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- Quintana-Lacaci, Guillermo, et al.
(författare)
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Hints of the Existence of C-rich Massive Evolved Stars
- 2019
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Ingår i: Astrophysical Journal. - : American Astronomical Society. - 1538-4357 .- 0004-637X. ; 876:2
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Tidskriftsartikel (refereegranskat)abstract
- We aim to study the properties of a particular type of evolved stars, C-rich evolved stars with high expansion velocities. For this purpose we have focused on the two best studied objects within this group, IRC+10401 and AFGL 2233. We focused on determining their luminosity by studying their spectral energy distribution. Also, we have obtained single-dish line profiles and interferometric maps of the CO J - 1-0 and J = 2-1. emission lines for both objects. We have modeled this emission using a LVG radiative transfer code to determine the kinetic temperature and density profiles of the gas ejected by these stars. We have found that the luminosities obtained for these objects (log(L/L-circle dot). =. 4.1 and 5.4) locate them in the domain of the massive asymptotic giant branch stars (AGBs) and the red supergiant stars (RSGs). In addition, the mass-loss rates obtained (1.5. x. 10(-5)-6. x 10(-3)M(circle dot) yr(-1)) suggest that while IRC+ 10401 might be an AGB star, AFGL 2233 could be an RSG star. All these results, together with those from previous works, suggest that both objects are massive objects, IRC+10401 a massive evolved star with M-init similar to 5-9M(circle dot). which could correspond to an AGB or an RSG and AFGL 2233 an RSG with M-init similar to 20M(circle dot), which would confirm the existence of massive C-rich evolved stars. Two scenarios are proposed to form these types of objects. The first one is capable of producing high-mass AGB stars up to similar to 8M(circle dot). and the second one is capable of forming C-rich RSGs like AFGL 2233.
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| 2. |
- Sánchez, Arancha, et al.
(författare)
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Replication fork collapse and genome instability in dCMP deaminase mutant
- 2012
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Ingår i: Molecular and Cellular Biology. - Washington : American Society Microbiology. - 0270-7306 .- 1098-5549. ; 32:21, s. 4445-4454
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Tidskriftsartikel (refereegranskat)abstract
- Ribonucleotide reductase (RNR) and deoxycytidylate deaminase (dCMP deaminase) are pivotal allosteric enzymes required to maintain adequate pools of deoxyribonucleoside triphosphates (dNTPs) for DNA synthesis and repair. Whereas RNR inhibition slows DNA replication and activates checkpoint responses, the effect of dCMP deaminase deficiency is largely unknown. Here, we report that deleting the Schizosaccharomyces pombe dcd1(+) dCMP deaminase gene (SPBC2G2.13c) increases dCTP ∼30-fold and decreases dTTP ∼4-fold. In contrast to the robust growth of a Saccharomyces cerevisiae dcd1Δ mutant, fission yeast dcd1Δ cells delay cell cycle progression in early S phase and are sensitive to multiple DNA damaging agents, indicating impaired DNA replication and repair. DNA content profiling of dcd1Δcells differs from an RNR-deficient mutant. Dcd1 deficiency activates genome integrity checkpoints enforced by Rad3 (ATR), Cds1 (Chk2) and Chk1, and creates critical requirements for proteins involved in recovery from replication fork collapse, including the γH2AX-binding protein Brc1 and Mus81 Holliday junction resolvase. These effects correlate with increased nuclear foci of the single-stranded DNA binding protein RPA and the homologous recombination repair protein Rad52. Moreover, Brc1 suppresses spontaneous mutagenesis in dcd1Δ cells. We propose that replication forks stall and collapse in dcd1Δ cells, burdening DNA damage and checkpoint responses to maintain genome integrity.
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