The star formation histories of dwarf galaxies in Local Group cosmological simulations

We use the apostle and Auriga cosmological simulations to study the star formation histories (SFHs) of field and satellite dwarf galaxies. Despite sizeable galaxy-to-galaxy scatter, the SFHs of apostle and Auriga dwarfs exhibit robust average trends with galaxy stellar mass: faint field dwarfs (105 < Mstar/M⊙ < 106) have, on average, steadily declining SFHs, whereas brighter dwarfs (107 < Mstar/M⊙ < 109) show the opposite trend. Intermediate-mass dwarfs have roughly constant SFHs. Satellites exhibit similar average trends, but with substantially suppressed star formation in the most recent ∼5 Gyr, likely as a result of gas loss due to tidal and ram-pressure stripping after entering the haloes of their primaries. These simple mass and environmental trends are in good agreement with the derived SFHs of Local Group (LG) dwarfs whose photometry reaches the oldest main-sequence turn-off. SFHs of galaxies with less deep data show deviations from these trends, but this may be explained, at least in part, by the large galaxy-to-galaxy scatter, the limited sample size, and the large uncertainties of the inferred SFHs. Confirming the predicted mass and environmental trends will require deeper photometric data than currently available, especially for isolated dwarfs

Erratum: Correction for Danovi et al. "Amplification of Mdmx (or Mdm4) Directly Contributes to Tumor Formation by Inhibiting p53 Tumor Suppressor Activity" (Molecular and cellular biology (2004) 24 13 (5835-5843) PII: e00150-19)

SCOPUS: er.jDecretOANoAutActifinfo:eu-repo/semantics/publishe

Amplification of Mdmx (or Mdm4) Directly Contributes to Tumor Formation by Inhibiting p53 Tumor Suppressor Activity

Human tumors are believed to harbor a disabled p53 tumor suppressor pathway, either through direct mutation of the p53 gene or through aberrant expression of proteins acting in the p53 pathway, such as p14(ARF) or Mdm2. A role for Mdmx (or Mdm4) as a key negative regulator of p53 function in vivo has been established. However, a direct contribution of Mdmx to tumor formation remains to be demonstrated. Here we show that retrovirus-mediated Mdmx overexpression allows primary mouse embryonic fibroblast immortalization and leads to neoplastic transformation in combination with HRas(V12). Furthermore, the human Mdmx ortholog, Hdmx, was found to be overexpressed in a significant percentage of various human tumors and amplified in 5% of primary breast tumors, all of which retained wild-type p53. Hdmx was also amplified and highly expressed in MCF-7, a breast cancer cell line harboring wild-type p53, and interfering RNA-mediated reduction of Hdmx markedly inhibited the growth potential of these cells in a p53-dependent manner. Together, these results make Hdmx a new putative drug target for cancer therapy