OTUB1 triggers lung cancer development by inhibiting RAS monoubiquitination

Activation of the RAS oncogenic pathway, frequently ensuing from mutations in RAS genes, is a common event in human cancer. Recent reports demonstrate that reversible ubiquitination of RAS GTPases dramatically affects their activity, suggesting that enzymes involved in regulating RAS ubiquitination may contribute to malignant transformation. Here, we identified the de-ubiquitinase OTUB1 as a negative regulator of RAS mono- and di-ubiquitination. OTUB1 inhibits RAS ubiquitination independently of its catalytic activity resulting in sequestration of RAS on the plasma membrane. OTUB1 promotes RAS activation and tumorigenesis in wild-type RAS cells. An increase of OTUB1 expression is commonly observed in non-small-cell lung carcinomas harboring wild-type KRAS and is associated with increased levels of ERK1/2 phosphorylation, high Ki67 score, and poorer patient survival. Our results strongly indicate that dysregulation of RAS ubiquitination represents an alternative mechanism of RAS activation during lung cancer development

Nuclear suppression of heavy quark production at forward rapidities in relativistic heavy ion collisions

We calculate nuclear suppression $R_{AA}$ of heavy quarks produced from the initial fusion of partons in nucleus-nucleus collisions at RHIC and LHC energies. We take the shadowing as well as the energy loss suffered by them while passing through Quark Gluon Plasma into account. We obtain results for charm and bottom quarks at several rapidities using different mechanisms for energy loss, to see if we can distinguish between them.Comment: 21 pages including 13 figures. To appear in J. Phys.

Prevalence of Toxoplasma gondii in Belgian wildlife

De Craeye, S., Speybroeck, N., Baert, K., Ajzenberg, D., Dardé, M.L., Collinet, F., Tavernier, P., Van Gucht, S., Dorny, P., Dierick, K

OTUB1 triggers lung cancer development by inhibiting RAS monoubiquitination

Activation of the RAS oncogenic pathway, frequently ensuing from mutations in RAS genes, is a common event in human cancer. Recent reports demonstrate that reversible ubiquitination of RAS GTPases dramatically affects their activity, suggesting that enzymes involved in regulating RAS ubiquitination may contribute to malignant transformation. Here, we identified the de-ubiquitinase OTUB1 as a negative regulator of RAS mono- and di-ubiquitination. OTUB1 inhibits RAS ubiquitination independently of its catalytic activity resulting in sequestration of RAS on the plasma membrane. OTUB1 promotes RAS activation and tumorigenesis in wild-type RAS cells. An increase of OTUB1 expression is commonly observed in non-small-cell lung carcinomas harboring wild-type KRAS and is associated with increased levels of ERK1/2 phosphorylation, high Ki67 score, and poorer patient survival. Our results strongly indicate that dysregulation of RAS ubiquitination represents an alternative mechanism of RAS activation during lung cancer developmen

41 GHz and 10.6 GHz low threshold and low noise InAs/InP quantum dash two-section mode-locked lasers in L band

International audienceThis paper reports recent results on InAs/InP quantum dash-based, two-section, passively mode- locked lasers pulsing at 41 GHz and 10.6 GHz and emitting at 1.59 lm at 20°C. The 41-GHz device (1 mm long) starts lasing at 25 mA under uniform injection and the 10.6 GHz (4 mm long) at 71 mA. Their output pulses are significantly chirped. The 41-GHz laser exhibits 7 ps pulses after propagation in 60 m of a single-mode fiber. The 10.6-GHz laser generates one picosecond pulses with 545 m of a single-mode fiber. Its single side-band phase noise does not exceed -80 dBc/Hz at 100 kHz offset, leading to an average timing jitter of 800 fs

Measurements of differential and double-differential Drell-Yan cross sections in proton-proton collisions at [Formula: see text][Formula: see text].

Measurements of the differential and double-differential Drell-Yan cross sections in the dielectron and dimuon channels are presented. They are based on proton-proton collision data at [Formula: see text] recorded with the CMS detector at the LHC and corresponding to an integrated luminosity of 19.7[Formula: see text]. The measured inclusive cross section in the [Formula: see text] peak region (60-120[Formula: see text]), obtained from the combination of the dielectron and dimuon channels, is [Formula: see text], where the statistical uncertainty is negligible. The differential cross section [Formula: see text] in the dilepton mass range 15-2000[Formula: see text] is measured and corrected to the full phase space. The double-differential cross section [Formula: see text] is also measured over the mass range 20 to 1500[Formula: see text] and absolute dilepton rapidity from 0 to 2.4. In addition, the ratios of the normalized differential cross sections measured at [Formula: see text] and 8[Formula: see text] are presented. These measurements are compared to the predictions of perturbative QCD at next-to-leading and next-to-next-to-leading (NNLO) orders using various sets of parton distribution functions (PDFs). The results agree with the NNLO theoretical predictions computed with fewz 3.1 using the CT10 NNLO and NNPDF2.1 NNLO PDFs. The measured double-differential cross section and ratio of normalized differential cross sections are sufficiently precise to constrain the proton PDFs