Results 151 to 160 of about 2,258 (240)

Coronal dimmings and what they tell us about solar and stellar coronal mass ejections. [PDF]

open access: yesLiving Rev Sol Phys
Veronig AM   +12 more
europepmc   +1 more source

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

open access: yesMolecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan   +16 more
wiley   +1 more source

Generation and characterization of a Cre-inducible MAP3K1 gain-of-function model. [PDF]

open access: yesDis Model Mech
Xiao B   +6 more
europepmc   +1 more source

M STARS IN THE TW HYA ASSOCIATION: STELLAR X-RAYS AND DISK DISSIPATION [PDF]

open access: green, 2016
Joel H. Kastner   +6 more
openalex   +1 more source

Heterozygous loss‐of‐function alleles associate the conserved 3′‐5′ exoribonuclease EXOSC10 with hypersensitivity to the anticancer drug 5‐fluorouracil

open access: yesMolecular Oncology, EarlyView.
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain   +10 more
wiley   +1 more source

Big-5 personality traits as predictors of allostatic load in Latino Americans: a longitudinal study. [PDF]

open access: yesJ Gerontol B Psychol Sci Soc Sci
Sevi B   +5 more
europepmc   +1 more source

Stellar Associations in the Andromeda Nebula.

open access: yesThe Astrophysical Journal Supplement Series, 1964
openaire   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

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