Results 61 to 70 of about 26,734 (323)

TRIP13PCH-2 promotes Mad2 localization to unattached kinetochores in the spindle checkpoint response. [PDF]

open access: yes, 2015
The spindle checkpoint acts during cell division to prevent aneuploidy, a hallmark of cancer. During checkpoint activation, Mad1 recruits Mad2 to kinetochores to generate a signal that delays anaphase onset.
Bhalla, Needhi   +3 more
core   +1 more source

Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration

open access: yesFrontiers in Neuroscience, 2018
Tau is an essential protein that physiologically promotes the assembly and stabilization of microtubules, and participates in neuronal development, axonal transport, and neuronal polarity.
María J. Pérez   +5 more
doaj   +1 more source

Ribonucleolytic resection is required for repair of strand displaced nonhomologous end-joining intermediates [PDF]

open access: yes, 2013
Nonhomologous end-joining (NHEJ) pathways repair DNA double-strand breaks (DSBs) in eukaryotes and many prokaryotes, although it is not reported to operate in the third domain of life, archaea. Here, we describe a complete NHEJ complex, consisting of DNA
Bartlett, Edward   +2 more
core   +1 more source

OsHOP2 regulates the maturation of crossovers by promoting homologous pairing and synapsis in rice meiosis.

open access: yesNew Phytologist, 2019
Meiotic recombination is closely linked with homologous pairing and synapsis. Previous studies have shown that HOMOLOGOUS PAIRING PROTEIN2 (HOP2), plays an essential role in homologous pairing and synapsis.
Wenqing Shi   +11 more
semanticscholar   +1 more source

Apoptosis in mouse fetal and neonatal oocytes during meiotic prophase one [PDF]

open access: yes, 2007
Background The vast majority of oocytes formed in the fetal ovary do not survive beyond birth. Possible reasons for their loss include the elimination of non-viable genetic constitutions arising through meiosis, however, the ...
Ghafari , Fataneh   +2 more
core   +4 more sources

Crystal structure of Hop2-Mnd1 and mechanistic insights into its role in meiotic recombination [PDF]

open access: yes, 2015
In meiotic DNA recombination, the Hop2-Mnd1 complex promotes Dmc1-mediated single-stranded DNA (ssDNA) invasion into homologous chromosomes to form a synaptic complex by a yet-unclear mechanism.
Alexandra-Styliani Kalantzi   +66 more
core   +3 more sources

Crossover recombination and synapsis are linked by adjacent regions within the N terminus of the Zip1 synaptonemal complex protein

open access: yesbioRxiv, 2018
Accurate chromosome segregation during meiosis relies on the prior establishment of at least one crossover recombination event between homologous chromosomes, which is often associated with the meiosis-specific MutSγ complex.
K. Voelkel-Meiman   +8 more
semanticscholar   +1 more source

On the origin of trisomy 21 Down syndrome [PDF]

open access: yes, 2008
Background: Down syndrome, characterized by an extra chromosome 21 is the most common genetic cause for congenital malformations and learning disability.
Hultén, Maj A.   +6 more
core   +2 more sources

Chromosome Synapsis Alleviates Mek1-Dependent Suppression of Meiotic DNA Repair

open access: yesPLoS Biology, 2016
Faithful meiotic chromosome segregation and fertility require meiotic recombination between homologous chromosomes rather than the equally available sister chromatid, a bias that in Saccharomyces cerevisiae depends on the meiotic kinase, Mek1.
Vijayalakshmi V. Subramanian   +7 more
semanticscholar   +1 more source

SNUPN‐Related Muscular Dystrophy: Novel Phenotypic, Pathological and Functional Protein Insights

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective SNUPN‐related muscular dystrophy or LGMDR29 is a new entity that covers from a congenital or childhood onset pure muscular dystrophy to more complex phenotypes combining neurodevelopmental features, cataracts, or spinocerebellar ataxia. So far, 12 different variants have been described.
Nuria Muelas   +18 more
wiley   +1 more source

Home - About - Disclaimer - Privacy