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Bub1 is required for kinetochore localization of BubR1, Cenp-E, Cenp-F and Mad2, and chromosome congression
TLDR
It is shown that Bub1 plays a key role in the assembly of checkpoint proteins at the kinetochore, being required for the subsequent localization of Cenp-F, BubR1, Cen p-E and Mad2.
Kinetochore localisation and phosphorylation of the mitotic checkpoint components Bub1 and BubR1 are differentially regulated by spindle events in human cells.
TLDR
BUB1 and BubR1 may integrate different 'spindle assembly signals' into a single signal which can be interpreted by downstream cell cycle regulators, and are part of a common complex during mitosis.
Farnesylation of Cenp-F is required for G2/M progression and degradation after mitosis.
TLDR
Observations suggest that farnesylation of Cenp-F is required not only for its localisation to the nuclear envelope and kinetochores but also for timely progression through G2/M and its degradation after mitosis.
Silencing Cenp-F weakens centromeric cohesion, prevents chromosome alignment and activates the spindle checkpoint
TLDR
It is shown that, following repression of Cenp-F by RNA interference, the processes of metaphase chromosome alignment, anaphase chromosome segregation and cytokinesis all fail and, although kinetochores attach to microtubules in CenP-F-deficient cells, the oscillatory movements that normally occur following K-fibre formation are severely dampened.
Pediatric brain tumor cancer stem cells: cell cycle dynamics, DNA repair, and etoposide extrusion
TLDR
These cell lines and the approach taken provide a robust model system that can be used to develop the understanding of the biology of CSCs in pediatric brain tumors and other cancer types and to preclinically test therapeutic agents.
Microarray Expression Data Identify DCC as a Candidate Gene for Early Meningioma Progression
TLDR
DCC may constitute a valid biomarker to identify those benign meningiomas at risk for progression based on its expression levels, and is identified as a predicted top upstream regulators beta-estradiol, TGFB1, Tgf beta complex, LY294002, and dexamethasone.
d-&dgr;-Tocotrienol-Mediated Suppression of the Proliferation of Human PANC-1, MIA PaCa-2, and BxPC-3 Pancreatic Carcinoma Cells
TLDR
Suppression of mevalonate pathway activities, be it by modulators of HMG CoA reductase (statins, tocotrienols, and farnesol), farnesyl transferase (farnesyltransferase inhibitors), and/or mevalanate pyrophosphate decarboxylase (phenylacetate) activity, may have a potential in pancreatic cancer chemotherapy.
Chronic hypoxia promotes hypoxia-inducible factor-1α–dependent resistance to etoposide and vincristine in neuroblastoma cells
TLDR
It is suggested that prolonged hypoxia leads to resistance to clinically relevant drugs in neuroblastoma and that therapies aimed at inhibiting HIF-1α function may be useful in overcoming drug resistance in this tumor.
Mevalonate deprivation mediates the impact of lovastatin on the differentiation of murine 3T3-F442A preadipocytes
TLDR
The impact of lovastatin on intracellular triglyceride content and expression of the adipogenic genes was reversed by supplemental mevalonate, hypothesized to have essential roles in promoting adipogenic gene expression and adipocyte differentiation.
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