Olaf Stemmann ◽  
Michael R Speicher
Open Biology ◽  
2014 ◽  
Vol 4 (6) ◽  
pp. 130108 ◽  
Author(s):  
Roshan L. Shrestha ◽  
Naoka Tamura ◽  
Anna Fries ◽  
Nicolas Levin ◽  
Joanna Clark ◽  
...  

Chromosomal instability can arise from defects in chromosome–microtubule attachment. Using a variety of drug treatments, we show that TAO1 kinase is required for ensuring the normal congression of chromosomes. Depletion of TAO1 reduces the density of growing interphase and mitotic microtubules in human cells, showing TAO1's role in controlling microtubule dynamics. We demonstrate the aneugenic nature of chromosome–microtubule attachment defects in TAO1-depleted cells using an error-correction assay. Our model further strengthens the emerging paradigm that microtubule regulatory pathways are important for resolving erroneous kinetochore–microtubule attachments and maintaining the integrity of the genome, regardless of the spindle checkpoint status.


Cell ◽  
2001 ◽  
Vol 105 (4) ◽  
pp. 445-457 ◽  
Author(s):  
Prasad V. Jallepalli ◽  
Irene C. Waizenegger ◽  
Fred Bunz ◽  
Sabine Langer ◽  
Michael R. Speicher ◽  
...  

2002 ◽  
Vol 72 (3) ◽  
pp. 147-153 ◽  
Author(s):  
Kei-Ichi Hirai ◽  
Jie-Hong Pan ◽  
Ying-Bo Shui ◽  
Eriko Simamura ◽  
Hiroki Shimada ◽  
...  

The possible protection of cultured human cells from acute dioxin injury by antioxidants was investigated. The most potent dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), caused vacuolization of the smooth endoplasmic reticulum and Golgi apparatus in cultured human conjunctival epithelial cells and cervical cancer cells. Subsequent nuclear damage included a deep irregular indentation resulting in cell death. A dosage of 30–40 ng/mL TCDD induced maximal intracellular production of H2O2 at 30 minutes and led to severe cell death (0–31% survival) at two hours. A dose of 1.7 mM alpha-tocopherol or 1 mM L-dehydroascorbic acid significantly protected human cells against acute TCDD injuries (78–97% survivals), but vitamin C did not provide this protection. These results indicate that accidental exposure to fatal doses of TCDD causes cytoplasmic free radical production within the smooth endoplasmic reticular systems, resulting in severe cytotoxicity, and that vitamin E and dehydroascorbic acid can protect against TCDD-induced cell damage.


2003 ◽  
Vol 104 ◽  
pp. 289-292 ◽  
Author(s):  
R. Ortega ◽  
B. Fayard ◽  
M. Salomé ◽  
G. Devès ◽  
J. Susini

2004 ◽  
Vol 36 (05) ◽  
Author(s):  
U Henning ◽  
K Krieger ◽  
S Loeffler ◽  
A Klimke
Keyword(s):  

2015 ◽  
Author(s):  
Gerard Ruiz Babot ◽  
Irene Hadjidemetriou ◽  
Sharon Jane Ajodha ◽  
David Taylor ◽  
Norman Taylor ◽  
...  

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