Rescuing stalled replication forks: MMS22L-TONSL,a novel complex for DNA replication fork repair in human cells

Comment on: Piwko W, et al. EMBO J 2010; 29:4210-22, Duro E, et al. Mol Cell 2010; 40:632–44, O’Connell BC, et al. Mol Cell 2010; 40:645–57 and O’Donnell L, et al. Mol Cell 2010; 40:619–31.     

Building a great wall around mitosis: Evolutionary conserved roles for the Greatwall/MASTL kinases in securing chromosome stability

Comment on: Voets E, et al. Cell Cycle 2010; 9:3591–3601 & Burgess A, et al. Proc Natl Acad Sci USA 2010; 107:12564–9.     

Ribosomal protein L37 and the p53 network

Comment on: Llanos S, et al. Cell Cycle 2010; 9:4005–2.     

Shifting senescence into quiescence by turning up p53

Comment on: Leontieva OV, et al. Cell Cycle 2010; 9:4323–7.     

Molecular dynamics simulations of transitions for ECD epidermal growth factor receptors show key differences between human and drosophila forms of the receptors

Recent X‐ray structural work on the Drosophila epidermal growth factor receptor (EFGR) has suggested an asymmetric dimer that rationalizes binding affinity measurements that go back decades (Alvarado et al., Cell 2010;142:568–579; Dawson et al., Structure 2007;15:942–954; Lemmon et al., Embo J 1997;16:281–294; Mattoon et al., Proc Natl Acad Sci USA 2004;101:923–928; Mayawala et al., Febs Lett 2005;579:3043–3047; Ozcan et al., Proc Natl Acad Sci USA 2006;103:5735–5740). This type of asymmetric structure has not been seen for the human EGF receptor family and it may or may not be important for function in that realm. We hypothesize that conformational changes in the Drosophila system have been optimized for the transition, whereas the barrier for the same transition is much higher in the human forms. To address our hypothesis we perform dynamic importance sampling (DIMS) (Perilla et al., J Comput Chem 2010;32:196–209) for barrier crossing transitions in both Drosophila and human EFGRs. For each set of transitions, we work from the hypothesis, based on results from the AdK system, that salt‐bridge pairs making and breaking connections are central to the conformational change. To evaluate the effectiveness of the salt‐bridges as drivers for the conformational change, we use the effective transfer entropy based on stable state MD calculations (Kamberaj and Der Vaart, Biophys J 2009;97:1747–1755) to define a reduced subset of degrees of freedom that seem to be important for driving the transition (Perilla and Woolf, J Chem Phys 2012;136:164101). Our results suggest that salt‐bridge making and breaking is not the dominant factor in driving the symmetric to asymmetric transition, but that instead it is a result of more concerted and correlated functional motions within a subset of the dimer structures. Furthermore, the analysis suggests that the set of residues involved in the transitions from the Drosophila relative to the human forms differs and that this difference in substate distributions relates to why the asymmetric form may be more common to Drosophila than to the human forms. We close with a discussion about the residues that may be changed in the human and the Drosophila forms to potentially shift the kinetics of the symmetric to asymmetric transition. Proteins 2013; 81:1113–1126. © 2013 Wiley Periodicals, Inc.     

PDK1-driven Myc signaling regulates cellular response to mTOR inhibitors

Comment on: Tan J, et al. Cancer Cell 2010; 18:459-71     

In the right place at the right time: Analysis of p53 serine 312 phosphorylation in vivo

Comment on: Slee EA, et al. Proc Natl Acad Sci USA 2010; 107:19479–84.     

Epstein-Barr virus DNA XII. A variable region of the Epstein-Barr virus genome is included in the P3HR-1 deletion.

The P3HR-1 subclone of Jijoye differs from Jijoye and from other Epstein-Barr virus (EBV)-infected cell lines in that the virus produced by P3HR-1 cultures lacks the ability to growth-transform normal B lymphocytes (Heston et al., Nature (London) 295:160-163, 1982; Miller et al., J. Virol. 18:1071-1080, 1976; Miller et al., Proc. Natl. Acad. Sci. U.S.A. 71:4006-4010, 1974; Ragona et al., Virology 101:553-557, 1980). The P3HR-1 virus was known to be deleted for a region which encodes RNA in latently infected, growth-transformed cells (Bornkamm et al., J. Virol. 35:603-618, 1980; Heller et al., J. Virol. 38:632-648, 1981; King et al., J. Virol. 36:506-518, 1980; Raab-Traub et al., J. Virol. 27:388-398, 1978; van Santen et al., Proc. Natl. Acad. Sci. U.S.A. 78:1930-1934, 1980). This deletion is now more precisely defined. The P3HR-1 genome contains less than 170 base pairs (and possibly none) of the 3,300-base pair U2 region of EBV DNA and is also lacking IR2 (a 123-base pair repeat which is the right boundary of U2). A surprising finding is that EBV isolates vary in part of the U2 region. Two transforming EB viruses, AG876 and Jijoye, are deleted for part of the U2 region including most or all of a fragment, HinfI-c, which encodes part of one of the three more abundant cytoplasmic polyadenylated RNAs of growth-transformed cells (King et al., J. Virol. 36:506-518, 1980; King et al., J. Virol. 38:649-660, 1981; van Santen et al., Proc. Natl. Acad. Sci. U.S.A. 78:1930-1934).     

p16Ink4A,not only a G1 inhibitor?

Comment on: Chien WW, et al. Cell Cycle 2010; 9:3286-96.     

Skirmish between the mighty p53 protein and the complex retrovirus HIV-1

Comment on: Mukerjee R, et al. Cell Cycle 2010; 9(22):in press.     

Regulation of vitamin metabolism by p53 and p63 in development and cancer

Comment on: Kirschner KR, et al. Cell Cycle 2010; 9:2177-88.     

Hedgehog signaling in T-cell development: A non-redundant role for Gli1

Comment on: Drakopoulou E, et al. Cell Cycle 2010; 9:4144–52.     

A combination of 1α,25-dihydroxyvitamin D3, a plant-derived antioxidant and an inhibitor of the Cot1/Tlp2 oncogene as molecularly targeted weapons in the hematologist’s battle against acute myeloid leukemias

Comment on: Wang X, et al. Cell Cycle 2010; 9:4542–51.     

Dancing with p53: The role of p38MAPK in mitosis of p53-deficient tetraploid cells

Comment on: Vitale I, et al. Cell Cycle 2010; 9:2823-9.     

A spotlight on regulatory networks connecting EMT and cancer stem cells

Comment on: Fuxe, J, et al. Cell Cycle 2010; 9:2363-74.     

TRPM7 and magnesium,metabolism, mitosis: An old path with new pebbles

Comment on: Sahni J, et al. Cell Cycle 2010; 9:3565-74.     

p38α as an inducer of aneuploidy in p53-/- tetraploid cells

Comment on: Vitale I, et al. Cell Cycle 2010; 9:2823-9.     

A natural oocyte component required for the reprogramming of somatic cell nuclei

Comment on: Jullien J, et al. Proc Natl Acad Sci USA 2010; 107:5483-8.