Results 91 to 100 of about 2,127,079 (302)

An asymptotically normal test for the selective neutrality hypothesis

open access: yes, 2008
An important parameter in the study of population evolution is $\theta=4N\nu$, where $N$ is the effective population size and $\nu$ is the rate of mutation per locus per generation. Therefore, $\theta$ represents the mean number of mutations per site per
Aluísio Pinheiro   +3 more
core   +2 more sources

Nucleotide Conformations [PDF]

open access: yesScience, 1972
S, Arnott   +4 more
openaire   +2 more sources

Genetic attenuation of ALDH1A1 increases metastatic potential and aggressiveness in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Aldehyde dehydrogenase 1A1 (ALDH1A1) is a cancer stem cell marker in several malignancies. We established a novel epithelial cell line from rectal adenocarcinoma with unique overexpression of this enzyme. Genetic attenuation of ALDH1A1 led to increased invasive capacity and metastatic potential, the inhibition of proliferation activity, and ultimately ...
Martina Poturnajova   +25 more
wiley   +1 more source

IMPDH inhibition enhances cytarabine efficacy in SAMHD1‐expressing leukaemia cells via guanine nucleotide depletion

open access: yesMolecular Oncology, EarlyView.
Cytarabine is a key therapy for acute myeloid leukaemia (AML), but its efficacy is limited by the dNTPase SAMHD1, which hydrolyses its active metabolite. Screening nucleotide biosynthesis inhibitors revealed that IMPDH inhibitors selectively sensitise SAMHD1‐proficient AML cells to cytarabine.
Miriam Yagüe‐Capilla   +9 more
wiley   +1 more source

Keratin 19 as a prognostic marker and contributing factor of metastasis and chemoresistance in high‐grade serous ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Keratin 19 (KRT19) is overexpressed in high‐grade serous ovarian cancer with high levels of Kallikrein‐related peptidases (KLK) 4–7 and is associated with poor survival. In vivo analyses demonstrate that elevated KRT19 increases peritoneal tumour burden.
Sophia Bielesch   +13 more
wiley   +1 more source

Structural basis of the allosteric trigger of the Hsp70 chaperone proteins. [PDF]

open access: yes, 2008
This work solves a decades-old dilemma that stood in the way of understanding the allosteric mechanism of Hsp70 (heat shock 70 kDa) chaperone proteins. Hsp70s are central to protein folding, refolding, and trafficking in organisms ranging from Archae to ...
Akash Bhattacharya   +4 more
core   +1 more source

Electronic signature of DNA nucleotides via transverse transport

open access: yes, 2004
We report theoretical studies of charge transport in single-stranded DNA in the direction perpendicular to the backbone axis. We find that, if the electrodes which sandwich the DNA have the appropriate spatial width, each nucleotide carries a unique ...
Di Ventra, Massimiliano, Zwolak, Michael
core   +1 more source

Somatic mutational landscape in von Hippel–Lindau familial hemangioblastoma

open access: yesMolecular Oncology, EarlyView.
The causes of central nervous system (CNS) hemangioblastoma in Von Hippel–Lindau (vHL) disease are unclear. We used Whole Exome Sequencing (WES) on familial hemangioblastoma to investigate events that underlie tumor development. Our findings suggest that VHL loss creates a permissive environment for tumor formation, while additional alterations ...
Maja Dembic   +5 more
wiley   +1 more source

Mutagenesis of the conserved 51-nucleotide region of Sindbis virus [PDF]

open access: yes, 1990
We have constructed 25 site-specific mutations in a domain of 51 nucleotides in Sindbis virus that is highly conserved among all alphaviruses sequenced to date.
Niesters, Hubert G. M.   +1 more
core  

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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